Lower mitochondrial DNA content but not increased mutagenesis associates with decreased base excision repair activity in brains of AD subjects

• Published in: Neurobiology of aging Vol. 73; pp. 161 - 170
• Main Authors: Soltys, Daniela T., Pereira, Carolina P.M., Rowies, Fernanda T., Farfel, José M., Grinberg, Lea T., Suemoto, Claudia K., Leite, Renata E.P., Rodriguez, Roberta D., Ericson, Nolan G., Bielas, Jason H., Souza-Pinto, Nadja C.
• Format: Journal Article
• Language: English
• Published: United States Elsevier Inc 01.01.2019
• Subjects: Aged; Aged, 80 and over; Alzheimer Disease - genetics; Alzheimer Disease - pathology; Alzheimer's disease; Base excision repair; Brain - metabolism; DNA Repair - genetics; DNA, Mitochondrial - genetics; DNA, Mitochondrial - metabolism; DNA-(Apurinic or Apyrimidinic Site) Lyase - metabolism; Female; Gene Dosage; Humans; Male; Middle Aged; mtDNA depletion; mtDNA mutation; Mutation; Oxidative Stress - genetics; Temporal Lobe - metabolism; Uracil-DNA Glycosidase - metabolism; mtDNA mutation; mtDNA depletion; Base excision repair; Alzheimer's disease

Accumulation of oxidative mitochondrial DNA (mtDNA) damage and impaired base excision repair (BER) in brains have been associated with Alzheimer's disease (AD). However, it is still not clear how these affect mtDNA stability, as reported levels of mtDNA mutations in AD are conflicting. Thus, we...