<HashMap><database>biostudies-literature</database><scores/><additional><submitter>Alavi MV</submitter><funding>National Institute of Allergy and Infectious Diseases</funding><funding>NIA NIH HHS</funding><funding>National Institutes of Health</funding><funding>National Institute on Aging</funding><pagination>119116</pagination><full_dataset_link>https://www.ebi.ac.uk/biostudies/studies/S-EPMC8525314</full_dataset_link><repository>biostudies-literature</repository><omics_type>Unknown</omics_type><volume>1868(12)</volume><pubmed_abstract>The neuropathological hallmarks of Alzheimer's Disease are plaques and neurofibrillary tangles. Yet, Alzheimer's is a complex disease with many contributing factors, such as energy-metabolic changes, which have been documented in autopsy brains from individuals with Alzheimer's and animal disease models alike. One conceivable explanation is that the interplay of age-related extracellular and intracellular alterations pertaining to Alzheimer's, such as cerebrovascular changes, protein aggregates and inflammation, evoke a mitochondrial response. However, it is not clear if and how mitochondria can contribute to Alzheimer's pathophysiology. This study focuses on one particular aspect of this question by investigating the functional interaction between the microtubule-associated protein tau an</pubmed_abstract><journal>Biochimica et biophysica acta. Molecular cell research</journal><pubmed_title>Tau phosphorylation and OPA1 proteolysis are unrelated events: Implications for Alzheimer's Disease.</pubmed_title><pmcid>PMC8525314</pmcid><funding_grant_id>R43AG063642</funding_grant_id><funding_grant_id>R43 AG063642</funding_grant_id><pubmed_authors>Alavi MV</pubmed_authors></additional><is_claimable>false</is_claimable><name>Tau phosphorylation and OPA1 proteolysis are unrelated events: Implications for Alzheimer's Disease.</name><description>The neuropathological hallmarks of Alzheimer's Disease are plaques and neurofibrillary tangles. Yet, Alzheimer's is a complex disease with many contributing factors, such as energy-metabolic changes, which have been documented in autopsy brains from individuals with Alzheimer's and animal disease models alike. One conceivable explanation is that the interplay of age-related extracellular and intracellular alterations pertaining to Alzheimer's, such as cerebrovascular changes, protein aggregates and inflammation, evoke a mitochondrial response. However, it is not clear if and how mitochondria can contribute to Alzheimer's pathophysiology. This study focuses on one particular aspect of this question by investigating the functional interaction between the microtubule-associated protein tau an</description><dates><release>2021-01-01T00:00:00Z</release><publication>2021 Nov</publication><modification>2025-04-05T13:44:14.893Z</modification><creation>2025-04-05T13:44:14.893Z</creation></dates><accession>S-EPMC8525314</accession><cross_references><pubmed>34400172</pubmed><doi>10.1016/j.bbamcr.2021.119116</doi></cross_references></HashMap>