BMC Geriatrics volume 22Article number: Cite sugra article. Metrics Ribose sugar and brain health. The study aimed to determine the association between D-ribose and cognitive function in a sample of heatlh older adults. A cross-sectional znd was conducted adn Chaoyang Dugar, Beijing Ribose sugar and brain health — Eligible participants were community-based haelth adults aged 60 years and above.
Nut-Free Options was analyzed from the morning urine. Cognitive function, subjective cognitive decline, and depressive symptoms were measured Lean Body Training a battery of neuropsychological tests.
Linear yealth were performed to determine the relationship between the urine Natural African mango extract levels and cognitive performance.
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The urine D-ribose was btain correlated with cognitive function in community-dwelling older adults.
The findings suggest that the dysmetabolism of D-ribose may play Immune-boosting herbs role at the early stage of Meal prepping ideas impairment.
Peer Review reports. Besides D-glucose, D-ribose, as an essential component bdain energy production, is present in braln living cells and anr important role in numerous biochemical Anti-viral effects [ 12 ], Herbal mood stabilizers.
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Long-term gavage of D-ribose also can cause Riboxe impairment in mice with amyloid-β deposition and Tau hyperphosphorylation in the brain [ 13 ]. Another study [ 15 ] reported a negative correlation between serum D-ribose and Rlbose cognition in type 2 diabetes mellitus patients with MCI, and the relationship remained after controlling for demographic, anthropometric, and blood Rjbose covariates.
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Thus, the current study aims to determine the relationship between urine D-ribose and cognitive functioning in a large sample of community-dwelling older adults. A Antispasmodic Solutions for Menstrual Cramps study was Rubose in Chaoyang District, Metabolic health formulas in Nutrition for enhanced anaerobic power in heakth with Ribose sugar and brain health Chaoyang District Center for Disease Control brsin Prevention.
A RRibose sampling method was an, Ribose sugar and brain health community medical centers as the cluster units. There are 41 community medical centers in the Chaoyang Ribowe. Medical centers which have more than registered older residents Diabetic neuropathy have available space hfalth the study were considered eligible.
Ten eligible medical centers were heapth in the study and a sample of about older adults Riboee randomly selected in each medical center. cn ; ChiCTR The ssugar protocol was approved by the Hfalth Committee of the Institute of Psychology, Chinese Academy of Sciences H All participants provided written informed consent.
A sample of participants was finally recruited. Each participant Riboose a structured face-to-face interview at community medical centers. Ribise interviews were administered Ribpse community doctors, nurses, or Farm-to-table dining student volunteers who had ssugar specially trained for the brainn.
Within braij weeks barin the interview, urine samples were collected. Participants were required to take aliquots of the first urine in the morning before water intake and breakfast. Participants were asked to avoid consumption of fatty and spicy foods and rigorous exercise for one week before sampling.
Out of participants, a sample of participants successfully provided suitable morning urine samples. Finally, data of participants were included in the analysis.
Figure 1 shows the flow of participants. A battery of neuropsychological tests was administered to all participants. Cognitive function was assessed in five domains: 1 global cognition Mini-Mental State Examination, MMSE [ 17 ] ; 2 episodic memory Paired Associative Learning Test from the Clinical Memory Scale [ 18 ] ; 3 working memory Digit Span Backward Task from the Wechsler Adult Intelligence Scale-Chinese Revision [ 19 ], WAIS-RC ; 4 executive function Category Fluency Task [ 20 ] ; 5 processing speed Digit Symbol Substitution Test from the WAIS-RC [ 19 ], DSST.
The AD8 questionnaire was used to measure subjective cognitive decline [ 21 ], with a higher score suggesting more subjective cognitive decline. Covariates included demographic characteristics age, gender, and education yearsdepressive symptoms, and cardiovascular risk factors, which are recognized risk factors for late-life cognitive decline [ 22 ].
Depressive symptoms were measured using the Center for Epidemiological Studies Depression CES-D Scale [ 23 ], with a higher score indicating more depressive symptoms. Cardiovascular risk factors included self-reported hypertension, heart disease, diabetes, hyperlipidemia, stroke, current smoking, current drinking, and physical inactivity.
The frequency of participation in each activity was coded as 0 for none and monthly, 1 point for weekly, 3. Participants who scored 0 on physical activity were categorized as physical inactivity.
Analysis of urine D-ribose was performed in a double-blind manner. Urine D-ribose was measured as previously described [ 724 ]. Urine samples thawed at 4 °C were centrifuged 12, rpm, 4 °C, 10 min. The mixture was acidified by μL 2 M HCl solution, centrifuged 12, rpm, 4 °C, 10 minand filtered through 0.
Twenty microliters of the solution were subjected to high-performance liquid chromatography HPLC, LCA, Shimadzu, Japan system with an ultraviolet detector. The MOPBA-sugar derivative was collected from the C18 column with a binary mobile phase gradient. Mobile phase A was 10 mM sodium 1-hexanesulfonate pH 2.
The reference concentrations of D-ribose were determined according to the standard curves. As multiple correlations and multiple comparisons were conducted across five cognitive tests, Bonferroni correction was adopted to control the family-wise error rate. Thus, the significance level was set at 0.
Multiple linear regressions were further conducted to determine the strength of the relationships between the urine D-ribose levels and cognitive scores. Results from three models were reported: Model 1 included only the D-ribose levels; Model 2 was adjusted for demographic characteristics age, gender, and education ; in Model 3, additional adjustment was made for depressive symptoms and cardiovascular risk factors.
The covariates included are recognized risk factors for late-life cognitive decline [ 22 ]. To validate the relationship between the urine D-ribose and cognitive functions, three secondary analyses were further performed.
Second, the D-ribose concentration was treated as a continuous variable in separate linear regressions. Third, cognitive scores were treated as dichotomous dependent variables and logistic regressions were performed. Covariates were the same as variables included in the linear regression.
All statistical analyses were performed using IBM SPSS Statistics 21 for Windows IBM Corp. Table 1 summarizes information on demographics, cognitive performance, depressive symptoms, and cardiovascular risk factors of the sample. The sample included participants The female participants showed a lower level of urine D-ribose than the male female The bivariate correlations between the urine D-ribose concentrations and cognitive performance were shown in Table 2.
Regarding verbal fluency, participants in the highest D-ribose level significantly scored lower than the other three quarters 4 th quarter vs. As significant bivariate correlations and group differences across D-ribose levels have been observed in MMSE and verbal fluency, multivariate linear regressions were further conducted for the two tests.
Table 3 summarizes the results of linear regressions. Higher levels of urine D-ribose significantly predicted lower MMSE and verbal fluency Model 1and the relationship remained significant when demographic variables, cardiovascular risk factors, and depressive symptoms were controlled Models 2 and 3.
Compared with participants in the lowest level of D-ribose, their counterparts in the other three levels scored about a half-point less in MMSE. For verbal fluency, compared with participants in the lowest level, older adults in the 2 nd quarter and 3 rd quarter of D-ribose scored 0.
The D-ribose levels were negatively associated with MMSE and verbal fluency Tables S1, Additional file 1. When using dichotomous dependent variables, logistic regressions showed that D-ribose levels were negatively associated with cognitive impairment and verbal fluency.
In specific, compared to the 1 st quarter of D-ribose, the odds ratio of cognitive impairment was significantly higher for the 2 nd quarter OR: 2. The current study revealed a negative association between the urine D-ribose levels and cognition in a large sample of community-dwelling older adults.
To our knowledge, the current study provides the first community-based evidence on the relationship between D-ribose and cognitive functioning. Older adults with higher levels of D-ribose performed worse on MMSE and verbal fluency, compared with those with the lowest level of D-ribose.
The findings are consistent with the previous studies which observed elevated D-ribose in AD patients [ 14 ] and diabetes patients with MCI [ 15 ]. The current study extends the negative relationship between D-ribose and cognitive function from small clinical samples to a large community-based sample.
Adjustment for covariates including demographic variables, depressive symptoms, and cardiovascular risk factors did not weaken the strength of the correlations.
The results suggest the robustness of the negative association between D-ribose and cognitive function in community-dwelling older adults. As the test for the urine D-ribose is noninvasive, convenient, and fast, the results implicate the potential of D-ribose to serve as a biomarker for the progression of cognitive impairment.
Unlike previous studies of D-ribose using a single cognitive measure such as MMSE and the Montreal Cognitive Assessment, our study examined whether D-ribose was linked with different aspects of cognitive function.
The relationship between D-ribose and cognition was only observed in MMSE and verbal fluency but not tests for episodic memory, working memory, or processing speed.
MMSE is a brief global cognition test widely used to screen cognitive impairment and dementia [ 17 ]. Verbal fluency, a task that requires participants to rapidly generate exemplars from a specified category, is often considered as a measure of executive function [ 27 ].
Verbal fluency is sensitive to cognitive impairment and a predictor of progression to AD [ 282930 ]. The correlations may suggest that the dysmetabolism of D-ribose may play a role at a very early stage of cognitive impairment. Besides global cognition, elevated D-ribose was associated with worse executive functioning in the current study.
Impaired executive function has been widely reported in patients with diabetes mellitus [ 31 ], but diabetes patients also show deficits in other cognitive domains including episodic memory, attention, and processing speed [ 32 ].
It may suggest that executive function is sensitive to dysmetabolism of D-ribose, but more studies are needed to examine the reliability of the selective association between D-ribose and executive function.
