Omega-3 Fatty Acid-Type Docosahexaenoic Acid Protects against A?-Mediated Mitochondrial Deficits and Pathomechanisms in Alzheimer's Disease-Related Animal Model.

ABSTRACT: It has been reported that damage to the mitochondria affects the progression of Alzheimer's disease (AD), and that mitochondrial dysfunction is improved by omega-3. However, no animal or cell model studies have confirmed whether omega-3 inhibits AD pathology related to mitochondria deficits. In this study, we aimed to (1) identify mitigating effects of endogenous omega-3 on mitochondrial deficits and AD pathology induced by amyloid beta (A?) in fat-1 mice, a transgenic omega-3 polyunsaturated fatty acids (PUFAs)-producing animal; (2) identify if docosahexaenoic acid (DHA) improves mitochondrial deficits induced by A? in HT22 cells; and (3) verify improvement effects of DHA administration on mitochondrial deficits and AD pathology in B6SJL-Tg(APPSwFlLon,PSEN1*M146L*L286V)6799Vas/Mmjax (5XFAD), a transgenic A?-overexpressing model. We found that omega-3 PUFAs significantly improved A?-induced mitochondrial pathology in fat-1 mice. In addition, our in vitro and in vivo findings demonstrate that DHA attenuated AD-associated pathologies, such as mitochondrial impairment, A? accumulation, neuroinflammation, neuronal loss, and impairment of adult hippocampal neurogenesis.

SUBMITTER: Park YH 

PROVIDER: S-EPMC7312360 | biostudies-literature | 2020 May

REPOSITORIES: biostudies-literature