<HashMap><database>biostudies-literature</database><scores/><additional><submitter>Abdelmoaty MM</submitter><funding>Margaret R. Larson Professorship</funding><funding>NIA NIH HHS</funding><funding>NIDA NIH HHS</funding><funding>NIMH NIH HHS</funding><funding>Fogarty International Center</funding><funding>NINDS NIH HHS</funding><funding>Carol Swarts, MD Emerging Neuroscience Research Laboratory</funding><funding>Frances and Louie Blumkin and Harriet Singer Research Foundations</funding><pagination>317-330</pagination><full_dataset_link>https://www.ebi.ac.uk/biostudies/studies/S-EPMC10659760</full_dataset_link><repository>biostudies-literature</repository><omics_type>Unknown</omics_type><volume>2(3)</volume><pubmed_abstract>&lt;h4>Objectives&lt;/h4>To evaluate the linkage between age and deficits in innate and adaptive immunity which heralds both Alzheimer's disease (AD) onset and progression. The pathobiological events which underlie and tie these outcomes remain not fully understood.&lt;h4>Methods&lt;/h4>To investigate age-dependent immunity in AD, we evaluated innate and adaptive immunity in coordinate studies of regulatory T cell (Treg) function, T cell frequencies, and microglial integrity. These were assessed in blood, peripheral lymphoid tissues, and the hippocampus of transgenic (Tg) amyloid precursor protein/presenilin 1 (APP/PS1) against non-Tg mice. Additionally, immune arrays of hippocampal tissue were performed at 4, 6, 12, and 20 months of age.&lt;h4>Results&lt;/h4>APP/PS1 mice showed progressive impairment of Tr</pubmed_abstract><journal>NeuroImmune pharmacology and therapeutics</journal><pubmed_title>Immune senescence in aged APP/PS1 mice.</pubmed_title><pmcid>PMC10659760</pmcid><funding_grant_id>P01 DA028555</funding_grant_id><funding_grant_id>R01 NS036126</funding_grant_id><funding_grant_id>P01 NS031492</funding_grant_id><funding_grant_id>P30 MH062261</funding_grant_id><funding_grant_id>P01 DA028555, R01 NS36126, P01 NS31492, P01 MH6457</funding_grant_id><funding_grant_id>P01 NS043985</funding_grant_id><funding_grant_id>R01 AG043540</funding_grant_id><funding_grant_id>P01 MH064570</funding_grant_id><funding_grant_id>R01 NS034239</funding_grant_id><pubmed_authors>Yeapuri P</pubmed_authors><pubmed_authors>Gendelman HE</pubmed_authors><pubmed_authors>Machhi J</pubmed_authors><pubmed_authors>Lu Y</pubmed_authors><pubmed_authors>Kadry R</pubmed_authors><pubmed_authors>Bhattarai S</pubmed_authors><pubmed_authors>Lu E</pubmed_authors><pubmed_authors>Mosley RL</pubmed_authors><pubmed_authors>Abdelmoaty MM</pubmed_authors><pubmed_authors>Namminga KL</pubmed_authors></additional><is_claimable>false</is_claimable><name>Immune senescence in aged APP/PS1 mice.</name><description>&lt;h4>Objectives&lt;/h4>To evaluate the linkage between age and deficits in innate and adaptive immunity which heralds both Alzheimer's disease (AD) onset and progression. The pathobiological events which underlie and tie these outcomes remain not fully understood.&lt;h4>Methods&lt;/h4>To investigate age-dependent immunity in AD, we evaluated innate and adaptive immunity in coordinate studies of regulatory T cell (Treg) function, T cell frequencies, and microglial integrity. These were assessed in blood, peripheral lymphoid tissues, and the hippocampus of transgenic (Tg) amyloid precursor protein/presenilin 1 (APP/PS1) against non-Tg mice. Additionally, immune arrays of hippocampal tissue were performed at 4, 6, 12, and 20 months of age.&lt;h4>Results&lt;/h4>APP/PS1 mice showed progressive impairment of Tr</description><dates><release>2023-01-01T00:00:00Z</release><publication>2023 Sep</publication><modification>2025-04-20T01:04:17.692Z</modification><creation>2025-04-20T01:04:17.692Z</creation></dates><accession>S-EPMC10659760</accession><cross_references><pubmed>38023614</pubmed><doi>10.1515/nipt-2023-0015</doi></cross_references></HashMap>