ArticleGenes & genomics2025
Hippocampal MCT4 as a key regulator in excessive exercise-induced cognitive impairment: involvement of neuroinflammation.
Article in Genes & genomics, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 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
4 citing papers in PubMed.
- Roles of Lcn2 and neuroinflammation in a scopolamine-induced cognitive impairment animal model: implication of the NLRP3 inflammasome pathway.Genes & genomics · 2026Article
- Red ginseng-mediated modulation of the NLRP3 Inflammasome in neuroinflammatory-related cognitive impairments.Journal of ginseng research · 2026Review
- Biomarkers for predominantly inattentive ADHD: potential involvement of Wnt/β-catenin/integrin signaling in a spontaneously hypertensive rat.Genes & genomics · 2026Article
- Myokine Cathepsin B as a Key Muscle-Brain Axis Regulator Mediates Treadmill-Running-Induced Hippocampal Neurogenesis and Cognitive Improvement in Mice.Research (Washington, D.C.) · 2026Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
4 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundAs human life expectancy increases, maintaining a healthy lifestyle has become crucial. However, excessive exercise (EE) can lead to negative consequences such as muscle damage and exercise addiction. Recently, numerous reports have indicated that EE negatively impacts cognitive performance, although the exact mechanism remains unclear.
objectiveThis study aimed to investigate the specific mechanisms underlying cognitive alterations induced by EE.
methodsWe conducted the Y-maze, Barnes maze, and Novel Object Recognition Test to assess both short-term and long-term memory, as well as object recognition ability. We then validated our findings using qRT-PCR to elucidate the underlying mechanisms. Additionally, Diclofenac (Dic), an anti-inflammatory drug, was administered to evaluate its effects on cognitive function and the results of the molecular experiments.
resultsEE-induced mice exhibited cognitive impairments, along with elevated expression of inflammatory cytokines such as tumor necrosis factor-α, interleukin (IL) -6, and IL-1β, and downregulated monocarboxylate transporters (MCTs) like MCT4. However, animals pre-treated with Dic regained cognitive function, alongside restored levels of IL-6, IL-1β, and MCT4.
conclusionMCT4 plays may play a crucial role in EE-induced cognitive impairments.
Indexed as
Identifiers
40244523What 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.