A comprehensive review on the prevention and regulation of Alzheimer's disease by tea and its active ingredients

被引:24
作者
Huang, Yi [1 ]
Wei, Yang [1 ]
Xu, Jia [1 ,2 ]
Wei, Xinlin [1 ]
机构
[1] Shanghai Jiao Tong Univ, Sch Agr & Biol, Shanghai, Peoples R China
[2] Shanghai Univ, Sch Environm & Chem Engn, Shanghai, Peoples R China
基金
中国博士后科学基金; 中国国家自然科学基金;
关键词
Tea active ingredients; Alzheimer's disease; neuroprotection; beta-amyloid; inflammation; intestinal flora; AMYLOID-BETA LEVELS; UNIQUE AMINO-ACID; GREEN TEA; L-THEANINE; COGNITIVE IMPAIRMENT; MEMORY IMPAIRMENT; INDUCED NEUROTOXICITY; MOUSE MODEL; EPIGALLOCATECHIN-3-GALLATE EGCG; INCIDENT DEMENTIA;
D O I
10.1080/10408398.2022.2081128
中图分类号
TS2 [食品工业];
学科分类号
0832 ;
摘要
Alzheimer's disease (AD) has brought a heavy burden to society as a representative neurodegenerative disease. The etiology of AD combines multiple factors, concluding family, gender, head trauma, diseases and social psychology. There are multiple hypotheses explaining the pathogenesis of AD such as beta-amyloid (A beta) deposition and tau hyperphosphorylation, which lead to extracellular amyloid plaques and neurofibrillary tangles in neurons. The existing therapeutic drugs have several disadvantages including single target, poor curative effect, and obvious side effects. Tea contains many bioactive components, such as tea polyphenols (TPP), L-theanine (L-TH), tea pigment, tea polysaccharides and caffeine. The epidemiological investigations have shown that drinking tea can reduce the risk of AD. The mechanisms of tea active ingredients in the prevention and regulation of AD includes reducing the generation and aggregation of A beta; inhibiting tau aggregation and hyperphosphorylation; inhibiting neuronal apoptosis and regulate neurotransmitters; relieving oxidative stress and neuroinflammation as well as the regulation of intestinal flora. This review summarizes the different signaling pathways that tea active ingredients regulate AD. Furthermore, we propose the main limitations of current research and future research directions, hoping to contribute to the development of natural functional foods based on tea active ingredients in the prevention and treatment of AD.
引用
收藏
页码:10560 / 10584
页数:25
相关论文
共 218 条
[1]  
Abe A., 2007, NIHON NNOUGEIKAGAKU, V302, P16
[2]   Recent progress in studies on the health benefits of pyrroloquinoline quinone [J].
Akagawa, Mitsugu ;
Nakano, Masahiko ;
Ikemoto, Kazuto .
BIOSCIENCE BIOTECHNOLOGY AND BIOCHEMISTRY, 2016, 80 (01) :13-22
[3]   Green Tea, A Medicinal Food with Promising Neurological Benefits [J].
Akbarialiabad, Hossein ;
Dahroud, Mohammad Dahri ;
Khazaei, Mohammad M. ;
Razmeh, Saeed ;
Zarshenas, Mohammad M. .
CURRENT NEUROPHARMACOLOGY, 2021, 19 (03) :349-359
[4]   Nuclear factor-kappa B (NF-ΚB) inhibition as a therapeutic target for plant nutraceuticals in mitigating inflammatory lung diseases [J].
Alharbi, Khalid Saad ;
Afzal, Obaid ;
Almalki, Waleed Hassan ;
Kazmi, Imran ;
Shaikh, Mohammad Arshad Javed ;
Thangavelu, Lakshmi ;
Gulati, Monica ;
Singh, Sachin Kumar ;
Jha, Niraj Kumar ;
Gupta, Piyush Kumar ;
Chellappan, Dinesh Kumar ;
Oliver, Brian George ;
Dua, Kamal ;
Gupta, Gaurav .
CHEMICO-BIOLOGICAL INTERACTIONS, 2022, 354
[5]   Purinergic P2 receptors trigger adenosine release leading to adenosine A2A receptor activation and facilitation of long-term potentiation in rat hippocampal slices [J].
Almeida, T ;
Rodrigues, RJ ;
De Mendonça, A ;
Ribeiro, JA ;
Cunha, RA .
NEUROSCIENCE, 2003, 122 (01) :111-121
[6]   The present and future of pharmacotherapy of Alzheimer's disease: A comprehensive review [J].
Anand, Abhinav ;
Patience, Albert Anosi ;
Sharma, Neha ;
Khurana, Navneet .
EUROPEAN JOURNAL OF PHARMACOLOGY, 2017, 815 :364-375
[7]   Therapeutics of Alzheimer's disease: Past, present and future [J].
Anand, R. ;
Gill, Kiran Dip ;
Mahdi, Abbas Ali .
NEUROPHARMACOLOGY, 2014, 76 :27-50
[8]   MATURATION OF CAFFEINE ELIMINATION IN INFANCY [J].
ARANDA, JV ;
COLLINGE, JM ;
ZINMAN, R ;
WATTERS, G .
ARCHIVES OF DISEASE IN CHILDHOOD, 1979, 54 (12) :946-949
[9]   Caffeine protects Alzheimer's mice against cognitive impairment and reduces brain β-amyloid production [J].
Arendash, G. W. ;
Schleif, W. ;
Rezai-Zadeh, K. ;
Jackson, E. K. ;
Zacharia, L. C. ;
Cracchiolo, J. R. ;
Shippy, D. ;
Tan, J. .
NEUROSCIENCE, 2006, 142 (04) :941-952
[10]   Caffeine Reverses Cognitive Impairment and Decreases Brain Amyloid-β Levels in Aged Alzheimer's Disease Mice [J].
Arendash, Gary W. ;
Mori, Takashi ;
Cao, Chuanhai ;
Mamcarz, Malgorzata ;
Runfeldt, Melissa ;
Dickson, Alexander ;
Rezai-Zadeh, Kavon ;
Tan, Jun ;
Citron, Bruce A. ;
Lin, Xiaoyang ;
Echeverria, Valentina ;
Potter, Huntington .
JOURNAL OF ALZHEIMERS DISEASE, 2009, 17 (03) :661-680