ArticleMolecular neurobiology2025
Gut Acetic Acid Alleviates Cognitive Impairment by Inhibiting Tau Hyperphosphorylation via Regulating FFAR3/Erk Pathway in Chronic Cerebral Ischemia Mice.
Article in Molecular neurobiology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
3 citing papers in PubMed.
- Short-chain fatty acids as key mediators of the microbiota-gut-brain axis in chronic cerebral hypoperfusion: mechanisms and therapeutics.Molecular medicine (Cambridge, Mass.) · 2026Review
- The Gut Mucosal Barrier-Neuroinflammation Axis in Vascular Cognitive Impairment Induced by Chronic Cerebral Ischemia: A Narrative Review of Candidate Mechanisms.International journal of molecular sciences · 2026Review
- Opposite regulatory effects ofFrontiers in neurologyArticle
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
13 authors.
Funding
Abstract
Chronic cerebral ischemia is a significant contributor to cognitive impairment, which plays a crucial role in the pathogenesis of vascular dementia (VaD). While tau hyperphosphorylation is acknowledged as a critical risk factor, the precise mechanisms underlying this process remain poorly understood. Recent studies have indicated a significant correlation between low abundance of intestinal short-chain fatty acids (SCFAs) and tau hyperphosphorylation. In this study, we assessed neurological function in mice subjected to chronic cerebral ischemia through bilateral common carotid artery stenosis (BCAS) and in cells through oxygen-glucose deprivation (OGD). In our investigation, we observed cognitive deficits in chronic cerebral ischemia mice. This was accompanied by dysbiosis of the intestinal microbiota, markedly reduced levels of acetic acid (Ace), aberrant Erk activation, and increased tau hyperphosphorylation. Notably, supplementation with Ace exhibits a significant neuroprotective effect. Utilizing both BCAS mice and OGD cell models, our study elucidated that Ace can ameliorate cognitive impairment induced by chronic cerebral ischemia. The underlying mechanism may involve a reduction in tau hyperphosphorylation, potentially mediated through the inhibition of Erk activity via the free fatty acid receptor 3 (FFAR3)/Erk signaling pathway. This research provides novel insights into the pathophysiology of VaD resulting from chronic cerebral ischemia and offers potential therapeutic strategies for its clinical management, highlighting the significance of targeting metabolic dysregulation in the prevention and treatment of cognitive decline.
Indexed as
Identifiers
41276732What OpenQuestion holds
Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.