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Shop the look. Choose Options. Close Edit Option. Close Back In Stock Notification. this is just a warning. Login Close. Forgot your password? For studies that compared the results of groups treated with different D -ribose doses with those of a single control group, the data from the latter were utilized in each of the dose intervention meta-analyses.

The mean score and standard deviation [SD] were extracted for the meta-analysis. Data were analyzed using the Review Manager version 5. A total of 3, reports were identified including from PubMed, from Embase, from Scopus, from Web of Science, from CNKI, from Wanfang, from SinoMed, and 38 from Cqvip.

Subsequently, 1, records were retained after all the searches were pooled and duplicates were deleted. After construing all the titles and abstracts, 1, records were found to be irrelevant the majority of these were excluded as they were conference publications or studies focused on other topics.

After reading the full text of the remaining records, 5 studies met the predefined eligibility criteria.

Non-consensus on the inclusion of these articles was not applicable. The representation of the article selection process is shown in Figure 1. Most of the included studies were published in the last decade, and 2 were published in the past 3 years.

All the male rodent models were 8—10 weeks old and no study reported the animal weights. For the D -ribose treatment, the most frequently selected duration was 30 days 2 studies , followed by 10 days 1 study , 28 days 1 study , and days 1 study.

Intraperitoneal injection was the most commonly used route for D -ribose administration, except for two studies, which employed intravenous tail injection and gavage administration, respectively.

The specific characteristics of the included studies are shown in Table 1. In the ARRIVE guidelines for assessing the quality of studies, all showed the four items, comprising the title, objectives, experimental outcomes, and estimated outcomes. The specific results of the quality assessment were shown in Table 2.

All studies described the effects of D -ribose on cognition in the Morris water maze test, and these studies were included in the meta-analysis.

Three studies reported the number of platform crossings; four studies reported the percentage of the distance traversed in the target quadrant; five studies reported the percentage of time spent in the target quadrant, and all studies reported the escape latency.

The number of platform crossings, the percentage of the distance traversed in the target quadrant, and the percentage of time spent in the target quadrant were counted and analyzed by RevMan in trials to test memory functions Vorhees and Williams, Meta-analysis indicated that D -ribose reduced the number of platform crossings Figure 2 ; SMD: —0.

Moreover, in a total of animals, the meta-analysis showed less percentage of the distance traversed in the target quadrant in the D -ribose-treated group as compared to the control group, with an SMD of —1. The D -ribose group showed a substantially decreased percentage of time spent in the target quadrant relative to the control group Figure 4 ; SMD: —0.

The heterogeneity in the sensitivity analysis obviously declined after excluding the data in the low-dose group in the study reported by Han et al. Figure 3. Forest plot of the percentage of distance in target quadrant in the Morris water maze test.

Figure 4. Forest plot of the percentage of time in target quadrant in the Morris water maze test. The escape latency was assessed and analyzed by RevMan in trials to test spatial learning ability Vorhees and Williams, Meta-analysis revealed that D -ribose intervention had no significant effects on escape latency Figure 5 ; SMD: 0.

Advanced glycation end products have been investigated extensively owing to their involvement in cognitive diseases such as AD Vlassara et al. Serum AGEs were adopted as an outcome in three studies, and the analysis showed the effects of D -ribose in significantly elevating AGEs in mouse blood Figure 6 ; SMD: 0.

The brain AGEs were adopted as an outcome in three studies, and D -ribose intervention significantly increased the levels of AGEs in the mouse brain Figure 7 ; SMD: 0.

The heterogeneity in the sensitivity analysis completely disappeared after excluding the data of the high-dose group in the study reported by Han et al. In addition, D -ribose intervention showed no significant influence on escape latency.

The specific results of the subgroup analysis are shown in Table 3. Metabolic disorder of ribose is associated with adverse effects on cognition Siddiqui et al. Although studies focused on D -ribose intervention show inconsistent findings, no systematic review of D -ribose on cognitive alterations has been published.