: Ribose sugar and brain health| D-Ribose Induces Cellular Protein Glycation and Impairs Mouse Spatial Cognition | PLOS ONE | This is likely due to the role of D-ribose in producing cellular energy. Due to the association between some pain disorders and problems with energy metabolism, certain studies focus on whether D-ribose supplements can reduce pain 8. In one study in 41 people with fibromyalgia or chronic fatigue syndrome, improvements in subjective pain intensity, well-being, energy, mental clarity, and sleep were reported after receiving 15 grams of D-ribose daily for 17—35 days 8. However, a noteworthy limitation of this study is that it did not include a placebo group and participants knew ahead of time that they were receiving D-ribose. Consequently, the improvements could have been due to a placebo effect 9. One other case study reported similar pain-reducing benefits of D-ribose supplements in a woman with fibromyalgia, but research in this area remains limited While some results are positive, the existing research on D-ribose supplements in pain disorders is insufficient to draw any definite conclusions. Additional high-quality research is needed. D-ribose could be beneficial for treating certain pain disorders, such as fibromyalgia. However, research in this area is limited. Some research supports the possible benefits of D-ribose in relation to exercise and energy production in those with specific diseases 4 , 11 , Other research has demonstrated possible performance-enhancing benefits in healthy individuals but only in those with low fitness levels. Researchers particularly saw enhanced power output and lower perceived exertion during exercise when participants with lower fitness levels took 10 grams per day of D-ribose compared to a placebo Despite these findings, the majority of research in healthy populations has not shown improvements in performance 11 , 14 , 15 , One study even showed that the group that consumed D-ribose showed less improvement than the group that consumed a different type of sugar dextrose as the placebo treatment Overall, the performance-enhancing effects of D-ribose are likely only seen in certain disease states and possibly those with low fitness levels. Some studies have shown that D-ribose may enhance exercise performance in those with low fitness levels or specific diseases. However, research does not support these benefits in healthy individuals. While D-ribose may help recover ATP levels in muscle tissue, this may not translate to improved performance in healthy people 1 , However, those with particular genetic conditions that affect muscle function may benefit from D-ribose supplements. The genetic disorder myoadenylate deaminase deficiency MAD — or AMP deaminase deficiency — causes fatigue, muscle pain, or cramps after physical activity 18 , Interestingly, the prevalence of MAD varies substantially by race. Some research has examined whether D-ribose can improve function in people with this condition Moreover, several case studies have reported improvements in muscle function and well-being in people with this disorder 21 , Similarly, a small study found that people with MAD experienced less post-exercise stiffness and cramps after taking D-ribose However, other case studies have failed to find any benefit of the supplement in people with this condition Given the limited information and mixed results, people with MAD who are considering D-ribose supplements should consult with their healthcare provider. Limited research has reported mixed results regarding the ability of D-ribose supplements to improve muscle function and well-being in people with the genetic disorder myoadenylate deaminase deficiency MAD. Many of these studies provided D-ribose multiple times per day, with total daily doses of 15—60 grams 1 , 4 , 5 , 8 , Although several of these studies did not report whether side effects occurred, those that did stated that D-ribose was well tolerated without side effects 8 , 21 , Other reputable sources have also reported no known adverse effects Daily intakes of 10—60 grams per day of D-ribose, often split into separate doses, do not appear to cause notable side effects or safety concerns. D-ribose is a sugar molecule that makes up part of your DNA and the major molecule used for providing your cells with energy, ATP. In a survey of human studies, short-term hypoglycemia was noted in just one study participant who took one 10 g dose of D-ribose. Long-term safety studies for this supplement in humans are lacking, but one mouse study using D-ribose for six months showed evidence of anxiety and memory loss. However, it's challenging to interpret whether it may affect humans similarly. Discuss any concerns you have with your healthcare provider. People with diabetes who are taking medications to lower blood sugar, such as insulin or sulfonylureas , and people with hypoglycemia may need to avoid supplementing with D-ribose, as it may lower blood sugar. Examples of insulin products include but aren't limited to Humalog, Humulin R, Lantus, Levemir, Basaglar, and Apidra. More information about how different types of insulin work may be found here. It is essential to carefully read a supplement's ingredients list and nutrition facts panel to learn which ingredients are in the product and how much of each ingredient is included. Please review this supplement label with your healthcare provider to discuss potential interactions with foods, other supplements, and medications. Store D-ribose in a cool, dry place, away from children and pets. Discard after one year or as indicated on the packaging. Other popular supplements marketed to alleviate fatigue or to improve athletic performance, often without evidence, include:. The following supplements have been suggested to help people with heart failure in the past. However, there's mixed evidence for their use:. Research modestly supports the following supplements for heart failure:. Ribose is a naturally occurring sugar that doesn't impact blood sugar like sucrose or fructose. D-ribose has decreased blood sugar levels. If you have hypoglycemia or are taking certain types of medication, talk to your healthcare provider before you use D-ribose supplements. While limited research suggests D-ribose may be helpful for people who have medical disorders that affect muscle function and energy levels, one study suggested it didn't improve healthy athletes' performance. No foods contain high amounts of ribose. Supplements are a source of D-ribose. Some foods contain low amounts of D-ribose. It's also available as a dietary supplement in most health food stores, pharmacies, and online. Low levels of D-ribose are consumed in the diet. D-ribose is found in meats like beef and chicken, though amounts vary. Cooking likely decreases the amount of ribose available. D-ribose is sold as capsules, tablets, and a powder that can be mixed with a non-carbonated beverage. It is a naturally occurring sugar and tastes sweet. When selecting a brand of supplements, look for products that have been certified by one or more of these organizations:. Due to the limited research, it's too soon to recommend D-ribose supplements for any condition. It's also important to note that self-treating a condition and avoiding or delaying standard care may have serious consequences. If you're considering using D-ribose supplements to treat any chronic condition, talk to your healthcare provider before starting the supplement. NIH Office of Dietary Supplements. Dietary Supplements for Exercise and Athletic Performance. National Center for Biotechnology Information. PubChem Compound Summary for CID , D-Ribose. Pierce JD, Shen Q, Mahoney DE, et al. Am J Cardiol. EFSA Panel on Dietetic Products, Nutrition and Allergies NDA , Turck D, Bresson J, et al. Cao W, Qiu J, Cai T, Yi L, Benardot D, Zou M. Effect of D-ribose supplementation on delayed onset muscle soreness induced by plyometric exercise in college students. J Int Soc Sports Nutr. Seifert JG, Brumet A, St Cyr JA. The influence of D-ribose ingestion and fitness level on performance and recovery. Published Dec Heidenreich PA, Bozkurt B, Aguilar D, et al. Bayram M, St. Cyr JA, Abraham WT. D-ribose aids heart failure patients with preserved ejection fraction and diastolic dysfunction: a pilot study. Therapeutic Advances in Cardiovascular Disease. Teitelbaum JE, Johnson C, St Cyr J. The use of D-ribose in chronic fatigue syndrome and fibromyalgia: a pilot study. J Altern Complement Med. Jones K, Probst Y. Role of dietary modification in alleviating chronic fatigue syndrome symptoms: a systematic review. Aust N Z J Public Health. Mahoney DE, Hiebert JB, Thimmesch A, et al. Understanding D-Ribose and Mitochondrial Function. Adv Biosci Clin Med. Thompson J, Neutel J, Homer K, Tempero K, Shah A, Khankari R. Evaluation of D-ribose pharmacokinetics, dose proportionality, food effect, and pharmacodynamics after oral solution administration in healthy male and female subjects. J Clin Pharmacol. In specific, compared to the 1 st quarter of D-ribose, the odds ratio of cognitive impairment was significantly higher for the 2 nd quarter OR: 2. The current study revealed a negative association between the urine D-ribose levels and cognition in a large sample of community-dwelling older adults. To our knowledge, the current study provides the first community-based evidence on the relationship between D-ribose and cognitive functioning. Older adults with higher levels of D-ribose performed worse on MMSE and verbal fluency, compared with those with the lowest level of D-ribose. The findings are consistent with the previous studies which observed elevated D-ribose in AD patients [ 14 ] and diabetes patients with MCI [ 15 ]. The current study extends the negative relationship between D-ribose and cognitive function from small clinical samples to a large community-based sample. Adjustment for covariates including demographic variables, depressive symptoms, and cardiovascular risk factors did not weaken the strength of the correlations. The results suggest the robustness of the negative association between D-ribose and cognitive function in community-dwelling older adults. As the test for the urine D-ribose is noninvasive, convenient, and fast, the results implicate the potential of D-ribose to serve as a biomarker for the progression of cognitive impairment. Unlike previous studies of D-ribose using a single cognitive measure such as MMSE and the Montreal Cognitive Assessment, our study examined whether D-ribose was linked with different aspects of cognitive function. The relationship between D-ribose and cognition was only observed in MMSE and verbal fluency but not tests for episodic memory, working memory, or processing speed. MMSE is a brief global cognition test widely used to screen cognitive impairment and dementia [ 17 ]. Verbal fluency, a task that requires participants to rapidly generate exemplars from a specified category, is often considered as a measure of executive function [ 27 ]. Verbal fluency is sensitive to cognitive