<HashMap><database>biostudies-literature</database><scores/><additional><submitter>Valerio RR</submitter><funding>Conselho Nacional de Desenvolvimento Científico e Tecnológico</funding><funding>INOVA Fiocruz Program</funding><funding>Coordenação de Aperfeiçoamento de Pessoal de Nível Superior</funding><funding>FOCEM</funding><funding>Fundação Carlos Chagas Filho de Amparo à Pesquisa do Estado do Rio de Janeiro</funding><funding>National Institute of Science and Technology on Neuroimmunomodulation (INCT-NIM)</funding><pagination>e70341</pagination><full_dataset_link>https://www.ebi.ac.uk/biostudies/studies/S-EPMC12758097</full_dataset_link><repository>biostudies-literature</repository><omics_type>Unknown</omics_type><volume>170(1)</volume><pubmed_abstract>Microglia are the main innate immune cells residing in the brain parenchyma. Their activation and resulting neuroinflammation have emerged as major pathogenic mechanisms in neurodegenerative disorders, particularly in Alzheimer's disease (AD). The accumulation of amyloid-β oligomers (AβOs) and microglia activation play crucial roles in the pathogenesis of AD. In a second vein, the development of innate immune memory in response to different stimuli is a vital mechanism that enables microglia to adjust their response to subsequent inflammatory challenges. While there is increasing evidence that repeated bouts of peripheral inflammation lead to training or tolerance in microglia, the impact of tolerance on the inflammatory response induced by AβOs remains to be determined. In this study, we </pubmed_abstract><journal>Journal of neurochemistry</journal><pubmed_title>Innate Immune Tolerance Regulates Microglia Response to Aβ Oligomers.</pubmed_title><pmcid>PMC12758097</pmcid><funding_grant_id>E‐26/200.169/2023</funding_grant_id><funding_grant_id>E-26/201.419/2021</funding_grant_id><funding_grant_id>E-26/200.169/2023</funding_grant_id><funding_grant_id>E‐26/201.419/2021</funding_grant_id><funding_grant_id>403742/2016‐1</funding_grant_id><funding_grant_id>E‐26/010.000983/2019</funding_grant_id><funding_grant_id>E‐26/203.195/2016</funding_grant_id><funding_grant_id>403742/2016-1</funding_grant_id><funding_grant_id>E‐26/010.002418/2019</funding_grant_id><funding_grant_id>E‐26/202.807/2019</funding_grant_id><funding_grant_id>E-26/202.807/2019</funding_grant_id><funding_grant_id>E-26/203.195/2016</funding_grant_id><funding_grant_id>E-26/010.002418/2019</funding_grant_id><funding_grant_id>E-26/010.000983/2019</funding_grant_id><funding_grant_id>VPPCB-008-FIO-18-2-52</funding_grant_id><pubmed_authors>De Felice FG</pubmed_authors><pubmed_authors>Martins R</pubmed_authors><pubmed_authors>Bonomo A</pubmed_authors><pubmed_authors>Ferreira ST</pubmed_authors><pubmed_authors>Santos AR</pubmed_authors><pubmed_authors>Bernardi A</pubmed_authors><pubmed_authors>Savino W</pubmed_authors><pubmed_authors>Valerio RR</pubmed_authors><pubmed_authors>Nobrega AHL</pubmed_authors><pubmed_authors>Frozza RL</pubmed_authors></additional><is_claimable>false</is_claimable><name>Innate Immune Tolerance Regulates Microglia Response to Aβ Oligomers.</name><description>Microglia are the main innate immune cells residing in the brain parenchyma. Their activation and resulting neuroinflammation have emerged as major pathogenic mechanisms in neurodegenerative disorders, particularly in Alzheimer's disease (AD). The accumulation of amyloid-β oligomers (AβOs) and microglia activation play crucial roles in the pathogenesis of AD. In a second vein, the development of innate immune memory in response to different stimuli is a vital mechanism that enables microglia to adjust their response to subsequent inflammatory challenges. While there is increasing evidence that repeated bouts of peripheral inflammation lead to training or tolerance in microglia, the impact of tolerance on the inflammatory response induced by AβOs remains to be determined. In this study, we </description><dates><release>2026-01-01T00:00:00Z</release><publication>2026 Jan</publication><modification>2026-06-06T09:33:19.632Z</modification><creation>2026-05-28T03:12:21.063Z</creation></dates><accession>S-EPMC12758097</accession><cross_references><pubmed>41480929</pubmed><doi>10.1111/jnc.70341</doi></cross_references></HashMap>