We examined animal studies to assess the effects of D -ribose on cognition through a systematic review and meta-analysis of the impact of differential D -ribose doses on cognition. D -ribose treatment caused cognitive impairment, and the cognition deteriorated with increasing dose.

We assessed the effects of different doses of D -ribose on cognitive changes in mice and rats according to the results of the Morris water maze, the number of platform crossings, the percentage of the distance traversed in the target quadrant, and the percentage of time spent in the target quadrant to test memory function and escape latency to assess spatial learning abilities.

The meta-analysis revealed that D -ribose intervention produced a significant impairment in the spatial learning task but not in the spatial memory task.

We verified that D -ribose caused cognitive impairment, consistent with previous studies, which suggest that metabolic disorders due to D -ribose are a possible risk factor for age-related neurodegenerative disorders such as AD Zhu et al.

Lyu et al. A cross-sectional study reported that T2DM-MCI patients had higher serum concentrations of D -ribose and were correlated negatively with the MoCA score Lu et al.

In addition, our subgroup analysis revealed that the group with a high D -ribose dose intervention injured cognitive function more significantly than the group with a low D -ribose dose intervention.

It was clear that the impaired spatial memory ability was more prominent in the high-dose group than the low-dose D -ribose-treated group. D -ribose at a low dose did not cause a decline in the spatial learning ability in rodents, and only D -ribose at a high dose led to a significant decrease in the spatial learning ability.

For the increase in brain AGEs, D -ribose at a high dose had a stronger impact relative to the low-dose D -ribose group. Moreover, only a high dose of D -ribose but not a low dose led to the rise in AGEs in serum.

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. Abramov, A. The role of an astrocytic NADPH oxidas e in the neurotoxicity of amyloid beta peptides. B Biol.

doi: PubMed Abstract CrossRef Full Text Google Scholar. Akhter, F. Antigenic role of the adaptive immune response to d-ribose glycated LDL in diabetes, atherosclerosis and diabetes atherosclerotic patients.

Life Sci. Acquired immunogenicity of calf thymus DNA and LDL modified by D-ribose: a comparative study. An immunohistochemical analysis to validate the rationale behind the enhanced immunogenicity of D-ribosylated low density lipo-protein.

PLoS One 9:e Bio-physical characterization of ribose induced glycation: a mechanistic study on DNA perturbations. Alzheimers Dementia, Alzheimers Dement. But a word of caution here: Always seek professional healthcare advice before beginning any new supplementation, especially if you have an existing heart condition.

This sugary molecule could improve cognitive performance and mood 7 Jacob E Teitelbaum et al, The use of D-ribose in chronic fatigue syndrome and fibromyalgia: a pilot study J Altern Complement Med. D-Ribose also plays a role in the pentose phosphate pathway, producing NADPH 8 Guoyao Wu et al, Glutathione metabolism and its implications for health J Nutr.

Moreover, D-Ribose assists in nucleotide synthesis. These nucleotides are the building blocks for our DNA and RNA — essential for cell growth, repair, and communication 9 Diane E. Mahoney et al, Understanding D-Ribose and Mitochondrial Function Adv Biosci Clin Med. Intriguingly, a cross-sectional study on patients aged 60 and older associated elevated urinary D-Ribose levels with increased cognitive decline rates 10 Xinyi Zhu et al, Urine D-ribose levels correlate with cognitive function in community-dwelling older adults BMC Geriatrics.

This could mean D-Ribose might be a practical, non-invasive biomarker for mental impairment progression. However, no negative correlation between D-Ribose and cognitive function was seen in episodic memory, working memory, or processing speed tests.

A systematic review of animal studies reveals that D-ribose treatment might induce cognitive impairment, with more significant effects at higher doses 13 Ying Song et al, A systematic review and meta-analysis of cognitive and behavioral tests in rodents treated with different doses of D-ribose Front.

Aging Neurosci. In rodents, D-ribose affected spatial learning tasks but not spatial memory tasks. Moreover, high D-ribose doses increased AGEs in the brain and serum, potentially causing cognitive impairment.

