<HashMap><database>biostudies-literature</database><scores/><additional><submitter>Petrozziello T</submitter><funding>NIA NIH HHS</funding><funding>NINDS NIH HHS</funding><pagination>267-281</pagination><full_dataset_link>https://www.ebi.ac.uk/biostudies/studies/S-EPMC11823699</full_dataset_link><repository>biostudies-literature</repository><omics_type>Unknown</omics_type><volume>12(3)</volume><pubmed_abstract>&lt;h4>Background&lt;/h4>To date, it is still controversial whether tau phosphorylation plays a role in Huntington's disease (HD), as previous studies demonstrated either no alterations or increases in phosphorylated tau (pTau) in HD postmortem brain and mouse models.&lt;h4>Objective&lt;/h4>The goal of this study was to determine whether total tau and pTau levels are altered in HD.&lt;h4>Methods&lt;/h4>Immunohistochemistry, cellular fractionations, and western blots were used to measure total tau and pTau levels in a large cohort of HD and control postmortem prefrontal cortex (PFC). Furthermore, western blots were performed to assess tau, and pTau levels in HD and control isogenic embryonic stem cell (ESC)-derived cortical neurons and neuronal stem cells (NSCs). Similarly, western blots were used to assess </pubmed_abstract><journal>Journal of Huntington's disease</journal><pubmed_title>Age-Dependent Increase in Tau Phosphorylation at Serine 396 in Huntington's Disease Prefrontal Cortex.</pubmed_title><pmcid>PMC11823699</pmcid><funding_grant_id>R01 NS126420</funding_grant_id><funding_grant_id>P30 AG062421</funding_grant_id><pubmed_authors>Connors TR</pubmed_authors><pubmed_authors>Wu M</pubmed_authors><pubmed_authors>Quinn JP</pubmed_authors><pubmed_authors>Pouladi MA</pubmed_authors><pubmed_authors>Huntress SS</pubmed_authors><pubmed_authors>DiFiglia M</pubmed_authors><pubmed_authors>Sunderesh SR</pubmed_authors><pubmed_authors>Rosas HD</pubmed_authors><pubmed_authors>Boudi A</pubmed_authors><pubmed_authors>Liu S</pubmed_authors><pubmed_authors>Petrozziello T</pubmed_authors><pubmed_authors>Mills AN</pubmed_authors><pubmed_authors>Mouro Pinto R</pubmed_authors><pubmed_authors>Mahmood F</pubmed_authors><pubmed_authors>Sadri-Vakili G</pubmed_authors><pubmed_authors>Castillo-Torres AL</pubmed_authors><pubmed_authors>Auger CA</pubmed_authors><pubmed_authors>Arnold SE</pubmed_authors><pubmed_authors>Kim SE</pubmed_authors><pubmed_authors>Hyman BT</pubmed_authors><pubmed_authors>Kivisakk P</pubmed_authors><pubmed_authors>Kegel-Gleason K</pubmed_authors><pubmed_authors>Sapp E</pubmed_authors></additional><is_claimable>false</is_claimable><name>Age-Dependent Increase in Tau Phosphorylation at Serine 396 in Huntington's Disease Prefrontal Cortex.</name><description>&lt;h4>Background&lt;/h4>To date, it is still controversial whether tau phosphorylation plays a role in Huntington's disease (HD), as previous studies demonstrated either no alterations or increases in phosphorylated tau (pTau) in HD postmortem brain and mouse models.&lt;h4>Objective&lt;/h4>The goal of this study was to determine whether total tau and pTau levels are altered in HD.&lt;h4>Methods&lt;/h4>Immunohistochemistry, cellular fractionations, and western blots were used to measure total tau and pTau levels in a large cohort of HD and control postmortem prefrontal cortex (PFC). Furthermore, western blots were performed to assess tau, and pTau levels in HD and control isogenic embryonic stem cell (ESC)-derived cortical neurons and neuronal stem cells (NSCs). Similarly, western blots were used to assess </description><dates><release>2023-01-01T00:00:00Z</release><publication>2023</publication><modification>2025-04-05T09:39:26.604Z</modification><creation>2025-04-05T09:39:26.604Z</creation></dates><accession>S-EPMC11823699</accession><cross_references><pubmed>37694372</pubmed><doi>10.3233/JHD-230588</doi><doi>10.3233/jhd-230588</doi></cross_references></HashMap>