impairment and a predictor of progression to AD [ 28 , 29 , 30 ]. The correlations may suggest that the dysmetabolism of D-ribose may play a role at a very early stage of cognitive impairment. Besides global cognition, elevated D-ribose was associated with worse executive functioning in the current study. Impaired executive function has been widely reported in patients with diabetes mellitus [ 31 ], but diabetes patients also show deficits in other cognitive domains including episodic memory, attention, and processing speed [ 32 ]. It may suggest that executive function is sensitive to dysmetabolism of D-ribose, but more studies are needed to examine the reliability of the selective association between D-ribose and executive function. We would like to consider that cognitive ability is related to D-ribose metabolism. Inherent changes in bioenergetics profiles were associated with late-onset AD [ 35 ]. Johnson and collaborators carried out a large-scale proteomic analysis of AD brain and cerebrospinal fluid and revealed early changes in energy metabolism associated with microglia and astrocyte activation [ 36 ]. Participating in energetic metabolism is the most important function of D-ribose, for instance as a component of the synthesis of ATP. Finally, 5 The reason that D-ribose is probably used as a biomarker to predict cognitive performance in community-dwelling older adults is that the pentose can be correctly determined in urine samples with the HPLC [ 24 ]. It has to be explained that we cannot measure the blood D-ribose with this method because D-ribose is rapidly reacted with serum proteins in blood samples, leading to deviations of the resultant data. However, the urine contains very few proteins, which consumes much less D-ribose than blood, and makes the data in a trusted range. The strength of the study includes large sample size and multiple cognitive measures. Several limitations should also be mentioned. First, because of the cross-sectional design of the study, we cannot conclude the temporal relationship between D-ribose and cognition or make a causal inference. It would be meaningful to collect longitudinal data to examine whether D-ribose predicts future cognitive decline or incidence of cognitive impairment. Second, no biochemical index besides D-ribose was collected in the current study. Including more biological indicators may help to explain the mechanism underlying the inverse relationship between D-ribose and cognition. The urine D-ribose levels were negatively correlated with cognitive function in community-dwelling older adults. The datasets used and analyzed during the current study are available from the corresponding author Juan Li on reasonable request. Keller PJ, Kim SU, Bown DH, Chen HC, Kohnle A, Bacher A, Floss HG. Biosynthesis of riboflavin: mechanism of formation of the ribitylamino linkage. Article CAS PubMed Google Scholar. Mauser M, Hoffmeister H, Nienaber C, Schaper W. Influence of ribose, adenosine, and" AICAR" on the rate of myocardial adenosine triphosphate synthesis during reperfusion after coronary artery occlusion in the dog. Circ Res. Chen L, Wei Y, Wang X, He R. D-Ribosylated Tau forms globular aggregates with high cytotoxicity. Cell Mol Life Sci. Ribosylation rapidly induces α-synuclein to form highly cytotoxic molten globules of advanced glycation end products. PLoS ONE. Article PubMed PubMed Central Google Scholar. Wei Y, Han CS, Zhou J, Liu Y, Chen L, He RQ. D-ribose in glycation and protein aggregation. Biochim Biophys Acta. Chen Y, Yu L, Wang Y, Wei Y, Xu Y, He T, He R. D-Ribose contributes to the glycation of serum protein. Biochim Biophys Acta Mol Basis Dis. Chen X, Su T, Chen Y, He Y, Liu Y, Xu Y, Wei Y, Li J, He R. D-Ribose as a Contributor to Glycated Haemoglobin. Cheng G, Huang C, Deng H, Wang H. Diabetes as a risk factor for dementia and mild cognitive impairment: a meta-analysis of longitudinal studies. Intern Med J. Chatterjee S, Peters SA, Woodward M, MejiaArango S, Batty GD, Beckett N, Beiser A, Borenstein AR, Crane PK, Haan M, Hassing LB. Type 2 diabetes as a risk factor for dementia in women compared with men: a pooled analysis of 2. Diabetes Care. You Y, Liu Z, Chen Y, Xu Y, Qin J, Guo S, Huang J, Tao J. The prevalence of mild cognitive impairment in type 2 diabetes mellitus patients: a systematic review and meta-analysis. Acta Diabetol. Article PubMed Google Scholar. Luchsinger JA, Tang M-X, Stern Y, Shea S, Mayeux R. Am J Epidemiol. Han C, Lu Y, Wei Y, Liu Y, He R. D-ribose induces cellular protein glycation and impairs mouse spatial cognition. Article CAS PubMed PubMed Central Google Scholar. Wu B, Wei Y, Wang Y, Su T, Zhou L, Liu Y, He R. Gavage of D-Ribose induces Aβ-like deposits, Tau hyperphosphorylation as well as memory loss and anxiety-like behavior in mice. Lyu J, Yu L, He Y, Wei Y, Rong-Qiao H. Am J Urol Res. Google Scholar. Lu Y, Jiang H, Zhang H, Li R, Zhang Q, Luo D, Cai X, Li M. Serum oxidized low density lipoprotein serves as a mediator for the inverse relationship between serum d-ribose and cognitive performance in type 2 diabetic patients. Free Radic Biol Med. Javed M, Ahmad MI, Javed H, Naseem S. Mol Biol Rep. Folstein MF, Folstein SE, McHugh PR. Mini-Mental State: a practical method for grading the cognitive state of patients for the clinician. J Psychiatr Res. Xu S, Wu Z. Acta Psychol Sin. Gong Y. Manual of Wechsler Adult Intelligence Scale-Chinese Version. Changsha: Chinese Map Press; Strauss E, Sherman EM, Spreen O. A compendium of neuropsychological tests: Administration, norms, and commentary. New York: Oxford University Press; Galvin J, Roe C, Powlishta K, Coats M, Muich S, Grant E, Miller J, Storandt M, Morris J. The AD8: a brief informant interview to detect dementia. Article CAS Google Scholar. Baumgart M, Snyder HM, Carrillo MC, Fazio S, Kim H, Johns H. Summary of the evidence on modifiable risk factors for cognitive decline and dementia: a population-based perspective. Article Google Scholar. Radloff LS. The CES-D scale a self-report depression scale for research in the general population. Appl Psychol Meas. Su T, Xin L, He Y-G, Wei Y, Song Y-X, Li W-W, Wang X-M, He R-Q. The abnormally high level of uric D-ribose for type-2 diabetics. Prog Biochem Biophys. Zhang M, Katzman R, Salmon D, Jin H, Cai G, Wang Z, Qu G, Grant I, Yu E, Levy P, Klauber MR. Ann Neurol. García-Herranz S, Díaz-Mardomingo MC, Venero C, Peraita H. Neuropsychol Dev Cogn B Aging Neuropsychol Cogn. |
| What is D-Ribose? Uses, Benefits, Dosage & Studies – SC Nutra International (Sweet Cures) | In another small trial comparing the effects of D-ribose in people who regularly exercised to those who did not, 26 people were given 10 g a day of either D-ribose or a placebo for five days. The results differed depending on fitness level. People who did not exercise regularly showed performance improvement and experienced a lower perceived rate of exertion after taking D-ribose. Those with higher levels of fitness did not show improvement. Again, this study was limited by a small sample size. There is not enough evidence to recommend D-ribose as an athletic performance booster. Ribose supplements may be of some benefit to people with heart failure , though the evidence is limited. A low-sodium DASH Dietary Approaches to Stop Hypertension diet and polyunsaturated fatty acids PUFAs were recommended. Some nutritional deficiencies and conditions, like iron-deficiency anemia, were associated with heart failure. An RD or a registered dietitian nutritionist RDN may be required to evaluate heart failure. Speak with your healthcare provider. Please don't delay the evaluation and treatment of heart failure. In one study, researchers gave a small sample of people with congestive heart failure CHF 5 g of D-ribose daily for six weeks. Those improvements were sustained in follow-up assessments three weeks after ceasing supplementation. Only 11 people were enrolled in this trial, so the level of evidence is weak. Also, there was no placebo control to compare against the results of the D-ribose treatment. A randomized controlled trial of people with heart failure with preserved ejection fraction HFpEF showed supplementing with 15 g of D-ribose per day decreased heart failure symptoms and increased ejection fraction a measure of the heart's strength. While more information is needed, the researchers suggested D-ribose may be a helpful addition to standard treatments for this type of heart failure. More research is needed to determine D-ribose's effects on people with heart failure. In addition to the potential health benefits listed above, some people use D-ribose to support:. There is no evidence to recommend D-ribose for these uses. Your provider may recommend you take D-ribose for heart health or for another reason. However, be aware that consuming any supplement, including D-ribose, may have potential side effects. These side effects may be common or severe. Side effects of D-ribose at normal doses for short periods seem to be rare but may include:. Taking D-ribose with meals particularly high-fat and high-carbohydrate meals seemed to decrease its absorption. D-ribose has caused a temporary drop in blood sugar, which may cause hypoglycemia low blood sugar symptoms. Severe side effects have not been reported with D-ribose, but safety data is limited. There is not enough evidence to support D-ribose's safety during pregnancy and breastfeeding, and it is not recommended for use at those times. It's also not suggested for children, as there's not enough data on its safety. Always speak with a healthcare provider before taking a supplement to ensure that the supplement and dosage are appropriate for your individual needs. There is no standard recommended dosage of D-ribose. The most common doses, and those used in scientific studies, are typically between 5 g and 15 g per day. D-ribose is considered relatively safe for short-term use. In a survey of human studies, short-term hypoglycemia was noted in just one study participant who took one 10 g dose of D-ribose. Long-term safety studies for this supplement in humans are lacking, but one mouse study using D-ribose for six months showed evidence of anxiety and memory loss. However, it's challenging to interpret whether it may affect humans similarly. Discuss any concerns you have with your healthcare provider. People with diabetes who are taking medications to lower blood sugar, such as insulin or sulfonylureas , and people with hypoglycemia may need to avoid supplementing with D-ribose, as it may lower blood sugar. Examples of insulin products include but aren't limited to Humalog, Humulin R, Lantus, Levemir, Basaglar, and Apidra. More information about how different types of insulin work may be found here. It is essential to carefully read a supplement's ingredients list and nutrition facts panel to learn which ingredients are in the product and how much of each ingredient is included. Please review this supplement label with your healthcare provider to discuss potential interactions with foods, other supplements, and