<HashMap><database>biostudies-literature</database><scores/><additional><submitter>Terada T</submitter><funding>Japanese Ministry of Education, Culture, Sports, Science and Technology</funding><pagination>28</pagination><full_dataset_link>https://www.ebi.ac.uk/biostudies/studies/S-EPMC8074456</full_dataset_link><repository>biostudies-literature</repository><omics_type>Unknown</omics_type><volume>16(1)</volume><pubmed_abstract>&lt;h4>Background&lt;/h4>Mitochondrial electron transport chain abnormalities have been reported in postmortem pathological specimens of Alzheimer's disease (AD). However, it remains unclear how amyloid and tau are associated with mitochondrial dysfunction in vivo. The purpose of this study is to assess the local relationships between mitochondrial dysfunction and AD pathophysiology in mild AD using the novel mitochondrial complex I PET imaging agent [&lt;sup>18&lt;/sup>F]BCPP-EF.&lt;h4>Methods&lt;/h4>Thirty-two amyloid and tau positive mild stage AD dementia patients (mean age ± SD: 71.1 ± 8.3 years) underwent a series of PET measurements with [&lt;sup>18&lt;/sup>F]BCPP-EF mitochondrial function, [&lt;sup>11&lt;/sup>C]PBB3 for tau deposition, and [&lt;sup>11&lt;/sup>C] PiB for amyloid deposition. Age-matched normal control </pubmed_abstract><journal>Molecular neurodegeneration</journal><pubmed_title>Mitochondrial complex I abnormalities is associated with tau and clinical symptoms in mild Alzheimer's disease.</pubmed_title><pmcid>PMC8074456</pmcid><funding_grant_id>16H06402A01</funding_grant_id><funding_grant_id>17H04247</funding_grant_id><funding_grant_id>17K09797</funding_grant_id><pubmed_authors>Tsukada H</pubmed_authors><pubmed_authors>Ouchi Y</pubmed_authors><pubmed_authors>Rosa-Neto P</pubmed_authors><pubmed_authors>Lussier F</pubmed_authors><pubmed_authors>Benedet A</pubmed_authors><pubmed_authors>Bunai T</pubmed_authors><pubmed_authors>Tissot C</pubmed_authors><pubmed_authors>Obi T</pubmed_authors><pubmed_authors>Terada T</pubmed_authors><pubmed_authors>Pascoal TA</pubmed_authors><pubmed_authors>Wang YT</pubmed_authors><pubmed_authors>Matsudaira T</pubmed_authors><pubmed_authors>Therriault J</pubmed_authors><pubmed_authors>Kang MSP</pubmed_authors><pubmed_authors>Savard M</pubmed_authors></additional><is_claimable>false</is_claimable><name>Mitochondrial complex I abnormalities is associated with tau and clinical symptoms in mild Alzheimer's disease.</name><description>&lt;h4>Background&lt;/h4>Mitochondrial electron transport chain abnormalities have been reported in postmortem pathological specimens of Alzheimer's disease (AD). However, it remains unclear how amyloid and tau are associated with mitochondrial dysfunction in vivo. The purpose of this study is to assess the local relationships between mitochondrial dysfunction and AD pathophysiology in mild AD using the novel mitochondrial complex I PET imaging agent [&lt;sup>18&lt;/sup>F]BCPP-EF.&lt;h4>Methods&lt;/h4>Thirty-two amyloid and tau positive mild stage AD dementia patients (mean age ± SD: 71.1 ± 8.3 years) underwent a series of PET measurements with [&lt;sup>18&lt;/sup>F]BCPP-EF mitochondrial function, [&lt;sup>11&lt;/sup>C]PBB3 for tau deposition, and [&lt;sup>11&lt;/sup>C] PiB for amyloid deposition. Age-matched normal control </description><dates><release>2021-01-01T00:00:00Z</release><publication>2021 Apr</publication><modification>2025-04-04T07:47:27.386Z</modification><creation>2022-02-09T18:07:49.698Z</creation></dates><accession>S-EPMC8074456</accession><cross_references><pubmed>33902654</pubmed><doi>10.1186/s13024-021-00448-1</doi></cross_references></HashMap>