Experimental Evidence Supporting the Neuroprotective Role of Epigallocatechin-3-Gallate in Parkinson’s Disease
Ahsas Goyal, Sparsh Kaushal, Partyaksha Ruhella, Nandini Dubey, Harlokesh Narayan YadavIntroduction:
Parkinson’s Disease (PD) is a progressive neurodegenerative disorder characterized by motor and non-motor symptoms due to the loss of dopaminergic neurons in the substantia nigra. Most current therapies are symptomatic and do not arrest the disease course. There is growing interest in nutraceuticals that have the potential to modify disease. Epigallocatechin- 3-gallate (EGCG), a major polyphenol in green tea, has been shown to have neuroprotective properties related to the etiology of Parkinson's disease.
Methods:
The databases PubMed, Scopus, Web of Science, and Google Scholar were systematically searched. To uncover original research papers, reviews, and meta-analyses on EGCG and its activities in PD, the search strategy was developed by combining keywords such as “Parkinson’s disease,” “Epigallocatechin-3-gallate,” “Neuroprotective,” and “Preclinical”. Non-English articles, conference papers, and studies not connected to neuroprotective processes were excluded. Divergent results were attributed to methodological variations or biological variability, and current high-quality studies were prioritized to address inconsistencies. Seminal articles before 2020 were included to provide historical context and basic mechanical principles.
Results:
Evidence from preclinical models has repeatedly shown neuroprotective effects of EGCG in a number of PD animal models. EGCG decreases oxidative stress by activating antioxidant pathways, reduces neuroinflammation by suppressing pro-inflammatory cytokines, and attenuates apoptosis via modulating mitochondrial and STAT3-related signaling. Moreover, EGCG prevents α-synuclein aggregation, preserves striatal dopamine levels, protects dopaminergic neurons, and enhances motor performance in animal models.
Discussion:
EGCG’s pleiotropic characteristics permit the simultaneous targeting of many pathological processes involved in the evolution of Parkinson’s disease. It can pass the bloodbrain barrier, making it more therapeutically effective. However, the compounds' low oral bioavailability and rapid metabolism still pose difficulties for clinical translation.
Conclusion:
The available experimental results indicate that EGCG could be a successful neuroprotective and disease-modifying therapy for PD. More clinical studies and improved delivery systems are needed to confirm its therapeutic potential in humans.