D-Ribose is a monosaccharide like glucose, but its effect on blood glucose might be more adverse than we thought. Interestingly, D-Ribose outperforms other sugars in producing glycated serum protein GSP , a precursor to chronic diabetes complications 15 Yao Chen et al, d-Ribose contributes to the glycation of serum protein Biochim Biophys Acta Mol Basis Dis.

A notable observation here is that D-Ribose interacts more rapidly than glucose with non-enzymatic proteins in diabetic patients, leading to the formation of AGEs. The binding of these AGEs to their receptors triggers a series of events: the upregulation of vascular growth factors, increased vascular permeability, angiogenesis, and local inflammation 16 Alejandra Planas et al, Advanced Glycations End Products in the Skin as Biomarkers of Cardiovascular Risk in Type 2 Diabetes Int J Mol Sci.

This AGE-receptor pathway activation also stimulates oxidative stress reactions, contributing to chronic diabetes complications. Although D-Ribose might temporarily reduce blood sugar levels, its long-term accumulation can worsen diabetes complications. Consequently, monitoring D-ribose levels and glycosylated proteins in diabetic patients might help forecast potential clinical complications, providing an opportunity for proactive prevention.

Given the potential brain-health complications linked to high D-Ribose levels, classifying D-Ribose as a nootropic might be a stretch. However, numerous natural nootropics can prevent cognitive decline and boost brain health.

As you can see, the question as to whether you can benefit from D-ribose supplementation is tricky. While there are many positive aspects, many adverse outcomes correlate to high serum d-ribose. As more research comes to light, we can hopefully get a more straightforward answer, especially regarding brain health.

Check with your doctor to determine whether D-ribose is right for you! Join us at Holistic Nootropics as we journey through all facets of health and wellness.

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D-Ribose: A Simple Sugar With A Complex Story Erik Abramowitz, FNTP. Last Updated: June 7, No Comments.

Evidence shows that dysregulated D -ribose metabolism causes several neurodegenerative diseases such as AD. As a reactive sugar, D -ribose can bind to protein or lipid molecules for non-enzymatic glycation, resulting in the production of advanced glycation end products AGEs Wei et al.

Reports show that AGEs are involved in the pathogenesis of aging, diabetes, and neurodegenerative diseases Akhter et al. Moreover, AGEs are neurotoxic in cultured neurons, and their precursors, including methylglyoxal and glyoxal, also promote intracellular aggregation of amyloid-beta carboxy-terminal fragments and cytotoxicity Takeuchi et al.

An animal study also reported that D -ribose accelerated the formation of AGEs in astrocytes, ultimately activating the NF-κB pathway in the brain and causing cognitive impairment Han et al. Chen et al. Animal experiments show that D -ribose impairs the spatial learning and memory of mice. For example, Han et al.

Notably, not all studies suggest that D -ribose significantly affects spatial learning and memory, especially those using low-dose D -ribose intervention. The inconsistent results might be due to the differences in the intervention doses of D -ribose. To date, D -ribose and its role in cognition remain unclear.

Therefore, we systematically reviewed and analyzed the available evidence to clarify the actual effects of D -ribose and its differential doses on cognition. In the beginning, no filters were applied for the search, including language, publication date, dose of administration, route of administration, and duration of administration.

Two reviewers SY and YD examined the papers to ensure that they met the inclusion criteria for the meta-analysis. A third member YL was consulted in case of a disagreement. The systematic review was limited to published studies, i.

An intact design with at least one healthy control group of rodents treated with vehicle saline, phosphate-buffered saline, or a similar solution and at least an experimental group of rodents treated with D -ribose was an inclusion criterion.

All the included studies reported at least one measure of learning and memory after the intervention. Studies with incomplete data in the published text or Supplementary material, or in cases of D -ribose administered with other components, were excluded.