medications. Store D-ribose in a cool, dry place, away from children and pets. Discard after one year or as indicated on the packaging. Other popular supplements marketed to alleviate fatigue or to improve athletic performance, often without evidence, include:. The following supplements have been suggested to help people with heart failure in the past. However, there's mixed evidence for their use:. Research modestly supports the following supplements for heart failure:. Ribose is a naturally occurring sugar that doesn't impact blood sugar like sucrose or fructose. D-ribose has decreased blood sugar levels. If you have hypoglycemia or are taking certain types of medication, talk to your healthcare provider before you use D-ribose supplements. While limited research suggests D-ribose may be helpful for people who have medical disorders that affect muscle function and energy levels, one study suggested it didn't improve healthy athletes' performance. No foods contain high amounts of ribose. Supplements are a source of D-ribose. Some foods contain low amounts of D-ribose. It's also available as a dietary supplement in most health food stores, pharmacies, and online. Low levels of D-ribose are consumed in the diet. D-ribose is found in meats like beef and chicken, though amounts vary. Cooking likely decreases the amount of ribose available. D-ribose is sold as capsules, tablets, and a powder that can be mixed with a non-carbonated beverage. It is a naturally occurring sugar and tastes sweet. When selecting a brand of supplements, look for products that have been certified by one or more of these organizations:. Due to the limited research, it's too soon to recommend D-ribose supplements for any condition. It's also important to note that self-treating a condition and avoiding or delaying standard care may have serious consequences. If you're considering using D-ribose supplements to treat any chronic condition, talk to your healthcare provider before starting the supplement. NIH Office of Dietary Supplements. Dietary Supplements for Exercise and Athletic Performance. National Center for Biotechnology Information. PubChem Compound Summary for CID , D-Ribose. Pierce JD, Shen Q, Mahoney DE, et al. Am J Cardiol. EFSA Panel on Dietetic Products, Nutrition and Allergies NDA , Turck D, Bresson J, et al. Cao W, Qiu J, Cai T, Yi L, Benardot D, Zou M. Effect of D-ribose supplementation on delayed onset muscle soreness induced by plyometric exercise in college students. J Int Soc Sports Nutr. Seifert JG, Brumet A, St Cyr JA. The influence of D-ribose ingestion and fitness level on performance and recovery. Published Dec Heidenreich PA, Bozkurt B, Aguilar D, et al. Bayram M, St. Cyr JA, Abraham WT. D-ribose aids heart failure patients with preserved ejection fraction and diastolic dysfunction: a pilot study. Therapeutic Advances in Cardiovascular Disease. Teitelbaum JE, Johnson C, St Cyr J. The use of D-ribose in chronic fatigue syndrome and fibromyalgia: a pilot study. J Altern Complement Med. Jones K, Probst Y. Role of dietary modification in alleviating chronic fatigue syndrome symptoms: a systematic review. Aust N Z J Public Health. Mahoney DE, Hiebert JB, Thimmesch A, et al. Understanding D-Ribose and Mitochondrial Function. Adv Biosci Clin Med. This unstable aldofuranose ring is vulnerable to reactions with amino groups, giving rise to its high efficiency in protein glycation. Therefore, comparing ribosylation with glucosylation should provide new clues for clarifying some of the important complications caused by advanced glycation end products in vivo. In vitro studies on the role of Rib in glycation have been carried out. Rib can glycate rat tail tendon collagen in vitro and the structure of the collagen is significantly altered by Rib-induced glycation [10]. Luciano and colleagues prepared glycated fetal calf serum with Rib and found that while ribosylation reduces the proliferation of pancreatic islet beta-cells, cell necrosis and cell apoptosis rate increase correspondingly [11]. Ribosylated bovine serum albumin polymerizes and forms globule-like aggregates with high cytotoxicity [12]. However, the relationship between ribosylation and neurodegenerative diseases is still unknown. In this laboratory we have observed that glycation induces inactivation and conformational change of D-glyceraldehydephosphate dehydrogenase [13] , [14]. We have also compared the characteristics of ribosylation on neuronal Tau protein [15] , and α-synuclein [16] with those of glucosylation in vitro , showing that ribosylation occurs much more rapidly than glucosylation. Ribosylated neuronal protein is much more cytotoxic than glucosylated protein. Nevertheless, little is known about whether Rib can rapidly induce glycation in cells and the AGEs produced by ribosylation can impair the cognitive function. Here, we treated cultured cells and mice with Rib and Glc to compare ribosylation and glucosylation for the production of AGEs. We found that Rib reacted rapidly with proteins and produced significant amounts of AGEs in cultured cells and mouse brain tissues, and that accumulation of AGEs impaired mouse spatial cognition. This finding implies that Rib-derived AGEs may be related to impairments of learning and memory ability. To investigate whether Rib leads to decreases in cell viability, SH-SY5Y human neuroblastoma SH-SY5Y cells and Human embryonic kidney T HEKT cells were incubated with D-ribose or D-glucose at different concentrations. Cell viability was measured by MTT assays at 2 and 3 days after addition of the monosaccharide. MTT assays also gave the same results after 3 days of Rib treatment Fig 1H and J. Furthermore, the number of SH-SY5Y and HEK cells was markedly lower after treatment with 50 mM Rib for 3 days compared with Glc-treated and control cells Fig 1A to F. The morphology of SH-SY5Y cells was observed by inverted contrast microscopy after incubation with 50 mM Rib A , or 50 mM Glc B for 3 days. Untreated cells were used as controls C. HEKT cells treated with the same concentration of Rib D , Glc E and control cells F were imaged under the same conditions. SH-SY5Y G and H and HEKT I and J cells were incubated with Rib or Glc as indicated and cell viability was measured using the MTT assay at day 2 G and I , and day 3 H and J after addition of the monosaccharides. It is known that AGEs have cytotoxicity [15] , [17] and can inhibit cell proliferation [18]. Rib and Glc react with protein amino groups to initiate a non-enzymatic glycation process which results in AGE formation. Thus, we detected the presence of AGEs in SH-SY5Y, HEK cell lines and primary cultured hippocampal neurons incubated with Rib for 2 days by Western blotting. However, in the presence of Glc, the level of AGEs did not increase significantly under the experimental conditions used. Similarly, the level of AGEs in both HEKT cells and primary cultured hippocampal neurons was also enhanced significantly after Rib treatment Fig 2B and C. These results indicate that Rib is much more active in protein glycation resulting in high yields of AGEs and reduced cell viability. SH-SY5Y cells panel A , HEKT cells panel B and primary cultured rat neurons panel C were treated with Rib and Glc as indicated for 2 days. AGEs were detected with anti-AGEs 6D12 monoclonal antibody. β-Actin was used as a loading control. The control value was set as 1. All values are expressed as means ± S. Having determined that Rib but not Glc is able to glycate proteins rapidly and produce high levels of AGEs in cultured cells in vitro , we investigated whether Rib is able to induce AGE formation in vivo. Mice were injected i. with Rib as indicated for 30 days and serum was taken for assays of glycated serum protein. Mice injected with Glc and saline were used as controls. Having established that injection of Rib leads to an increase in glycated serum proteins, we measured changes in serum AGE formation in mice treated with Rib and Glc to determine whether high levels of glycation lead to AGE production Fig 4. Strikingly, serum AGEs were markedly elevated in the sera of mice that had been injected with Rib. Those treated with Glc were not significantly different from the control group. Similar results were also obtained when the anti-pentosidine antibody was used. Serum pentosidine level was markedly increased in the presence of Rib both 0. These results demonstrate that Rib significantly elevates the glycation of proteins in the blood resulting in accelerated AGE formation under our experimental conditions. Conditions for the injection of monosaccharides were the same as those given in Fig 3 , except that serum AGEs were detected with an anti-AGEs monoclonal antibody panel A and an anti-pentosidine monoclonal antibody panel B. Serum albumin level was used as a loading control. The saline control value was set as 1. Rib can pass through the blood-brain barrier and enter the brain by simple diffusion [19]. To investigate whether injected Rib can elevate the glycation of proteins in the brain, we measured AGEs in the mouse brain by Western blotting. As shown in Fig 5 , intraperitoneal injection of Rib led to the formation of significantly more AGEs in the mouse brain. However, Glc did not have a significant effect on AGE formation in the brain compared to the control. This suggests that Rib can react effectively with proteins and increase AGEs in the mouse brain. Conditions for the injection of Rib were the same as those given in Fig 3 , except that AGEs in the mouse brain were detected by Western blotting using anti-AGEs 6D12 monoclonal antibody, panel A. β-Actin level was used as a loading control. Quantification results are shown in panel B. To confirm the effect of Rib on accelerating the formation and accumulation of AGEs in the brain, we performed immunohistochemistry staining on microtome sections of the mouse brain Fig 6. Compared with the control group, AGEs were observed to increase throughout the hippocampus of mice that had been injected with Rib for 30 days. However, no obvious differences in the hippocampus were found in the Glc-treated and control mice groups. Furthermore, AGE signals were more clearly evident in the cortex of Rib-treated mice, compared with those treated with Glc. This indicates that the rapid formation of Rib-induced AGEs occurred in both the hippocampus and cortex. AGEs in the mouse brain were detected by immunohistochemistry using anti-AGEs monoclonal antibody. We used immunofluorescent staining to further demonstrate that Rib is able to induce AGE formation in the mouse brain. As shown in Fig 7 , AGE signals were clearly visible in the cortex of mice treated with Rib but not in those treated with Glc or saline. The fluorescent signals of AGEs were mainly localized outside the nucleus. Similar results were also observed in the hippocampus of the Rib group though the signals were relatively lower than those in the cortex. AGEs in the mouse brain were detected by immunofluorescent staining. The brain sections were double-labeled for AGEs green and nuclei