Neurodegenerative and neuropsychiatric diseases have attracted global attention with an overwhelming burden on families and society. Tea contains many bioactive compounds, such as polyphenols and theanine, which could contribute to the neuroprotective effects of tea. The possible mechanisms of action include regulating signaling pathways and gut microbiota; inhibiting abnormal protein aggregation; normalizing the hyperactivity of the hypothalamic-pituitary-adrenal axis; as well as antioxidant and anti-inflammatory properties of tea for Parkinson’s disease, Alzheimer’s disease, and depression. In this narrative revie w, the effects of tea on these diseases were summarized, and special attention was paid to the mechanisms of action.
Abbreviations: AChE, acetylcholinesterase; ACTH, adrenocorticotropin; AKT, serine-threonine protein kinase; BChE, butyrylcholinesterase; BDNF, brain-derived neurotrophic factor; CI, confidence interval; COX-2, cyclooxygenase-2; CRH, corticotrophin-releasing hormone; CREB, cyclic adenosine monophosphate response element-binding protein; EC, epicatechin; ECG, epicatechin-3-gallate; EGC, epigallocatechin; EGCG, epigallocatechin gallate; ERK, extracellular signal-regulated kinase; GABA, gamma-aminobutyric acid; GSK-3β, glycogen synthase kinase-3β; HPA, hypothalamic-pituitary-adrenal; HR, hazard ratio; IL, interleukin; MAOB, monoamine oxidase B; MPTP, 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine; NFκB, nuclear factor kappa-light-chain-enhancer of activated B cells; Nrf2, nuclear factor erythroid 2-related factor 2; NOS, nitric oxide species; OR, odds ratio; PGC-1α; peroxisome proliferator-activated receptor gamma coactivator-1α; PI3K, phosphoinositide 3-kinase; PKC, protein kinase C; ROS, reactive oxygen species; RR, risk ratio; TLR4, Toll-like receptor 4; TNF-α; umor necrosis factor alpha; 6-OHDA, 6-hydroxydopamine.