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Open AccessArticle

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

1
Department of Biochemistry, College of Medicine, Konyang University, 158, Gwanjeodong-ro, Seo-gu, Daejeon 35365, Korea
2
Department of Nephrology, School of Medicine, Chungnam National University, Daejeon 35015, Korea
3
Department of Biochemistry, School of Medicine, Chungnam National University, Daejeon 35015, Korea
4
Myunggok Medical Research Institute, College of Medicine, Konyang University, Daejeon 35365, Korea
5
Department of Nursing, College of Nursing, Jeju National University, Jeju-si 63243, Korea
6
Biopharmaceutical Chemistry Major, School of Applied Chemistry, Kookmin University, Seongbuk-gu, Seoul 02707, Korea
*
Authors to whom correspondence should be addressed.
These authors contributed equally to this work.
Int. J. Mol. Sci. 2020, 21(11), 3879; https://doi.org/10.3390/ijms21113879
Received: 26 April 2020 / Revised: 27 May 2020 / Accepted: 27 May 2020 / Published: 29 May 2020
(This article belongs to the Special Issue Mechanism of Adult Neurogenesis)
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 (Aβ) 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 Aβ 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 Aβ-overexpressing model. We found that omega-3 PUFAs significantly improved Aβ-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, Aβ accumulation, neuroinflammation, neuronal loss, and impairment of adult hippocampal neurogenesis. View Full-Text
Keywords: Alzheimer’s disease; mitochondria; omega-3; DHA; fat-1 mice; 5XFAD mice Alzheimer’s disease; mitochondria; omega-3; DHA; fat-1 mice; 5XFAD mice
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Park, Y.H.; Shin, S.J.; Kim, H.; Hong, S.B.; Kim, S.; Nam, Y.; Kim, J.-J.; Lim, K.; Kim, J.-S.; Kim, J.-I.; Jeon, S.G.; Moon, M. Omega-3 Fatty Acid-Type Docosahexaenoic Acid Protects against Aβ-Mediated Mitochondrial Deficits and Pathomechanisms in Alzheimer’s Disease-Related Animal Model. Int. J. Mol. Sci. 2020, 21, 3879.

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