Alzheimer’s Disease and Green Tea: Epigallocatechin-3-Gallate as a Modulator of Inflammation and Oxidative Stress

Modulation of PKC-mediated pathways by EGCG in Alzheimer’s disease. EGCG can induce the activation of PKC pathways (1), specifically the isoform PKCζ (2) that enhances long-term memory (3), PKCα (4) that results in an increase in memory function (5) and PKCε (6) that activates BDNF factor (7), promoting synaptogenesis (8), neuronal survival (9), Ca2+ liberation (10) and changes of synaptic structures (11), altogether promoting neuroprotection (12). The generation of Aβ produces Aβ plaques (13), promoting neurodegeneration processes (14). Aβ also inhibits the PKC pathway (15) and RACK (16), whose receptors are required to activate PKC (17), and blocks BDNF (18). Moreover, the isoforms PKCα and PKCε activate α-secretase (19), promoting the generation of sAPPα (20) that inhibits Aβ production (21). PKCε activates ECE1 (22), which degrades Aβ (21). The activation of the PKC pathway inhibits GSK3β (23), which is involved in tau hyperphosphorylation (24) that finally leads to neurodegeneration processes (14). EGCG produces the reduction in protein Bax (25) and promotes the degradation of protein Bad (26) through the proteasomal system (27).

Publication

Alzheimer’s Disease and Green Tea: Epigallocatechin-3-Gallate as a Modulator of Inflammation and Oxidative Stress. (2023) Víctor Valverde-Salazar, et al. Antioxidants (Basel). 2023 Jul;12(7):1460. Figure: F5. Homo sapiens

Disease mentions