blue. AGEs, which have been found in the brains of senile dementia patients [20] , are cytotoxic [12] , [17]. To assess changes in the spatial learning and memory of mice whose brain AGE levels were elevated after injection of Rib, we tested their behavior in the Morris water maze. During the training session, all mice improved their performance as indicated by shortened escape latencies over successive days, and mice from each treatment group had the same level of performance no significant individual effect was observed in the first three trials on day 1 prior to treatment. Escape latencies of mice injected with Rib 0. Conditions for the injection of Rib were the same as those given in Fig 3. The length of time mice took to find the hidden platform was recorded as latency of escape during each of the seven training days panel A and B. The length of the searching time spent in the quadrant when the platform was removed during the probe trial is shown in panel C. Withdrawal of the platform induced a general tendency to swim in the quadrant where the platform was previously located and in the platform zone, in preference to other equivalent zones. Control, Rib 0. These results indicate that spatial learning and memory ability in Rib-treated mice are significantly impaired. As a reducing saccharide, Rib reacts with protein amino groups to initiate a post-translational modification process widely known as non-enzymatic glycation [1]. This reaction proceeds from reversible Schiff bases to stable, covalently-bonded Amadori rearrangement products. Once formed, the Amadori products undergo further chemical rearrangements to form irreversibly bound AGEs, which are a heterogeneous group of structures including pyrraline, pentosidine, crossline, and carboxymethyl-lysine [3]. As described previously, Rib is much more active in protein glycation than Glc in vitro [12] , [15] , [16]. Here, we also found that Rib reacts rapidly with proteins and showed that Rib treatment results in a significantly higher level of AGEs both in cultured cells and in the mouse serum and brain. This demonstrates that AGEs result from ribosylation not only in mixtures of Rib and proteins in a test-tube, but also in cultured cells, and in the mammalian serum and brain. Even though glycation of proteins with reducing saccharides has been widely studied, the formation of monosaccharide-induced intracellular AGEs has not previously been observed. Here, 10 mM Rib enhanced AGE formation in cultured cells, and diminished cell viability. This work is the first to show that Rib enhances the yield of AGEs in HEKT and SH-SY5Y cells and primary cultured hippocampal neurons. Rib showed significantly higher cytotoxicity than Glc in cell culture. The high cytotoxicity of Rib may result from the rapid formation of AGEs as a result of ribosylation under these experimental conditions. Furthermore, this monosaccharide also enhances the yield of AGEs in both the hippocampus and cortex of the mouse brain after intraperitoneal injection. Impairment of spatial cognition was observed to be coincident with these increases in intracellular AGEs when Rib-treated mice were tested in the Morris water maze. Glc, however, was unable to elevate the yield of AGEs under our experimental conditions. This clearly demonstrates that an overload of Rib may result in a high level of AGEs in the brain and neurons. We would like to emphasize that Rib is much more effective than Glc in the glycation of proteins not only in vitro, but also in vivo. The intracellular AGE-enhanced cell model and the AGE-enhanced cognitive impairment mouse model successfully established here can be used for further investigation of the mechanisms behind the phenomena observed. As shown in the results of Western blotting Fig 2 and 5 , a low level of glycated proteins or AGEs is already present under physiological conditions in both cells and the mouse brain since cells and blood contain certain concentrations of reducing saccharides. High levels of Rib are not only able to enhance AGE formation in vivo , but also induce dysfunction of spatial cognition. This is the first time that Rib-induced cognitive impairment has been observed in mice. The spatial learning and memory ability of mice markedly declined after 30 days of Rib administration. However, those that were injected with the same concentration of Glc did not show significant impairments of spatial cognition compared with saline controls. This suggests that Rib overload for a relatively long period may be harmful to brain function. This treatment paradigm of inducing high levels of AGEs in the brain by administration of Rib can be used as a model for the study of dementia. Here, we believe that the decline in learning and the loss of memory are due to ribosylation and its resultant AGEs; glycation with Rib induces mouse spatial cognitive impairment. This viewpoint is based on the following observations and data. Finally, 7 Decline in learning and memory is observed in Rib-injected mice, but not in Glc-injected and control mice. AGEs were clearly evident in the hippocampus and cortex of Rib-injected mice Fig 6. Glc, however, did not significantly elevate AGEs in the mouse brain under the same conditions. Toxic AGEs have previously been implicated in diabetes [3] , cataracts [23] , renal failure [24] , and other disorders [25]. Immunohistochemical studies have demonstrated the presence of AGEs in the senile plaques of brains from Alzheimer' disease patients [20] , suggesting a link between AGEs and senile plaque formation. Takeda and colleagues have reported that AGE deposits are markedly increased in the hippocampus and the parahippocampus of the brains of Alzheimer's disease patients [26]. Furthermore, it has recently become clear that glycation is also involved in other neurodegenerative diseases and cognitive disorders [27]. This indicates that an AGE overload in the brain may be related to the dysfunction of learning and memory. The relationship between AGE accumulation, cognitive decline and neurodegenerative disease is still under active investigation. Multiple studies have suggested that AGEs are directly neurotoxic to cultured neurons [15] , [17]. AGEs and their precursors methylglyoxal and glyoxal may increase the aggregation and cytotoxicity of intracellular amyloid-beta carboxy-terminal fragments [28]. AGEs, as a kind of specific ligand, can also interact with receptors for advanced glycation end products RAGE and activate an array of signal transduction cascades [29]. By the interaction with RAGE, AGEs may be involved in the generation of ROS and inflammation, and may play a role as activating factors for neuroglia cells such as astrocytes or microglias [30] , [31] , inducing them to produce cytotoxic cytokinelike molecules which then may induce further neuronal cell injury and death and dysfunction of the brain. However, whether AGEs induced by Rib are the same as those generated spontaneously in vivo , and the mechanism by which Rib-induced AGEs impair spatial learning and memory, need further investigations. As a readily available source of energy, ribose is used to improve athletic performance and the ability to exercise by boosting muscle energy. It has also been used to improve symptoms of conditions such as chronic fatigue syndrome, fibromyalgia, and coronary artery disease [32] , [33] , [34]. Rib, as a bioactive ingredient is used widely in nutrition and medicine. Large quantities of Rib are consumed as health supplements and in functional food and beverage formulations each year. However, Rib is very active in the glycation of proteins and its associated chronic risks should be taken into consideration. Our results have shown that administration of high doses of Rib over a long period can lead to high yields of AGEs in vivo and cognitive dysfunction. Glycation affects the biological functions of proteins and crosslinking by glycation results in the formation of detergent-insoluble and protease-resistant aggregates. Thus, the effects of ribosylation on the human brain should be regularly examined during long term administrations of Rib as a drug. Our findings on the importance of ribosylation are relevant to medical professionals monitoring the therapeutic use of Rib. In summary, we have shown that Rib rapidly reacts with proteins and produces AGEs in cells, inducing a decrease in cell viability. Administration of Rib to mice leads to the accumulation of a significantly high concentration of AGEs in the brain and subsequent impairment of spatial learning and memory ability. Administration of Rib can thus be used to establish a mouse model of dysfunction in spatial cognition. The handling of mice and experimental procedures were approved by the Animal Welfare and Research Ethics Committee of the Institute of Biophysics, Chinese Academy of Sciences Permit Number: SYXK Primary hippocampal neuron cultures were prepared from day-old Sprague-Dawley rat embryos as described previously [39]. Mature hippocampal neurons cultured for 14 days were prepared for treatment. For all experiments, the culture medium was replaced with serum-free medium before Rib or Glc treatment. Cells were incubated with Rib Amresco, USA or Glc Sigma, USA at concentrations of 10 mM and 50 mM for 48 hours. Cells were then collected to prepare cellular extracts for Western blots. To determine cell viability, we used the standard 3- 4, 5-dimethylthiazolyl -2, 5-diphenyl tetrazolium bromide MTT; Sigma, USA test, with the slight modifications suggested by Mayo and Stein [40]. After 24 hours, the culture medium was replaced with serum-free medium in the presence of Rib or Glc at different concentrations. Medium without monosaccharides was used as a control. After 48 or 96 hours of treatment, MTT final concentration 0. The reaction was stopped by replacement of the MTT-containing medium with µl DMSO Amresco, USA , and absorbance at nm was measured on a Multiscan MK3 spectrophotometer Thermo, USA. After 1 week of acclimatization to the cages, mice were randomly divided into five groups and received intraperitoneal injections each day for 30 days with Rib at doses of 0. All mice were maintained in animal facilities under pathogen-free conditions. After days of injections, the Morris water maze MWM test was performed as described previously [41]. The experimental apparatus consisted of a circular water tank 90 cm in diameter, 35 cm in height , containing water 23±1°C to a depth of A platform 4. The water tank was located in a test room, which contained various prominent visual cues. Each mouse received three periods of training per day for seven consecutive days. Latency to escape from the water maze finding the submerged escape platform was calculated for each trial. On day 8, the probe test was carried out by removing the platform and allowing each mouse to swim freely for 60 seconds. The time that mice spent swimming in the target quadrant where the platform had been located during hidden platform training was measured. All data were recorded with a computerized video