Mitochondrial dysfunction and Alzheimer's disease

Article ID	Journal	Published Year	Pages	File Type
5845126	Progress in Neuro-Psychopharmacology and Biological Psychiatry	2011	11 Pages	PDF

Abstract

To date, one of the most discussed hypotheses for Alzheimer's disease (AD) etiology implicates mitochondrial dysfunction and oxidative stress as one of the primary events in the course of AD. In this review we focus on the role of mitochondria and mitochondrial DNA (mtDNA) variation in AD and discuss the rationale for the involvement of mitochondrial abnormalities in AD pathology. We summarize the current data regarding the proteins involved in mitochondrial function and pathology observed in AD, and discuss the role of somatic mutations and mitochondrial haplogroups in AD development.

Keywords

MPTP PiB MFN2 Cyclophilin D PrEP ApoE3 LHON Mfn1 CMRGlc NFT tRNA CypD APOE4 FDG APP Mitochondrial haplogroups PDHc COX OXPHOS Aβ TCA APOE2 rRNA DLP1 tom40 2-[18F]fluoro-2-deoxy-d-glucose Mitochondrial DNA Mitochondrial DNA (mtDNA)opa1 ROS ATP Mitochondrial dysfunction mild cognitive impairment tricarboxylic acid ribosomal ribonucleic acid transfer ribonucleic acid amyloid beta Alzheimer's disease Oxidative stress Positron emission tomography mtDNA electron transport chain cytochrome c oxidase Oxidative phosphorylation ABAD Control region neurofibrillary tangles mitofusin 1 mitofusin 2 cerebral metabolic rate for glucose Leber's hereditary optic neuropathy MCI ETc PET dynamin-like protein 1 amyloid precursor protein Pittsburgh compound B presequence protease Reactive oxygen species