Authors
Nadia V Harerimana, Devashi Paliwali, Carmen Romero-Molina, David A Bennett, Judy Pa, Alison Goate, Russell H Swerdlow, Shea J Andrews
Published in
Alzheimer's & dementia : the journal of the Alzheimer's Association. Volume 19. Issue 5. Pages 2069-2083. Epub Oct 12, 2022.
Abstract
Mitochondrial dysfunction is an early and prominent feature of Alzheimer's disease (AD), with impaired energy metabolism preceding the onset of clinical symptoms. Here we propose an update to the mitochondrial dysfunction hypothesis of AD based on recent results examining the role of mitochondrial genome abundance in AD. In a large post mortem study, we show that lower brain mitochondrial genome abundance is associated with a greater odds of AD neuropathological change and worse cognitive performance. We hypothesize that lower mitochondrial genome abundance impairs mitochondrial function by reducing mitochondrial bioenergetics, thereby impacting neuronal and glial cell function. However, it remains to be determined if mitochondrial dysfunction causes, mediates, or is a by-product of AD pathogenesis. Additional support for this hypothesis will be generated by linking peripheral blood mitochondrial genome abundance to AD and establishing clinical trials of compounds that upregulate total mitochondrial genome abundance or boost mitochondrial mass.
PMID:
36224040
Bibliographic data and abstract were imported from PubMed on 17 Sep 2026.
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