Chlorogenic Acid: Characteristics, Neuroprotective Effects, and Potential Mechanisms.
This review synthesizes animal and mechanistic studies indicating that chlorogenic acid (a dietary polyphenol) exerts neuroprotective effects relevant to Parkinson's disease through anti-inflammatory, antioxidant, and autophagy-modulating actions, while highlighting gaps in molecular specificity…
What the AI sees
This review synthesizes animal and mechanistic studies indicating that chlorogenic acid (a dietary polyphenol) exerts neuroprotective effects relevant to Parkinson's disease through anti-inflammatory, antioxidant, and autophagy-modulating actions, while highlighting gaps in molecular specificity…
Research significance
CGA engages multiple PD-relevant pathways (neuroinflammation, oxidative stress, protein aggregation, autophagy) and could be a low-risk repurposing candidate, but its translational value is tempered by limited mechanistic resolution and pharmacokinetic/bioavailability challenges.
Source 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.