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Mol Neurobiol. 2019 Aug;56(8):5556-5567. doi: 10.1007/s12035-019-1469-6. Epub 2019 Jan 16.

Procyanidins and Alzheimer's Disease.

Zhao S1,2,3, Zhang L4, Yang C1,2,3, Li Z5, Rong S6,7,8.

Author information

1
Department of Nutrition and Food Hygiene, School of Public Health, Medical College, Wuhan University of Science and Technology, Wuhan, 430065, China.
2
Institute of Nutrition and Chronic Diseases, Wuhan University of Science and Technology, Wuhan, 430065, China.
3
Hubei Province Key Laboratory of Occupational Hazard Identification and Control, Wuhan University of Science and Technology, Wuhan, 430065, China.
4
Department of Neurology, Hubei Provincial Hospital of Integrated Chinese & Western Medicine, Wuhan, 430015, China.
5
Wuhan Puren Guanghui Hospital, Wuhan, 430084, China.
6
Department of Nutrition and Food Hygiene, School of Public Health, Medical College, Wuhan University of Science and Technology, Wuhan, 430065, China. rongshuang@wust.edu.cn.
7
Institute of Nutrition and Chronic Diseases, Wuhan University of Science and Technology, Wuhan, 430065, China. rongshuang@wust.edu.cn.
8
Hubei Province Key Laboratory of Occupational Hazard Identification and Control, Wuhan University of Science and Technology, Wuhan, 430065, China. rongshuang@wust.edu.cn.

Abstract

Procyanidins, the oligomeric compounds formed from catechin and epicatechin molecules, are potentially effective targets as nutraceuticals or pharmaceuticals in the prevention and treatment of Alzheimer's disease (AD). Natural procyanidins can attenuate AD pathological features, extracellular amyloid deposits, and neurofibrillary tangles via reducing Aβ accumulation and tau pathology. The enhancement of cognition as well as modulation of synaptic plasticity by these compounds also participated in the alleviation of AD. Notably, procyanidins and some of their metabolites have been observed to upregulate SIRT1 (silent information regulator 1) which is essential for normal cognitive and synaptic plasticity, and stimulate CREB (cAMP response element binding) which acts as a molecular switch from short- to long-term memory. Based on the interplay of CREB-SIRT1 axis, it is therefore conceivable that the regulation of procyanidins by the means of CREB-SIRT1 could promote the cognitive function and is thus conducive for AD pathogenesis. This review focuses on the role of procyanidins, the main group of flavonoids, on AD and the potential mechanism involved CREB-SIRT1 axis.

KEYWORDS:

Alzheimer’s disease; CREB; Procyanidins; SIRT1; Synaptic plasticity

PMID:
30649713
DOI:
10.1007/s12035-019-1469-6

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