ArticleCNS & neurological disorders drug targets2026
Chlorogenic Acid as a Neuroprotective Agent: Enhancing Plasticity and Promoting Brain Health and Functional Reserve.
Article in CNS & neurological disorders drug targets, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.
What it found
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The trial behind it
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Who cites it
5 citing papers in PubMed.
- Investigating the effects of chlorogenic acid on novel object recognition memory impairment, hyperlocomotion, and prefrontal BDNF expression in a sub-chronic ketamine-induced schizophrenia-like rat model.IBRO neuroscience reports · 2026Article
- The Therapeutic Architecture of Chlorogenic Acids: Molecular Mechanisms in Chronic Disease Prevention.Nutrients · 2026Review
- Early-stage olfactory bulbectomy induces hyperlocomotion with increased astrocyte and microglial density in the prefrontal cortex of male rats.Brain structure & function · 2026Article
- Recent Advances in Chlorogenic Acids for Food Preservation and Shelf-Life Extension.Antioxidants (Basel, Switzerland) · 2026Review
- Trends and Perspectives in the Rational Management of CNS Disorders.CNS & neurological disorders drug targets · 2026Article
Corrections and comments
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Authors and funding
8 authors.
Funding
Abstract
introductionFunctional reserve, the process that warrants the brain to have resources to maintain key functions and processes when facing neurodegeneration, may be strengthened in nominally healthy subjects by measures that prompt neural plasticity throughout life.
methodsIn this work, we administered Chlorogenic Acid (CGA) to evaluate its ability to promote functional morphological plasticity in the frontal cortical-striatal circuit of healthy mice, a pathway exposed constantly to oxidative challenges, excitotoxicity, and neuroinflammation. The magnitude of neural plasticity was estimated by assessing spontaneous motor behavior (open field), the relative magnitude of neuronal activation (number of c-Fos positive neurons), dendritic remodeling (Golgi- Cox impregnation), the availability of Brain-Derived Neurotrophic Factor (BDNF) (semiquantitative Western blotting), and lipid peroxidation (TBARS assay) in CGA- or vehicle-administered C57BL/6 male mice.
resultsCGA administration increased c-Fos in the Dorsal striatum (Ds), changed the availability of BDNF and Pro-BDNF in the Frontal Cortex (FC) and Ds, induced dendritic remodeling in FC and DS neurons, and reduced FC and DS lipid peroxidation without affecting motor performance or the availability of TrkB receptor isoforms.
conclusionOur findings suggest that CGA increases functional reserve by promoting neuronal plasticity in healthy male mice. Future research should determine whether these additional resources indeed protect against neurodegeneration.
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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.