The Animal Research: Reporting in vivo Experiments ARRIVE guidelines checklist 2. Two reviewers SY and YD independently extracted the data in a standardized format suited for animal study design from the reports that met the inclusion criteria.

The items recorded were as follows: fundamental information name of the author, year of publication, and nation ; animals animal species, age, weight, gender, and sample size ; study design dose, route, and duration of D -ribose manipulation ; and measurement outcomes behavioral test results such as those of the Morris water maze test and biochemistry such as AGEs.

If data were not obtained in a table or in text, the Web Plot Digitizer software to extract data from images was used to obtain these from the published figures Drevon et al.

For studies that compared the results of groups treated with different D -ribose doses with those of a single control group, the data from the latter were utilized in each of the dose intervention meta-analyses. The mean score and standard deviation [SD] were extracted for the meta-analysis. Data were analyzed using the Review Manager version 5.

A total of 3, reports were identified including from PubMed, from Embase, from Scopus, from Web of Science, from CNKI, from Wanfang, from SinoMed, and 38 from Cqvip.

Subsequently, 1, records were retained after all the searches were pooled and duplicates were deleted. After construing all the titles and abstracts, 1, records were found to be irrelevant the majority of these were excluded as they were conference publications or studies focused on other topics.

After reading the full text of the remaining records, 5 studies met the predefined eligibility criteria. Non-consensus on the inclusion of these articles was not applicable.

The representation of the article selection process is shown in Figure 1. Most of the included studies were published in the last decade, and 2 were published in the past 3 years. All the male rodent models were 8—10 weeks old and no study reported the animal weights.

For the D -ribose treatment, the most frequently selected duration was 30 days 2 studies , followed by 10 days 1 study , 28 days 1 study , and days 1 study. Intraperitoneal injection was the most commonly used route for D -ribose administration, except for two studies, which employed intravenous tail injection and gavage administration, respectively.

The specific characteristics of the included studies are shown in Table 1. In the ARRIVE guidelines for assessing the quality of studies, all showed the four items, comprising the title, objectives, experimental outcomes, and estimated outcomes. The specific results of the quality assessment were shown in Table 2.

All studies described the effects of D -ribose on cognition in the Morris water maze test, and these studies were included in the meta-analysis. Three studies reported the number of platform crossings; four studies reported the percentage of the distance traversed in the target quadrant; five studies reported the percentage of time spent in the target quadrant, and all studies reported the escape latency.

The number of platform crossings, the percentage of the distance traversed in the target quadrant, and the percentage of time spent in the target quadrant were counted and analyzed by RevMan in trials to test memory functions Vorhees and Williams, Meta-analysis indicated that D -ribose reduced the number of platform crossings Figure 2 ; SMD: —0.

Moreover, in a total of animals, the meta-analysis showed less percentage of the distance traversed in the target quadrant in the D -ribose-treated group as compared to the control group, with an SMD of —1. The D -ribose group showed a substantially decreased percentage of time spent in the target quadrant relative to the control group Figure 4 ; SMD: —0.

The heterogeneity in the sensitivity analysis obviously declined after excluding the data in the low-dose group in the study reported by Han et al. Figure 3. Forest plot of the percentage of distance in target quadrant in the Morris water maze test.

Figure 4. Forest plot of the percentage of time in target quadrant in the Morris water maze test. The escape latency was assessed and analyzed by RevMan in trials to test spatial learning ability Vorhees and Williams, Meta-analysis revealed that D -ribose intervention had no significant effects on escape latency Figure 5 ; SMD: 0.

Advanced glycation end products have been investigated extensively owing to their involvement in cognitive diseases such as AD Vlassara et al.

Serum AGEs were adopted as an outcome in three studies, and the analysis showed the effects of D -ribose in significantly elevating AGEs in mouse blood Figure 6 ; SMD: 0. The brain AGEs were adopted as an outcome in three studies, and D -ribose intervention significantly increased the levels of AGEs in the mouse brain Figure 7 ; SMD: 0.

