{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,10,14]],"date-time":"2026-10-14T12:19:40Z","timestamp":1791980380159,"version":"4.4.0"},"reference-count":47,"publisher":"Wiley","issue":"5","license":[{"start":{"date-parts":[[2022,1,22]],"date-time":"2022-01-22T00:00:00Z","timestamp":1642809600000},"content-version":"vor","delay-in-days":0,"URL":"http:\/\/onlinelibrary.wiley.com\/termsAndConditions#vor"}],"content-domain":{"domain":["onlinelibrary.wiley.com"],"crossmark-restriction":true},"short-container-title":["Euro J of Neurology"],"published-print":{"date-parts":[[2022,5]]},"abstract":"<jats:title>Abstract<\/jats:title><jats:sec><jats:title>Background and purpose<\/jats:title><jats:p>Abnormal mitochondrial metabolism has been described in the Alzheimer's disease (AD) brain. However, the relationship between AD pathophysiology and key mitochondrial processes remains elusive. The purpose of this study was to investigate whether mitochondrial complex I dysfunction is associated with amyloid aggregation or glucose metabolism and brain atrophy in patients with mild AD using positron emission tomography (PET).<\/jats:p><\/jats:sec><jats:sec><jats:title>Methods<\/jats:title><jats:p>Amyloid\u2010 and tau\u2010positive symptomatic AD patients with clinical dementia rating 0.5 or 1 (<jats:italic>N<\/jats:italic>\u00a0=\u00a030; mean age\u00a0\u00b1\u00a0standard deviation: 71.8\u00a0\u00b1\u00a07.6\u00a0years) underwent magnetic resonance imaging and PET scans with [<jats:sup>18<\/jats:sup>F]2\u2010tert\u2010butyl\u20104\u2010chloro\u20105\u20132H\u2010pyridazin\u20103\u2010one (BCPP\u2010EF), [<jats:sup>11<\/jats:sup>C]Pittsburgh Compound\u2010B (PiB) and [<jats:sup>18<\/jats:sup>F]fluorodeoxyglucose (FDG) to assess brain atrophy, mitochondrial complex I dysfunction, amyloid deposition, and glucose metabolism, respectively. Local cortical associations among these biomarkers and gray matter volume were evaluated with voxel\u2010based regressions models.<\/jats:p><\/jats:sec><jats:sec><jats:title>Results<\/jats:title><jats:p>[<jats:sup>18<\/jats:sup>F]BCPP\u2010EF standardized uptake value ratio (SUVR) was positively correlated with [<jats:sup>18<\/jats:sup>F]FDG SUVR in the widespread brain area, while its associations with gray matter volume were restricted to the parahippocampal gyrus. Reductions in [<jats:sup>18<\/jats:sup>F]BCPP\u2010EF SUVR were associated with domain\u2010specific cognitive performance. We did not observe regional associations between mitochondrial dysfunction and amyloid burden.<\/jats:p><\/jats:sec><jats:sec><jats:title>Conclusions<\/jats:title><jats:p>In symptomatic cases, although mitochondrial complex I reduction is linked to a wide range of downstream neurodegenerative processes such as hypometabolism, atrophy, and cognitive decline, a link to amyloid was not observable. The data presented here support [<jats:sup>18<\/jats:sup>F]BCPP\u2010EF as an excellent imaging tool to investigate mitochondrial dysfunction in AD.<\/jats:p><\/jats:sec>","DOI":"10.1111\/ene.15246","type":"journal-article","created":{"date-parts":[[2022,1,10]],"date-time":"2022-01-10T17:13:16Z","timestamp":1641834796000},"page":"1324-1334","update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":27,"title":["Mitochondrial complex I abnormalities underlie neurodegeneration and cognitive decline in Alzheimer\u2019s disease"],"prefix":"10.1111","volume":"29","author":[{"ORCID":"https:\/\/orcid.org\/0000-0002-0783-5508","authenticated-orcid":false,"given":"Tatsuhiro","family":"Terada","sequence":"first","affiliation":[{"name":"Translational Neuroimaging Laboratory McGill University Research Centre for Studies in Aging Douglas Research Institute Le Centre int\u00e9gr\u00e9 universitaire de sant\u00e9 et de services sociaux (CIUSSS) de 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