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- W3030735989 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 (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." @default.
- W3030735989 created "2020-06-05" @default.
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- W3030735989 date "2020-05-29" @default.
- W3030735989 modified "2023-10-15" @default.
- W3030735989 title "Omega-3 Fatty Acid-Type Docosahexaenoic Acid Protects against Aβ-Mediated Mitochondrial Deficits and Pathomechanisms in Alzheimer’s Disease-Related Animal Model" @default.
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- W3030735989 doi "https://doi.org/10.3390/ijms21113879" @default.
- W3030735989 hasPubMedCentralId "https://www.ncbi.nlm.nih.gov/pmc/articles/7312360" @default.
- W3030735989 hasPubMedId "https://pubmed.ncbi.nlm.nih.gov/32486013" @default.
- W3030735989 hasPublicationYear "2020" @default.
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