system. After behavioral testing, mice were sacrificed and their blood about 0. Glycated serum protein GSP [43] and blood glucose [44] were measured using kits obtained from the Nanjing Jiancheng Bioengineering Institute China according to the manufacturer' guidelines. The activity of the serum enzymes alanine aminotransferase ALT [45] , aspartate aminotransferase AST [46] and serum creatinine [47] was determined using a spectrophotometric diagnostic kit from Biosino Biotechnology Company Ltd. The level of AGEs or pentosidine was determined in cultured cells, brain tissues, and mice sera as described previously [12]. Membranes were then incubated respectively with anti-AGE 6D12 monoclonal antibody TransGenic, Japan , anti-pentosidine PEN12 monoclonal antibody TransGenic, Japan or anti-β actin monoclonal antibody Sigma, USA overnight at 4°C. Each membrane was washed three times with PBS with 0. The membranes were again washed three times with PBST, and then immunoreactive bands were visualized using enhanced chemiluminescence detection reagents Applygen, China. The protein bands were visualized after exposure of the membranes to Kodak X-ray film and quantified by Quantity One 1D analysis software 4. After fixation, brains were embedded in paraffin blocks. Five to eight micrometer thick sections were processed for immunohistochemical analyses. Deparaffinized and hydrated sections were incubated in Target Retrieval Solution at 95°C for 30 minutes for enhancement of immunoreactivity, then permeabilized with 0. The specimens were incubated overnight at 4°C in anti-AGEs 6D12 monoclonal antibody solution diluted in PBS. After washing with PBS, sections were subsequently incubated with biotin-labeled secondary antibodies 37°C, 1 hour. The immunoreaction was detected using horseradish peroxidase-labeled antibodies 37°C, 1 hour and red staining was visualized with an AEC system Nikon Optical, Japan. Immunofluorescent staining was performed as described [48]. Bound antibodies were visualized with Alexa conjugated anti-mouse IgG Invitrogen, USA and cell nuclei were stained with the DNA-specific fluorescent reagent Hoechst Immunolabeled tissues were observed under an Olympus FV laser scanning confocal microscope Olympus, Japan. All values reported are means ± standard errors SE unless otherwise indicated. Data analysis was performed by one way analysis of variance ANOVA using Origin 7. Conceived and designed the experiments: CH Y. Lu YW Y. Liu RH. Performed the experiments: CH Y. |
| Introduction | Data are the means ± standard error of mean. Jinni Hong et al, D-ribose induces nephropathy through RAGE-dependent NF-κB inflammation Arch Pharm Res. Sports Med. Lustig, R. There are 41 community medical centers in the Chaoyang District. |
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Is D-Ribose a Healthy SugarRibose sugar and brain health -
Overall, the pilot study found that D-ribose significantly reduced clinical symptoms for those with fibromyalgia and chronic fatigue syndrome.
Myoadenylate deaminase deficiency MAD is a metabolic muscle disease that interferes with the processing of ATP by muscle cells. Symptoms of this condition can include cramps, muscle pain and exercise intolerance. However, having no symptoms is also possible. For people struggling with MAD, there is some evidence that taking D-ribose by mouth or receiving it intravenously from a health care professional may effectively prevent symptoms, such as cramping, pain and stiffness after exercise.
This naturally occurring sugar may also offer impressive benefits for skin health, especially when it comes to anti-aging efforts. As we age, our cells naturally produce less ATP. The good news is that this naturally occurring sugar boosts ATP regeneration.
One study tested a topical D-ribose-based 0. The female subjects were objectively and subjectively evaluated at 14 and 28 days while applying the lotion on a daily basis. What did they find? After 14 days, there was a significant reduction of After 28 days, total wrinkle surface area remained at Overall, 67 percent of the subjects thought their skin looked more glowing and radiant after the treatment.
These results show that this natural carbohydrate is a potential anti-aging supplement for skin health. What foods are high in ribose? It can be found in the following food sources :. It can be difficult to get enough from dietary sources, however. This natural sugar is available in health stores and online in supplement form as a powder, chewable tablet or capsule.
You can take the powder in water or add it to other beverages, like smoothies, or mix it into kefir or yogurt. Powder form is definitely a popular way to take it, but reading D-ribose reviews may help you to determine which supplement is best for your you.
It is also a component of multi-ingredient supplements for energy. How much D-ribose should you take in supplement form? Most makers of these supplements recommend doses between one to 10 grams per day.
When should I take D-ribose? To improve the ability of people with coronary artery disease to exercise, the following D-ribose dosage by mouth has been studied: 15 grams four times daily taken one hour prior to exercise until the end of the exercise session.
In other words, take three grams every 10 minutes during exercises. This has been used to decrease muscle stiffness and cramps caused by exercising.
Ribose and deoxyribose are both five-carbon sugars that each contain 10 hydrogen atoms. The molecular formula of ribose is C 5 H 10 O 5, and the molecular formula of deoxyribose 2-deoxyribose is C 5 H 10 O 4. Does DNA contain ribose? It is a component of RNA while deoxyribose is part of DNA.
RNA stands for ribonucleic acid, and it is a complex compound that plays a vital role in cellular production of proteins. It also replaces DNA deoxyribonucleic acid as a carrier of genetic codes in some viruses. The biggest difference between deoxyribose vs. Our previous work has shown that d -ribose RIB -induced depressive-like behaviors in mice.
However, the relationship between variations in RIB levels and depression as well as potential RIB participation in depressive disorder is yet unknown. Here, a reanalysis of metabonomics data from depressed patients and depression model rats is performed to clarify whether the increased RIB level is positively correlated with the severity of depression.
The results show that RIB caused intestinal epithelial barrier impairment and microbiota-gut-brain axis dysbiosis. These microbial and metabolic modules are consistently enriched in peripheral fecal, colon wall, and serum and central hippocampus glycerophospholipid metabolism.
These findings suggest that the disturbances of gut microbiota by RIB may contribute to the onset of depressive-like behaviors via regulating glycerophospholipid metabolism, and providing new insight for understanding the function of microbiota-gut-brain axis in depression.
D-ribose RIB is a naturally occurring monosaccharide that is found in riboflavin-containing foods such as wheat bran, eggs, and meat. Meanwhile, because RIB can bypass part of the pentose pathway to produce d -ribosephosphate for the production of energy, it has been utilized as a daily nutritional or energy supplement 1 , notably for patients with chronic fatigue syndrome and coronary artery disease 2 , 3.
RIB is also a crucial component of several important biomolecules including adenosine and adenosine triphosphate, which are involved in a variety of metabolic activities 4.
However, as described by the European Food Safety Authority, the toxicological effects of RIB should not be ignored 5. Several studies have reported that RIB can be involved in the onset of encephalopathy 6 , 7.
Depression is one of the most prevalent serious mental disorders, characterized by a lack of interest, pessimism, appetite loss, and even suicidal behavior 8 , 9. Finding relevant risk variables is crucial for depression prevention and screening.
Given that RIB has not been widely reported in depressive disorder and that a high-sugar diet may be an environmental risk factor for depression 11 , 12 , we recently gave normal mice prolonged RIB supplementation and found that these mice exhibited depressive-like behaviors and histological alterations, including obviously condensed and deeply-stained pyramidal cells in the hippocampus This finding implies that RIB has a significant impact on the development of depression.
The key scientific concerns that we will research, however, are whether the variation in RIB level was associated with depression and the underlying biological mechanism of RIB implicated in depressive illness.
Of note, some other monosaccharides, such as fructose and glucose, have been linked to changes in the gut microbiota, leading to microbial metabolite disorder in rodents 14 , A high intake of sugar can cause enteric dysbacteriosis. The latter increases the permeability of the intestinal mucosa, and results in abnormalities in intestinal immunity and glucolipid metabolism Moreover, hyperglycemia would increase the permeability of the intestinal barrier, giving microbes a better chance to enter the body and causing the proliferation of pathogenic bacteria Our groups previously found that depression was linked to altered gut microbiomes 19 , and germ-free mice exhibit depressive-like behaviors after receiving gut microbiota from depressed patients 19 , Furthermore, a recent study demonstrates that exogenous RIB can affect gut microbial architecture As a result, we proposed that changes in microbiota might account for the connection between RIB intake and depression.
At first, we reanalyzed the metabonomics data from our earlier studies to clarify the change of RIB in the urine of depressed patients and in the hippocampus of depression model rats. Then, in the current study, to further investigate the possible mechanism of RIB-induced depression, eight weeks of RIB-fed mice were constructed.
The intestinal barrier impairment was evaluated using hematoxylin and eosin, immunohistochemistry, and electron microscopy. The distinct gut microbiota was initially identified by 16S rRNA gene sequencing analysis.
Moreover, by systematic analysis of relevant biological samples, including peripheral fecal, colon wall, and serum and central hippocampus specimens from the RIB-fed mice and control mice, comparative untargeted metabolomics was used to capture the functions of the altered gut microbiome. Finally, by integrating these multi-omics data, we sought to understand how the gut microbiota contributed to the development of depressive-like behaviors and to pinpoint a putative way between the gut and the brain in RIB-fed mice.
The results indicate that a tight connection may exist between elevated RIB and depressive illness. c There was a negative relationship between the percentage of sucrose preference SP and the relative abundance of RIB.
d There was a significant positive correlation between immobility time IT and the relative abundance of RIB. Data are the means ± standard error of mean.