The heterogeneity in the sensitivity analysis completely disappeared after excluding the data of the high-dose group in the study reported by Han et al.

In addition, D -ribose intervention showed no significant influence on escape latency. The specific results of the subgroup analysis are shown in Table 3.

Metabolic disorder of ribose is associated with adverse effects on cognition Siddiqui et al. Although studies focused on D -ribose intervention show inconsistent findings, no systematic review of D -ribose on cognitive alterations has been published.

We examined animal studies to assess the effects of D -ribose on cognition through a systematic review and meta-analysis of the impact of differential D -ribose doses on cognition. D -ribose treatment caused cognitive impairment, and the cognition deteriorated with increasing dose.

We assessed the effects of different doses of D -ribose on cognitive changes in mice and rats according to the results of the Morris water maze, the number of platform crossings, the percentage of the distance traversed in the target quadrant, and the percentage of time spent in the target quadrant to test memory function and escape latency to assess spatial learning abilities.

The meta-analysis revealed that D -ribose intervention produced a significant impairment in the spatial learning task but not in the spatial memory task. We verified that D -ribose caused cognitive impairment, consistent with previous studies, which suggest that metabolic disorders due to D -ribose are a possible risk factor for age-related neurodegenerative disorders such as AD Zhu et al.

Lyu et al. A cross-sectional study reported that T2DM-MCI patients had higher serum concentrations of D -ribose and were correlated negatively with the MoCA score Lu et al.

In addition, our subgroup analysis revealed that the group with a high D -ribose dose intervention injured cognitive function more significantly than the group with a low D -ribose dose intervention. It was clear that the impaired spatial memory ability was more prominent in the high-dose group than the low-dose D -ribose-treated group.

D -ribose at a low dose did not cause a decline in the spatial learning ability in rodents, and only D -ribose at a high dose led to a significant decrease in the spatial learning ability. For the increase in brain AGEs, D -ribose at a high dose had a stronger impact relative to the low-dose D -ribose group.

Moreover, only a high dose of D -ribose but not a low dose led to the rise in AGEs in serum. 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. Abramov, A. The role of an astrocytic NADPH oxidas e in the neurotoxicity of amyloid beta peptides.

B Biol. doi: PubMed Abstract CrossRef Full Text Google Scholar. Akhter, F. Antigenic role of the adaptive immune response to d-ribose glycated LDL in diabetes, atherosclerosis and diabetes atherosclerotic patients.

Life Sci. Acquired immunogenicity of calf thymus DNA and LDL modified by D-ribose: a comparative study. An immunohistochemical analysis to validate the rationale behind the enhanced immunogenicity of D-ribosylated low density lipo-protein. PLoS One 9:e Bio-physical characterization of ribose induced glycation: a mechanistic study on DNA perturbations.

Alzheimers Dementia, Alzheimers Dement. Ashraf, G. An overview on global trends in nanotechnological approaches for Alzheimer therapy. Drug Metab. Ashraf, J. Inhibiting effect of zinc oxide nanoparticles on advanced glycation products and oxidative modifications: A potential tool to counteract oxidative stress in neurodegenerative diseases.

Au, B. Sex differences in the prevalence and incidence of mild cognitive impairment: A meta-analysis. Ageing Res. Google Scholar. Batkulwar, K. ACS Chem. Borenstein, M. A basic introduction to fixed-effect and random-effects models for meta-analysis.

Methods 1, 97— Broom, A. Purine nucleosides. Further methylation studies of naturally occurring purine nucleosides. Biochemistry 3, — C Silva, T. Alzheimers Res. Cai, Y. Determination of several sugars in serum by high-performance anion-exchange chromatography with pulsed amperometric detection.

A , 98— Chen, L. D-Ribosylated Tau forms globular aggregates with high cytotoxicity. Policy More. Contact Us.

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Depleted cardiac energy storages are associated with increased cardiac stress, reduced blood flow to the periphery of the body, exhaustion and less exercise. Ribose is the main nutrient for restoring cardiac energy. To maximize athletic performance or to keep energy storages full during strenuous activities, slightly higher doses may be necessary.

