Urine D-ribose levels correlate with cognitive function in community-dwelling older adults

Zhu, Xinyi; Wei, Yan; He, Yingge; He, Rong; Li, Juan

doi:10.1186/s12877-022-03288-w

Cited by 6 publications

(5 citation statements)

References 40 publications

(40 reference statements)

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“…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, 2022 ). Lyu et al (2019) found that D -ribose levels in patients with AD were considerably higher than those in age-matched controls with normal cognition.…”

Section: Discussionsupporting

confidence: 91%

A systematic review and meta-analysis of cognitive and behavioral tests in rodents treated with different doses of D-ribose

Song

Du²,

An³

et al. 2022

Front. Aging Neurosci.

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BackgroundD-ribose is an aldehyde sugar and a necessary component of all living cells. Numerous reports have focused on D-ribose intervention in animal models to assess the negative effects of D-ribose on cognition. However, the results across these studies are inconsistent and the doses and actual effects of D-ribose on cognition remain unclear. This systematic review aimed to evaluate the effect of D-ribose on cognition in rodents.MethodsThe articles from PubMed, Embase, Sciverse Scopus, Web of Science, the Chinese National Knowledge Infrastructure, SinoMed, Wanfang, and Cqvip databases were screened. The results from the abstract on cognitive-related behavioral tests and biochemical markers from the included articles were extracted and the reporting quality was assessed.ResultsA total of eight trials involving 289 rodents met the eligibility criteria, and both low- and high-dose groups were included. Meta-analyses of these studies showed that D-ribose could cause a significant decrease in the number of platform crossings (standardized mean difference [SMD]: –0.80; 95% CI: –1.14, –0.46; p < 0.00001), percentage of distance traversed in the target quadrant (SMD: –1.20; 95% CI: –1.47, –0.92; p < 0.00001), percentage of time spent in the target quadrant (SMD: –0.93; 95% CI: –1.18, –0.68; p < 0.00001), and prolonged escape latency (SMD: 0.41; 95% CI: 0.16, 0.65; p = 0.001) in the Morris water maze test. Moreover, D-ribose intervention increased the levels of advanced glycation end products (AGEs) in the brain (SMD: 0.49; 95% CI: 0.34, 0.63; p < 0.00001) and blood (SMD: 0.50; 95% CI: 0.08, 0.92; p = 0.02). Subsequently, subgroup analysis for the dose of D-ribose intervention revealed that high doses injured cognitive function more significantly than low D-ribose doses.ConclusionD-ribose treatment caused 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 non-enzymatic glycosylation resulting in the generation of AGEs. These findings provide a new research idea for unveiling basic mechanisms and prospective therapeutic targets for the prevention and treatment of patients with cognitive impairment.

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Section: Discussionsupporting

confidence: 91%

A systematic review and meta-analysis of cognitive and behavioral tests in rodents treated with different doses of D-ribose

Song

Du²,

An³

et al. 2022

Front. Aging Neurosci.

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“…Of interest, two recent studies reported that urine D-ribose levels were correlated negatively with MMSE scores in an AD casecontrol cohort 46 and in a larger sample of community-dwelling older individuals, 47 which would be in line with this hypothesis. Another study reported a potential rescue of D-ribose dysmetabolism in rats with benfotiamine (BTMP) treatment, leading to decreased aging, tau hyperphosphorylation, and neurodegeneration.…”

Section: Discussionmentioning

confidence: 60%

Whole‐exome rare‐variant analysis of Alzheimer's disease and related biomarker traits

Küçükali

Neumann

Dongen

et al. 2022

Alzheimer's & Dementia

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Introduction: Despite increasing evidence of a role of rare genetic variation in the risk of Alzheimer's disease (AD), limited attention has been paid to its contribution to ADrelated biomarker traits indicative of AD-relevant pathophysiological processes. Methods: We performed whole-exome gene-based rare-variant association studies (RVASs) of 17 AD-related traits on whole-exome sequencing (WES) data generated in the European Medical Information Framework for Alzheimer's Disease Multimodal Biomarker Discovery (EMIF-AD MBD) study (n = 450) and whole-genome sequencing (WGS) data from ADNI (n = 808).Results: Mutation screening revealed a novel probably pathogenic mutation (PSEN1 p.Leu232Phe). Gene-based RVAS revealed the exome-wide significant contribution of rare coding variation in RBKS and OR7A10 to cognitive performance and protection against left hippocampal atrophy, respectively.Discussion: The identification of these novel gene-trait associations offers new perspectives into the role of rare coding variation in the distinct pathophysiological processes culminating in AD, which may lead to identification of novel therapeutic and diagnostic targets.

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“…The literature shows that the level of D-ribose in serum and urine is negatively correlated with cognitive function and induce anxiety-like behavior [ 2 , 21 , 22 ]. Therefore, the cognition and mood were checked through behavioral assessment in APP/PS1 mice.…”

Section: Resultsmentioning

confidence: 99%

Berberine Rescues D-Ribose-Induced Alzheimer‘s Pathology via Promoting Mitophagy

Wang

Zou

et al. 2023

IJMS

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Mitochondrial dysfunction is considered an early event of Alzheimer disease (AD). D-ribose is a natural monosaccharide that exists in cells, especially in mitochondria, and can lead to cognitive dysfunction. However, the reason for this is unclear. Berberine (BBR) is an isoquinoline alkaloid that can target mitochondria and has great prospect in the treatment of AD. The methylation of PINK1 reinforces the burden of Alzheimer’s pathology. This study explores the role of BBR and D-ribose in the mitophagy and cognitive function of AD related to DNA methylation. APP/PS1 mice and N2a cells were treated with D-ribose, BBR, and mitophagy inhibitor Mdivi-1 to observe their effects on mitochondrial morphology, mitophagy, neuron histology, AD pathology, animal behavior, and PINK1 methylation. The results showed that D-ribose induced mitochondrial dysfunction, mitophagy damage, and cognitive impairment. However, BBR inhibition of PINK1 promoter methylation can reverse the above effects caused by D-ribose, improve mitochondrial function, and restore mitophagy through the PINK1–Parkin pathway, thus reducing cognitive deficits and the burden of AD pathology. This experiment puts a new light on the mechanism of action of D-ribose in cognitive impairment and reveals new insights in the use of BBR for AD treatment.

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Urine D-ribose levels correlate with cognitive function in community-dwelling older adults

Cited by 6 publications

References 40 publications

A systematic review and meta-analysis of cognitive and behavioral tests in rodents treated with different doses of D-ribose

A systematic review and meta-analysis of cognitive and behavioral tests in rodents treated with different doses of D-ribose

Whole‐exome rare‐variant analysis of Alzheimer's disease and related biomarker traits

Berberine Rescues D-Ribose-Induced Alzheimer‘s Pathology via Promoting Mitophagy

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