{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,10,12]],"date-time":"2026-10-12T02:19:30Z","timestamp":1791771570436,"version":"4.3.4"},"reference-count":67,"publisher":"Wiley","issue":"5","license":[{"start":{"date-parts":[[2022,10,12]],"date-time":"2022-10-12T00:00:00Z","timestamp":1665532800000},"content-version":"vor","delay-in-days":0,"URL":"http:\/\/creativecommons.org\/licenses\/by-nc\/4.0\/"}],"content-domain":{"domain":["alz-journals.onlinelibrary.wiley.com"],"crossmark-restriction":true},"short-container-title":["Alzheimer's &amp;amp; Dementia"],"published-print":{"date-parts":[[2023,5]]},"abstract":"<jats:title>Abstract<\/jats:title>\n                  <jats:p>\n                    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\n                    <jats:italic>post mortem<\/jats:italic>\n                    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\u2010product 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.\n                  <\/jats:p>","DOI":"10.1002\/alz.12812","type":"journal-article","created":{"date-parts":[[2022,10,12]],"date-time":"2022-10-12T21:38:25Z","timestamp":1665610705000},"page":"2069-2083","update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":32,"title":["The role of mitochondrial genome abundance in Alzheimer's disease"],"prefix":"10.1002","volume":"19","author":[{"given":"Nadia V.","family":"Harerimana","sequence":"first","affiliation":[{"name":"Ronald M. Loeb Center for Alzheimer's Disease, Department of Genetics &amp; Genomic Sciences Icahn School of Medicine at Mount Sinai  New York New York USA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Devashi","family":"Paliwali","sequence":"additional","affiliation":[{"name":"Department of Genome Sciences, John Curtin School of Medical Research The Australian National University  Canberra Australian Capital Territory Australia"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Carmen","family":"Romero\u2010Molina","sequence":"additional","affiliation":[{"name":"Ronald M. Loeb Center for Alzheimer's Disease, Department of Genetics &amp; Genomic Sciences Icahn School of Medicine at Mount Sinai  New York New York USA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"David A.","family":"Bennett","sequence":"additional","affiliation":[{"name":"Rush Alzheimer's Disease Center Rush University Medical Center  Chicago Illinois USA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Judy","family":"Pa","sequence":"additional","affiliation":[{"name":"Department of Neurosciences, Alzheimer's Disease Cooperative Study (ADCS) University of California  San Diego California USA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Alison","family":"Goate","sequence":"additional","affiliation":[{"name":"Ronald M. Loeb Center for Alzheimer's Disease, Department of Genetics &amp; Genomic Sciences Icahn School of Medicine at Mount Sinai  New York New York USA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Russell H.","family":"Swerdlow","sequence":"additional","affiliation":[{"name":"University of Kansas Alzheimer's Disease Research Center  Kansas City Kansas USA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Shea J.","family":"Andrews","sequence":"additional","affiliation":[{"name":"Ronald M. Loeb Center for Alzheimer's Disease, Department of Genetics &amp; Genomic Sciences Icahn School of Medicine at Mount Sinai  New York New York USA"},{"name":"Department of Psychiatry and Behavioral Sciences University of California San Francisco  San Francisco California 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