| First Author | Park YH | Year | 2020 |
| Journal | Int J Mol Sci | Volume | 21 |
| Issue | 11 | PubMed ID | 32486013 |
| Mgi Jnum | J:352658 | Mgi Id | MGI:7704281 |
| Doi | 10.3390/ijms21113879 | Citation | Park YH, et al. (2020) Omega-3 Fatty Acid-Type Docosahexaenoic Acid Protects against Abeta-Mediated Mitochondrial Deficits and Pathomechanisms in Alzheimer's Disease-Related Animal Model. Int J Mol Sci 21(11) |
| abstractText | 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 (Abeta) 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 Abeta 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 Abeta-overexpressing model. We found that omega-3 PUFAs significantly improved Abeta-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, Abeta accumulation, neuroinflammation, neuronal loss, and impairment of adult hippocampal neurogenesis. |
