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Omega-3 Fatty Acid-Type Docosahexaenoic Acid Protects against Aβ-Mediated Mitochondrial Deficits and Pathomechanisms in Alzheimer’s Disease-Related Animal Model

Authors
  • park, yong
  • shin, soo jung
  • kim, hyeon soo
  • hong, sang bum
  • kim, sujin
  • nam, yunkwon
  • kim, jwa-jin
  • lim, kyu
  • kim, jong-seok
  • kim, jin-il
  • jeon, seong gak
  • moon, minho
Publication Date
May 29, 2020
Identifiers
DOI: 10.3390/ijms21113879
OAI: oai:mdpi.com:/1422-0067/21/11/3879/
Source
MDPI
Keywords
Language
English
License
Green
External links

Abstract

It has been reported that damage to the mitochondria affects the progression of Alzheimer&rsquo / 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&beta / ) 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&beta / 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&beta / -overexpressing model. We found that omega-3 PUFAs significantly improved A&beta / -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&beta / accumulation, neuroinflammation, neuronal loss, and impairment of adult hippocampal neurogenesis.

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