Ribose should be taken just before or immediately after training or physical activity. For longer training sessions, an additional 1 - 2 grams per training hour could be helpful. There are two known side effects of ribose when doses of 10 grams or more are taken on an empty stomach.

The first is transient hypoglycemia low blood sugar levels , which can be prevented if higher doses of ribose are combined with other carbohydrates such as juice. The second side effect that some people experience is loose stool. This side effect was only reported when very high doses over 10 grams were taken.

The total daily intake of ribose should be limited to 20 grams or around 4 heaped teaspoons. Ribose should be taken in single doses of up to 5 grams around 1 heaped teaspoon. Multiple doses of 5 grams taken 30 - 45 minutes apart can be taken without side effects. For some people, high intensity training means daily training for a marathon, 10 km run or a triathlon.

For others, it means going to the mailbox, climbing stairs or spending a day at the mall. However, for most of us it simply means stressing our muscles beyond normal levels.

Regardless of how you define high intensity, the effect on our body is the same. Intensive exertion strains our muscles and makes it difficult for them to remain energized. The resulting imbalance between the supply of energy and the demand for energy leads to a decrease in energy, which leads to the depletion of cellular energy reserves.

This loss of cellular energy is a catastrophe, because this energy can only be recharged slowly and at a metabolically expensive cost. Ribose increases the natural process of energy synthesis in the body. It helps reduce energy loss during stress and accelerated energy and tissue recovery.

Ribose helps the muscles regenerate lost energy and potentially minimize the physiological consequences of this low-energy situation. Whether you are running a marathon in under three hours or do a daily workout that keeps your heart and muscles healthy, Ribose can help you keep your muscles energetic and strong.

Everyone needs ribose. It is an essential ingredient for stimulating the natural energy production.

Research has shown that ribose reduces stress associated with strenuous activity and helps athletes achieve new top performances.

Ribose helps the heart and muscles maintain healthy energy levels and accelerates energy recovery when the tissue is stressed by strenuous exercise or overuse.

Regardless of whether you are a trained athlete, a weekend athlete or someone who is concerned about their cardiovascular health, ribose can give you the energy that your body needs. Scientific research shows that three to four training sessions per week does not mean enough rest periods between the units, which means that the energy storages of the heart and muscles can't reach their normal levels.

Taking ribose shortens the time it takes for the heart and muscle tissue to replace the energy lost through intense exercise. Keeping the energy storages full ensures that the heart and muscles are in a good physical condition, increases strength and endurance and reduces fatigue.

Current research has shown that taking a ribose supplement during exercise reduces free radical formation. Ribose can increase the effects of creatine and other energy supplements because the energy storage is kept at full capacity.

Creatine works by recycling energy that is already in the tissues. Another dietary supplement, carnitine, helps metabolize fatty acids. Others, such as pyruvate and coenzyme Q10, also help recycle energy. None of these other nutritional supplements actually help produce the energy components that the cell needs to maintain a healthy energy storage.

Only ribose has this important metabolic function. Remember: Ribose helps the body produce energy, while other supplements can help the body use energy more efficiently. quick delivery of the product and correct information about delivery time.

Home Counselor Ribose - New energy for the body. Ribose - New energy for the body Information, effects, deficiency, dosage, side effects. Table of contents. Ribose effect How is ribose produced in the body? How does the body get cell energy from ribose? Ribose - The crucial factor Ribose side effects Ribose and the heart Who should take Ribose?

Ribose and athletes Ribose and other food supplements. Recommended products. Ribose effect Ribose or D-ribose is a simple sugar that forms the carbohydrate portion of the DNA and RNA. Ribose improves exercise performance and physical function.

Ribose provides cardiac energy, which is needed to maintain normal cardiac function. Ribose increases cardiac efficiency and reduces stress during exercise. Ribose supports healthy energy levels in the heart and muscles. 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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