ReviewCurrent neuropharmacology2026
Chlorogenic Acid: Characteristics, Neuroprotective Effects, and Potential Mechanisms.
Review in Current neuropharmacology, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
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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.
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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.
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Who cites it
1 citing paper in PubMed.
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Authors and funding
6 authors.
Funding
Abstract
In this review, we explore recent evidence connecting chlorogenic acid (CGA) to neuropsychiatric disorders and critically discuss the biological mechanisms underlying these effects. CGA is a natural polyphenol that usually exists in fruits and vegetables. CGA has long been recommended for its broad pharmacological activities. Increasing evidence from animal studies has revealed that dietary CGA supplementation may confer protective effects on the nervous system. Here, we summarize multiple findings on CGA in animal models of neuropsychiatric disorders, including Parkinson's disease, Alzheimer's disease, stroke, depression, epilepsy, and other neuropsychiatric disorders. We place equal emphasis on chemical features, natural sources, bioavailability, and pharmacological properties of CGA; all of these can have a critical impact on CGA's intervention. Current experimental evidences suggest that the neuroprotective effects of CGA are driven by the convergence of several processes, including suppression of neuroinflammation, attenuation of oxidative stress, and context-dependent effects on synaptic and cellular homeostasis. In some models, CGA has also been associated with changes in autophagic activity and reduced accumulation of misfolded or aggregated proteins. Despite these advances, the field still lacks a coherent molecular framework that links CGA exposure to specific neural outcomes. Therefore, resolving this gap will be essential for the clinical application of CGA.
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