Regular ArticleDeficiency in Mitochondrial Aldehyde Dehydrogenase Increases the Risk for Late-Onset Alzheimer's Disease in the Japanese Population
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2020, Biochemical and Biophysical Research CommunicationsCitation Excerpt :Additionally, with acetaldehyde treatment, MC 3T3-E1 cells also accumulated 4HNE and induced proliferation loss and apoptosis. Increased levels of aldehyde adducts by ALDH2∗2 are implicated in various disease states and were detected in oxidized lipoproteins in osteoarthritic articular tissues, atherosclerotic lesions, cardiac tissue from patients with coronary artery disease, and the brains of individuals with Alzheimer’s disease [6–8]. Recently, ALDH2 rs671 is associated with hip fracture [9].
Interaction of oxidative stress and neurotrauma in ALDH2<sup>−/−</sup> mice causes significant and persistent behavioral and pro-inflammatory effects in a tractable model of mild traumatic brain injury
2020, Redox BiologyCitation Excerpt :This presents a dilemma for development of preclinical models that must demonstrate statistical significance with reasonable sample size, and usually leads to the forfeit of the heterogeneity observed in human patient populations in exchange for a genetically driven homogeneity in the animal model. The “Asian allele”, a loss-of-function mutation in ALDH2, prevalent in the East Asian population, has been proposed to contribute to AD risk in the general and APOE4 carrier populations [29–31,33]. Indeed, in transgenic mice carrying the ALDH2 mutation, 20% of 1 year old mice were reported to show signs of neurodegeneration [34].
Genetic resilience to Alzheimer's disease in APOE ε4 homozygotes: A systematic review
2019, Alzheimer's and Dementia
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To whom correspondence should be addressed at Department of Biochemistry and Cell Biology, Institute of Gerontology, Nippon Medical School, 1-396, Kosugi-cho, Nakahara-ku, Kawasaki City, Kanagawa-ken 211-8533 Japan. Fax: +81 44 733 1877. E-mail: [email protected].