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• W2897682153 abstract "Alzheimer's disease (AD) is a neurodegenerative disorder characterized by formation of amyloid plaques and neurofibrillary tangles, followed by neuronal death. Another characteristic of AD is a 30% decrease in cytochrome oxidase (COX) activity. COX is a complex of 13 polypeptide chains, 3 of which are encoded on mitochondrial DNA (mtDNA). Our laboratory identified a T->C mutation in COX subunit 3 at mtDNA position 9861 that results in a 2-fold greater reduction in COX activity than that seen in AD brains lacking the mutation. In this study, total RNA from frozen brains of control subjects and patients with autopsy-confirmed AD was isolated and gene expression was compared between AD samples lacking (AD) or containing (AD+) the T9861C COX mutation in order to assess differences in cellular energy production and associated biological and neurodegenerative pathways. Total RNA was isolated from 4 control brains and 9 brains with Alzheimer's Disease, 6 of which had the COX AD+ mutation. Total RNA was assessed using Nanodrop and Bioanalyzer analysis. cDNA was prepared and applied to the Human Mitochondrial Energy Metabolism RT2 Profiler™ PCR Array. The qPCR data was then analyzed using Qiagen Profiler Array Data Analysis version 3.5. The fold-regulation and p-value data was input into Ingenuity Pathway Analysis software to characterize the differences between the AD and AD+ brains. For the 14 COX subunit genes queried, there was an 8-fold decrease in COX gene expression in AD+ brains compared to AD brains without the mutation. There was a down-regulation of all respiratory chain complexes, and the gene expression values were found to be consistent with oxidative phosphorylation and mitochondrial dysfunction pathways. Major biologic processes and diseases overlapping with the gene expression patterns seen in the AD/AD+ differences included metabolic and neurological disease. The data indicate that the decrease in respiratory complex activity, especially COX activity, associated with Alzheimer's disease is even more pronounced in brains possessing the T9861C mtDNA mutation. This mutation may play a role in the mitochondrial dysfunction of AD, and possibly the formation of plaques and tangles as indicated by the link to neurological disease patterns." @default.
• W2897682153 created "2018-10-26" @default.
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• W2897682153 date "2018-07-01" @default.
• W2897682153 modified "2023-10-16" @default.
• W2897682153 title "P1‐223: THE MTDNA T9861C MUTATION EXACERBATES REDUCTIONS IN OXIDATIVE PHOSPHORYLATION PATHWAYS IN ALZHEIMER'S DISEASE BRAINS" @default.
• W2897682153 doi "https://doi.org/10.1016/j.jalz.2018.06.228" @default.
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