These results further confirm that RIB-fed induced depressive-like behaviors in mice. a , b Both body weight a and fasting blood b were similar between the two groups.
d Total distance was similar between the CON and RIB groups. e Center distance was significantly lower in the RIB group. f Compared to the CON group, the RIB group had a significantly higher immobility time. Homeostasis in the gut is important for brain function.
We investigated whether RIB feeding perturbed colonic homeostasis, including colonic barrier and gut microbiota. Electron microscopy also showed severe mitochondrial swelling, injury of tight junction and gap junction domains, reduced numbers of the desmosome, and increased distance between adjacent epithelial cells in the colon of RIB-fed mice Fig.
Moreover, immunohistochemistry analysis indicated that the expression of Occludin Fig. M mitochondria, TJ tight junction, De desmosome. Next, gut microbiota diversity and composition in response to RIB were analyzed using 16S rRNA gene sequencing. There were no significant differences in alpha diversity between the two groups Supplementary Fig.
As shown in Fig. The relative abundances of each phylum were described in Supplementary Data 1. a Principal coordinate analysis model showed that there were significantly differential gut microbiota compositions between CON and RIB-fed mice.
b Firmicutes, Bacteroidetes, and Verrucomicrobiota were the three major bacterial phyla in both groups. c In total, 22 differential genera responsible for the discrimination between CON and RIB-fed mice were identified using linear discriminant analysis effective size.
The relative abundance of glycerophospholipid metabolism was highest among these pathways. A1: Phenylalanine, tyrosine, and tryptophan biosynthesis; A2: Lysine degradation; A3: Valine, leucine, and isoleucine biosynthesis; A4: Histidine metabolism; L1: Secondary bile acid biosynthesis; L2: Glycerophospholipid metabolism; L3: Arachidonic acid metabolism; L4: Primary bile acid biosynthesis; L5: Fatty acid elongation; L6: Fatty acid biosynthesis.
CD center distance, IT immobility time, SP sucrose preference. Using linear discriminant analysis effective size, 22 differential genera responsible for the discrimination between CON and RIB-fed mice were identified Fig. Kyoto Encyclopedia of Genes and Genomes KEGG pathway analysis Fig.
The results Fig. In total, there were metabolites successfully annotated Supplementary Data 3. The built orthogonal partial least-squares discriminant analysis OPLS-DA model using microbial metabolites in feces showed that the RIB-fed mice were separate from CON with no overlap, suggesting the divergent microbial metabolic phenotypes between the two groups Fig.
The results of permutation testing demonstrated that this model was valid and not over-fitting Supplementary Fig. Detailed information on these microbial metabolites was described in Supplementary Data 4. The heat map consisting of these differential microbial metabolites showed a consistent clustering pattern within the individual groups Fig.
a OPLS-DA model showed that the two groups had significantly different fecal metabolic phenotypes. c KEGG pathway classification showed that these metabolites were mainly annotated into the metabolism category. d Using online software MetaboAnalyst, four significantly dysregulated metabolic pathways in KEGG metabolism category classifications at level 3 were identified via hypergeometric test each dot represents a KEGG path, the dot size represents the impact value, and the dot color represents the p-value, the more important the differential metabolites were in this pathway, the larger the dot.
In addition, KEGG pathway classification showed that these differential microbial metabolites were mainly annotated into the metabolism category Fig. Using online software MetaboAnalyst, four significantly affected metabolic pathways in KEGG metabolism category classifications at level 3 were identified via hypergeometric test Fig.
In total, metabolites were successfully annotated in the colon Supplementary Data 5. The built OPLS-DA model showed divergent metabolic phenotypes in the colon between the two groups Supplementary Fig. KEGG pathway classification showed that these differential microbial metabolites were mainly annotated into the metabolism category; and using the online software MetaboAnalyst, seven significantly affected metabolic pathways in KEGG metabolism category classifications at level 3 were identified via hypergeometric test Fig.
a Seven significantly dysregulated metabolic pathways were found using hypergeometric tests in colon tissue. b Eight significantly dysregulated metabolic pathways were identified using hypergeometric tests in blood.
c Three significantly dysregulated metabolic pathways were identified using hypergeometric tests in hippocampus. The online software MetaboAnalyst was used to conduct pathway analysis. Each dot represents a KEGG path, the dot size represents the impact value, and the dot color represents the p -value.
The more important the differential metabolites were in this pathway, the larger the dot. d A heat map representation comprising all the differential metabolites from the colon, blood, and hippocampus showed a consistent clustering pattern within the individual groups.
S3b and Supplementary Data 8. Using online software MetaboAnalyst, eight significantly affected metabolic pathways in KEGG metabolism category classifications at level 3 were identified via hypergeometric test Fig. S3c and Supplementary Data Using online software MetaboAnalyst, three significantly affected metabolic pathways in KEGG metabolism category classifications at level 3 were identified via hypergeometric test Fig.
A heat map representation comprising all the differential metabolites from colon, blood, and hippocampus showed a consistent clustering pattern within the individual groups Fig. This phenomenon was also observed in our previous nonhuman primate model of depression As such, the different components of a given metabolic pathway might synergistically modulate the function of the MGB axis in different tissues.
Thus, weighted correlation network analysis was used here to cluster the identified differential metabolites into the metabolic modules of the MGB axis. The results showed that there were seven different modules, in which four modules blue, red, black, and turquoise were significantly correlated with at least one type of depressive-like behavior Fig.
SP was significantly correlated with three metabolic modules blue, red, and black , and IT was significantly correlated with the turquoise metabolic module.
Red and green squares indicated positive and negative correlations, respectively. b The differential metabolites in the turquoise metabolic module were significantly correlated with IT mainly belonged to lipid metabolism, especially PE and PC.
c The differential metabolites in three metabolic modules blue, red, and black were significantly correlated with SP mainly belonging to PC, fatty acyls, organic compounds, and carboxylic acids and derivatives. Differential metabolites belonging to lipid metabolism were marked using different colors except for the gray, and other differential metabolites were marked using gray circles.
Circle size indicated the abundance of the metabolites belonging to this node. BW body weight, CD center distance, CL cardiolipin, FB fasting blood, IT immobility time, PA phosphatidic acid, PC phosphatidylcholine, PE phosphatidylethanolamine, PI phosphatidylinositol, PS phosphatidylserine, SP sucrose preference, TD total distance.
Module-trait analysis showed that the differential metabolites in the turquoise metabolic module significantly correlated with immobility time were mainly involved in peripheral and central glycerophospholipid metabolism within the MGB axis Fig.
Details regarding the module and chemical class of each compound were shown in Supplementary Data The abovementioned findings indicated that glycerophospholipid metabolism might play an important role in the crosstalk of gut microbiota and the brain.
The numbers associated with the metabolite names were just codes, for example, we used PC39 to represent 1-heptadecanoyl-glycerophosphate detailed information about the codes representing metabolites is shown in Supplementary Data PC phosphatidylcholine, PE phosphatidylethanolamine.
These results indicated that glycerophospholipid metabolism, especially PC and PE, might be the important bridge of gut microbiota in affecting brain functions. Dietary sugars, like fructose and glucose, are associated with psychosis-related higher brain dysfunctions 12 , Our previous study provided evidence that another simple sugar, RIB, could lead to depressive-like behaviors, and we demonstrated in mice that this was connected with altered hippocampus metabolic and transcriptome profiles 13 , but how the brain is affected by RIB remains poorly understood.
In this study, we clarified that the RIB level was significantly increased in the depressed patients and depression model rats, and there was an obvious correlation between the change of RIB and the severity of depression disorder. However, these studies only involved untargeted metabolomics analysis, which provides relative metabolite abundance rather than absolute quantification The results further suggested that high levels of RIB were correlated with depression.
We observed the RIB-fed mice were characterized by intestinal epithelial barrier impairment, alterations of microbial composition, function, and metabolic pathways of the MGB axis. Meanwhile, the altered microbial and metabolic modules linked the gut microbiome with dysregulation of peripheral and hippocampus glycerophospholipid metabolism in RIB-fed mice.
To our knowledge, this is the first report of RIB influencing gut microbiota, and gut dysbiosis may be responsible for mediating the depressive-like behaviors seen in RIB-fed mice by regulating the MGB metabolism.
We found that the RIB-fed mice had considerably impaired intestinal barrier as compared to the CON. The gut barrier function was regulated by the gut microbiota 24 , As a result, we deduced that the RIB might disrupt the gut microbiota, and that the gut dysbiosis would subsequently lead to depression via the MGB axis.
Akkermansia belonged to the Verrucomicrobiota phylum. Khan S et al. The mucus-degrading bacterium Akkermansia would regulate intestinal homeostasis and preserve the integrity of the gut barrier The increased Akkermansia might be the cause of intestinal barrier impairment in RIB-fed mice.
Interestingly, recent research has shown that Akkermansia has beneficial roles in human health 30 ; nevertheless, there is also strong evidence that Akkermansia promotes the etiology of colitis Similarly, Akkermansia was detected in much higher abundance in individuals with severe depressive symptoms, according to Zhang et al.
These contradictory findings might be the consequence of differences in participants, sequencing, and analytical approaches. Furthermore, we found that This result is in line with our earlier research that At the phylum level, disturbances of Firmicutes have been identified as a possible hallmark of depression 19 , Accordingly, these results suggested that RIB would induce the gut microbiota disordered, and that the bacterial phylum Firmicutes disturbances might be a significant contributing factor to RIB-caused depressive-like behaviors.
