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Chronic alpha-linolenic acid treatment alleviates age-associated neuropathology: Roles of PERK/eIF2 alpha signaling pathway

文献类型： 外文期刊

作者： Gao, Hui;Yan, Peipei;Han, Hao;Yang, Wei;Yao, Ping;Liu, Liegang;Gao, Hui;Yan, Peipei;Zhang, Shun;Han, Hao;Yang, Wei;Yao, Ping;Liu, Liegang;Nie, Shuke;Huang, Fenghong;Deng, Qianchun;Huang, Qingde;Xu, Jiqu;Huang, Fenghong;Deng, Qianchun;Huang, Qingde;Xu, Jiqu;Wu, Hailei;Ye, Keqiang

作者机构：

关键词： Aging;alpha-Linolenic acid;Learning and memory;Endoplasmic reticulum stress;Unfold protein response

期刊名称： BRAIN BEHAVIOR AND IMMUNITY

ISSN： 0889-1591

年卷期： 2016 年 57 卷

页码：

收录情况： SCI

摘要： Aging is a principal risk factor for neurodegenerative diseases and especially shares similar pathologic mechanisms to Alzheimer's disease (AD). Amyloid-beta (A beta) plaques deposition and neurofibrillary tangles (NFTs) are the prominent age-dependent pathologies implicated in the cognitive deficits. Accumulation of mis-folded proteins in the endoplasmic reticulum triggers a cellular stress response called the unfolded protein response (UPR), the activation of which is increased in AD patients. However, the UPR relates to the pathological hallmarks of aging is still elusive. In this study, we report that long-term supplement of alpha-linolenic acid (ALA), starting before the onset of disease symptoms (6 month-old), prevents the age-related memory deficits during natural aging. The amelioration of the memory impairment is associated with a decrease in UPR related markers [glucose regulated protein 78 (GRP78), protein kinase RNA-like endoplasmic reticulum kinase (PERK), eukaryotic Initiation Factor at (eIF2 alpha)]. ALA suppressed the PERK/eIF2 alpha signaling, which may be responsible for multifaceted memory-deteriorating and neurodegenerative mechanisms, including inhibition of A beta production by suppressing beta-site APP-cleaving enzyme 1 (BACE1) expression, enhancement of cAMP response element binding protein (CREB) function via down-regulating activating transcription factor 4 (ATF4), and suppression of Tau phosphorylation by inhibiting glycogen synthase kinase 3 beta (GSK-3 beta) pathway. Taken together, our findings provide new insights into the link between ALA and PERK/eIF2 alpha signaling, which could contribute to a better understanding of an ALA-mediated protective effect in aging-associated neuropathology. (C) 2015 Elsevier Inc. All rights reserved.

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