D-ribose and cognitive impairment in rodents: a sweet but troubling connection!

Published on November 9, 2022

Imagine a world where sugar not only tastes good, but also affects your brain! Well, that’s exactly what D-ribose does to rodents. In a systematic review and meta-analysis, scientists investigated the impact of different doses of D-ribose on cognition in these furry creatures. Turns out, the results were inconsistent, much like trying to predict how many licks it takes to get to the center of a Tootsie Pop! But hold on to your hats (or lab coats), because they did find something important. D-ribose treatment actually caused cognitive impairment in the rodents. And guess what? The higher the dose of D-ribose, the worse their cognition became! It’s like giving someone more and more candy until they can’t think straight anymore. But here’s where it gets really interesting – D-ribose seems to be forming these things called advanced glycation end products (AGEs) in the brain and blood. These AGEs may be responsible for the cognitive decline. So, if you’re curious to learn more about the sweet yet troubling connection between D-ribose and cognition, check out the full research article!

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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