According to previous research 36 , RIB levels in human urine were positively correlated with serum triglyceride levels, and Sprague-Dawley rats given RIB injection had considerably higher hepatic triglyceride levels, suggesting that RIB might regulate lipid metabolism.
Besides, lipids are crucial for brain neuronal activity 37 , and the lipid composition of the brain has a significant impact on emotional behavior and subjective mood Here, we found that both altered microbial and metabolic modules involving glycerophospholipid metabolism were highly correlated with depressive-like behaviors in RIB-fed mice.
Our previous studies revealed that the gut microbiota would significantly affect the glycerophospholipid metabolism in the mouse brain 41 , Meanwhile, the glycerophospholipid metabolism in the hippocampus was disturbed in the chronic unpredictable mild stress rat model of depression Thus, we concluded that in RIB-fed mice, peripheral and central glycerophospholipid metabolism was regulated by gut dysbiosis, which might be a contributing factor to the development of depressive-like behaviors.
In addition, we found that PC and PE had greater contributions to the overall correlation between differential genera and glycerophospholipids. Our previous study has also shown that they are remarkably increased in depressed patients and have favorable associations with depression severity Moreover, PC and PE are critical components of neuronal membranes.
The phospholipase A2 can deacylate PC and PE into lysophosphatidylcholine and lysophosphatidylethanolamine, which are then converted into glycerophosphocholine and glycerophosphoethanolamine.
Patients with depression have increased amounts of the neurotransmitter acetylcholine, which is produced by glycerophosphocholine Higher levels of glycerophosphoethanolamine have been found in the white matter of depressed individuals In light of this, our findings suggested that in RIB-fed mice, PC and PE might act as a link between gut dysbiosis and depressive-like behaviors.
Several limitations of this study are listed as follows: First, it was conducted in mice; however, human gut microbiota compositions do not exactly match those of rodents, clinical trials are required to further confirm the reported effects of RIB on human gut microbiota composition and function.
Second, we only focused on one region of the brain associated with emotions the hippocampus , whereas chronic stress caused lipidomic changes in a region-specific manner, and the disturbances of lipid metabolism in the prefrontal cortex were more obvious than those in the hippocampus As a result, future studies should take other brain regions to uncover more novel clues on the interactions between gut microbiota and RIB-caused depression.
Third, our data do not completely rule out the possibility of other direct effects of RIB on the host, even though we thoroughly defined host peripheral and hippocampus metabolism implicated in RIB-induced gut dysbiosis.
Future study on fecal microbiota transplantation is needed to clarify how the MGB axis links RIB to aberrant emotional-associated behavior.
Fourth, due to the dose of ribose being a constant here, we could not use mediation analyses to assess whether ribose directly induced depression or indirectly induced depression through influencing the gut microbiome or gut-brain axis glycerophospholipid metabolism.
Future studies should explore the role of RIB directly or indirectly in depression by designing gradient RIB dose experiments or modulating the important differential variables identified in this study bacterial taxa or metabolites. Considering that RIB induced depressive-like behavior, which correlated with intestinal barrier damage and gut microbiota imbalance, the issue of whether intervention or reversal of intestinal barrier damage and gut microbiota imbalance could circumvent the effects of RIB requires further investigation in future studies.
Sixth, due to the limitations of technologies and funds, we did not conduct further experiments to validate the functional relationship of RIB with the glycerophospholipids metabolism pathway. In conclusion, to our knowledge, this is the first study to reveal that oral RIB results in depressive-like behaviors, which may be partially explained by changes in microbial composition, function, and metabolism of the MGB axis.
This study highlights that simple sugars like RIB can have adverse effects on gut microbiota, MGB axis metabolism, and mental health. The relative abundance of RIB was defined as RIB level in metabonomics. The MDD patients were recruited from the Psychiatric Center of the First Affiliated Hospital of Chongqing Medical University, and the HC were recruited from the Medical Examination Center of the First Affiliated Hospital of Chongqing Medical University.
All included individuals were ethnically homogenous Han Chinese. The Hamilton Depression Scale score of MDD patients has to be more than 17, and all of them were first-episode drug-naïve MDD patients.
The human data used and study protocol have received ethical approval from the Medical Research Ethics Committee of Chongqing Medical University. All ethical regulations relevant to human research participants were followed, and a statement confirming that informed consent was obtained.
Following the protocol 49 , a typical depression phenotype caused by chronic mild stress was modeled in rats using a chronic social defeat stress paradigm. Animals were housed in a specific pathogen-free vivarium under standard conditions. All RIB group mice were administered the RIB 3.
Louis, MO, USA in drinking water for eight weeks. The dosage and time were determined by previously published studies 13 , Thus, here we used 3. The mice in the CON group were given access to normal purified water for feeding. Since food is one of the primary factors influencing changes in the gut microbiome, all the mice were fed the same food standard laboratory mouse diet to rule out any possible impacts.
These outcomes clearly suggested cognitive detriment due to D -ribose at a high dose. Sensitivity analysis explained most of the heterogeneity. In terms of the significant reduction of heterogeneity in the percentage of time spent in the target quadrant, contrary results were found in the study of Han et al.
Similarly, the obvious reduction of heterogeneity in the latency was attributed to the results reported by Wu et al. Regarding the brain AGEs, sensitivity analysis revealed the source of heterogeneity which may be attributed to differences in dose, sample size, and eligibility criteria Garcia-Alamino et al.
In the included studies, the rodents used were all male. Population-based studies suggest that gender may affect cognitive impairment Au et al. Nonetheless, owing to hormonal secretion, physical fitness, and other factors, males are usually selected as experimental subjects in animal studies Schaeffer, Hence, future research is needed to further address these gender-based differences.
As for sample size, due to ethical and economic reasons, a sample size calculation is not necessary for each experiment, and at least 7—10 animals are utilized per group in most animal studies Festing, ; Ricci et al.
The sample size can be further calculated based on power analysis, precision analysis, and other methods in future studies. Evidence suggests that D -ribose is involved in the generation of free oxygen radicals, glycation, protein aggregation, AGEs, and age-related neurodegenerative illnesses Chen et al.
According to cell-based experiments, D -ribose interacts with proteins and produces AGEs. Furthermore, the expression of the receptor of advanced glycation end products RAGE is linked to AGE elevation caused by ribosylation in both astrocytoma cells and astrocytes, resulting in RAGE-dependent NF-κB activation and astrocyte stimulation, further impairing the spatial learning and memory Han et al.
Our analysis of AGEs is consistent with the conclusions reported previously, i. These findings suggested that D -ribose-induced non-enzymatic glycosylation may play a role in the pathogenesis of cognitive impairment. However, the mechanisms underlying D -ribose-mediated cognitive impairment remain unclear, and these should be further investigated in the future.
This review, however, has some limitations, including a relatively small total sample size and the number of included studies. Furthermore, poor reporting quality increased the likelihood of bias and reduced the validity of the findings. To validate the harm caused by D -ribose in cognitive impairment and comprehensively study the underlying mechanisms, more precise and rigorous experiments with high sample sizes are warranted.
We summarized the effects of D -ribose intervention with different doses based on cognitive and behavioral tests and found that D -ribose was related to learning and memory functions. Our findings indicate that D -ribose intervention causes cognitive impairment, and cognition deteriorated with increasing dose.
Furthermore, the increase in AGEs in the blood and brain confirmed that D -ribose may be involved in cognitive impairment through glycosylation, resulting in the generation of AGEs. These provide a new research direction for unveiling basic mechanisms and prospective therapeutic targets for the prevention and treatment of cognitive impairment in these patients.
The raw data supporting the conclusions of this article will be made available by the authors, without undue reservation.
YS and YD completed the data analysis and wrote the manuscript. JZ contributed to the data analysis. YL and YA supervised the project.
All authors reviewed and approved the submitted version. This research was supported by grants from National Natural Science Foundation of China and the Fundamental Research Funds for the Central Universities.
The authors declare that the research was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest. All claims expressed in this article are solely those of the authors and do not necessarily represent those of their affiliated organizations, or those of the publisher, the editors and the reviewers.
Any product that may be evaluated in this article, or claim that may be made by its manufacturer, is not guaranteed or endorsed by the publisher.
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Supplemental Ribose sugar and brain health Rkbose been shown to heath cellular processes when there is mitochondrial dysfunction. D-ribose is a naturally occurring monosaccharide Herbal mood stabilizers the metabolic pathway that assists with ATP hexlth. Excess serum d-ribose is correlated to higher neurodegeneration. On the one hand, this simple sugar found in every cell is critical to your health and wellbeing 1 Zeba Siddiqui et al, Prevalence of auto-antibodies against D-ribose-glycated-hemoglobin in diabetes mellitus Glycobiology. On the other hand, some research points to poor health consequences when it is found in excess in the body. For more information about PLOS Bbrain Areas, click here. D-Ribose, an important reducing monosaccharide, is highly active in Rbiose glycation of proteins, and results in the rapid production of dugar glycation Brown rice benefits products AGEs in suvar. However, Herbal weight loss reviews D-ribose participates in glycation and leads to production of AGEs in vivo still requires investigation. Here we treated cultured cells and mice with D-ribose and D-glucose to compare ribosylation and glucosylation for production of AGEs. Treatment with D-ribose decreased cell viability and induced more AGE accumulation in cells. Administration of high doses D-ribose also accelerated AGE formation in the mouse brain and induced impairment of spatial learning and memory ability according to the performance in Morris water maze test.
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