<HashMap><database>biostudies-literature</database><scores/><additional><submitter>Li Y</submitter><funding>National Basic Research Program of China (973 Program)</funding><pagination>208</pagination><full_dataset_link>https://www.ebi.ac.uk/biostudies/studies/S-EPMC6694441</full_dataset_link><repository>biostudies-literature</repository><omics_type>Unknown</omics_type><volume>11</volume><pubmed_abstract>Mild cognitive impairment (MCI) is a transitional state between the cognitive changes in normal aging and Alzheimer's disease (AD), which induces abnormalities in specific brain regions. Previous studies showed that paired helical filaments Tau (PHF-Tau) protein is a potential pathogenic protein which may cause abnormal brain function and structure in MCI and AD patients. However, the understanding of the PHF-Tau protein network in MCI patients is limited. In this study, 225 subjects with PHF-Tau Positron Emission Tomography (PET) images were divided into four groups based on whether they carried Apolipoprotein E ε4 (APOE 4) or abnormal cerebrospinal fluid Total-Tau (CSF T-Tau). They are two important pathogenic factors that might cause cognitive function impairment. The four groups were: </pubmed_abstract><journal>Frontiers in aging neuroscience</journal><pubmed_title>The Influence of Cerebrospinal Fluid Abnormalities and APOE 4 on PHF-Tau Protein: Evidence From Voxel Analysis and Graph Theory.</pubmed_title><pmcid>PMC6694441</pmcid><funding_grant_id>2014CB744600</funding_grant_id><pubmed_authors>Massoglia D</pubmed_authors><pubmed_authors>Crawford K</pubmed_authors><pubmed_authors>Carmichael O</pubmed_authors><pubmed_authors>Belden CM</pubmed_authors><pubmed_authors>Taylor JL</pubmed_authors><pubmed_authors>Grossman H</pubmed_authors><pubmed_authors>Stark S</pubmed_authors><pubmed_authors>Brewer J</pubmed_authors><pubmed_authors>Rosen HJ</pubmed_authors><pubmed_authors>James O</pubmed_authors><pubmed_authors>Pierce A</pubmed_authors><pubmed_authors>Lane B</pubmed_authors><pubmed_authors>Carrillo M</pubmed_authors><pubmed_authors>Chertkow H</pubmed_authors><pubmed_authors>Hart D</pubmed_authors><pubmed_authors>DeCarli C</pubmed_authors><pubmed_authors>Gunter J</pubmed_authors><pubmed_authors>Figurski M</pubmed_authors><pubmed_authors>Lord JL</pubmed_authors><pubmed_authors>Bonakdarpour B</pubmed_authors><pubmed_authors>Rogalski E</pubmed_authors><pubmed_authors>Montine T</pubmed_authors><pubmed_authors>Villanueva-Meyer J</pubmed_authors><pubmed_authors>Taylor-Reinwald L</pubmed_authors><pubmed_authors>Petrella JR</pubmed_authors><pubmed_authors>Mathis C</pubmed_authors><pubmed_authors>Rachinsky I</pubmed_authors><pubmed_authors>Woo E</pubmed_authors><pubmed_authors>Frank R</pubmed_authors><pubmed_authors>Oyonumo NE</pubmed_authors><pubmed_authors>Reyes D</pubmed_authors><pubmed_authors>Creech ML</pubmed_authors><pubmed_authors>Geldmacher D</pubmed_authors><pubmed_authors>Duara R</pubmed_authors><pubmed_authors>Hu B</pubmed_authors><pubmed_authors>Reeder S</pubmed_authors><pubmed_authors>Grafman J</pubmed_authors><pubmed_authors>Pasternack S</pubmed_authors><pubmed_authors>Oates 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M</pubmed_authors><pubmed_authors>Morris JC</pubmed_authors><pubmed_authors>Daiello LA</pubmed_authors><pubmed_authors>Bodge C</pubmed_authors><pubmed_authors>Johnson PL</pubmed_authors><pubmed_authors>Raj BA</pubmed_authors><pubmed_authors>Jimenez G</pubmed_authors><pubmed_authors>Rountree S</pubmed_authors><pubmed_authors>Nguyen D</pubmed_authors><pubmed_authors>Allard J</pubmed_authors><pubmed_authors>Assaly M</pubmed_authors><pubmed_authors>Tariot P</pubmed_authors><pubmed_authors>Goldstein BS</pubmed_authors><pubmed_authors>Shaw LM</pubmed_authors><pubmed_authors>Sink KM</pubmed_authors><pubmed_authors>Kantarci K</pubmed_authors></additional><is_claimable>false</is_claimable><name>The Influence of Cerebrospinal Fluid Abnormalities and APOE 4 on PHF-Tau Protein: Evidence From Voxel Analysis and Graph Theory.</name><description>Mild cognitive impairment (MCI) is a transitional state between the cognitive changes in normal aging and Alzheimer's disease (AD), which induces abnormalities in specific brain regions. Previous studies showed that paired helical filaments Tau (PHF-Tau) protein is a potential pathogenic protein which may cause abnormal brain function and structure in MCI and AD patients. However, the understanding of the PHF-Tau protein network in MCI patients is limited. In this study, 225 subjects with PHF-Tau Positron Emission Tomography (PET) images were divided into four groups based on whether they carried Apolipoprotein E ε4 (APOE 4) or abnormal cerebrospinal fluid Total-Tau (CSF T-Tau). They are two important pathogenic factors that might cause cognitive function impairment. The four groups were: </description><dates><release>2019-01-01T00:00:00Z</release><publication>2019</publication><modification>2025-04-04T21:39:51.062Z</modification><creation>2019-08-26T07:02:42Z</creation></dates><accession>S-EPMC6694441</accession><cross_references><pubmed>31440157</pubmed><doi>10.3389/fnagi.2019.00208</doi></cross_references></HashMap>