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In vitro\n                      <jats:italic>,<\/jats:italic>\n                      microglia preferentially upregulate the iron importer, divalent metal transporter 1 (DMT1, gene name\n                      <jats:italic>Slc11a2<\/jats:italic>\n                      ) in response to inflammatory stimuli, and excess iron can augment cellular inflammation, suggesting a feed-forward loop between iron import mechanisms and inflammatory signaling. However, it is not understood whether microglial iron import mechanisms directly contribute to inflammatory signaling and chronic disease in vivo. These studies determined the effects of microglial-specific knockdown of\n                      <jats:italic>Slc11a2<\/jats:italic>\n                      on AD-related cognitive decline and microglial transcriptional phenotype.\n                    <\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Methods<\/jats:title>\n                    <jats:p>\n                      In vitro experiments and RT-qPCR were used to assess a role for DMT1 in amyloid-\u03b2-associated inflammation. To determine the effects of microglial\n                      <jats:italic>Slc11a2<\/jats:italic>\n                      knockdown on AD-related phenotypes in vivo, triple-transgenic\n                      <jats:italic>Cx3cr1<\/jats:italic>\n                      <jats:sup>\n                        <jats:italic>Cre\u2212ERT2<\/jats:italic>\n                      <\/jats:sup>\n                      <jats:italic>;Slc11a2<\/jats:italic>\n                      <jats:sup>flfl<\/jats:sup>\n                      <jats:italic>;APP\/PS1<\/jats:italic>\n                      <jats:sup>+or \u2013<\/jats:sup>\n                      mice were generated and administered corn oil or tamoxifen to induce knockdown at 5\u20136\u00a0months of age. Both sexes underwent behavioral analyses to assess cognition and memory (12\u201315\u00a0months of age). Hippocampal CD11b+\u00a0microglia were magnetically isolated from female mice (15\u201317\u00a0months) and bulk RNA-sequencing analysis was conducted.\n                    <\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Results<\/jats:title>\n                    <jats:p>\n                      DMT1 inhibition in vitro robustly decreased A\u03b2-induced inflammatory gene expression and cellular iron levels in conditions of excess iron. In vivo\n                      <jats:italic>, Slc11a2<\/jats:italic>\n                      <jats:sup>KD<\/jats:sup>\n                      <jats:italic>APP\/PS1<\/jats:italic>\n                      female, but not male, mice displayed a significant worsening of memory function in Morris water maze and a fear conditioning assay, along with significant hyperactivity compared to control WT and\n                      <jats:italic>APP\/PS1<\/jats:italic>\n                      mice. Hippocampal microglia from\n                      <jats:italic>Slc11a2<\/jats:italic>\n                      <jats:sup>KD<\/jats:sup>\n                      <jats:italic>APP\/PS1<\/jats:italic>\n                      females displayed significant increases in\n                      <jats:italic>Enpp2, Ttr,<\/jats:italic>\n                      and the iron-export gene,\n                      <jats:italic>Slc40a1,<\/jats:italic>\n                      compared to control\n                      <jats:italic>APP\/PS1<\/jats:italic>\n                      cells.\n                      <jats:italic>Slc11a2<\/jats:italic>\n                      <jats:sup>KD<\/jats:sup>\n                      cells from\n                      <jats:italic>APP\/PS1<\/jats:italic>\n                      females also exhibited decreased expression of markers associated with subsets of disease-associated microglia (DAMs), such as\n                      <jats:italic>Apoe, Ctsb, Ly9, Csf1,<\/jats:italic>\n                      and\n                      <jats:italic>Hif1\u03b1.<\/jats:italic>\n                    <\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Conclusions<\/jats:title>\n                    <jats:p>\n                      This work suggests a sex-specific role for microglial iron import gene\n                      <jats:italic>Slc11a2<\/jats:italic>\n                      in propagating behavioral and cognitive phenotypes in the\n                      <jats:italic>APP\/PS1<\/jats:italic>\n                      model of AD. These data also highlight an association between loss of a DAM-like phenotype in microglia and cognitive deficits in\n                      <jats:italic>Slc11a2<\/jats:italic>\n                      <jats:sup>KD<\/jats:sup>\n                      <jats:italic>APP\/PS1<\/jats:italic>\n                      female mice. Overall, this work illuminates an iron-related pathway in microglia that may serve a protective role during disease and offers insight into mechanisms behind disease-related sex differences.\n                    <\/jats:p>\n                  <\/jats:sec>","DOI":"10.1186\/s12974-024-03238-w","type":"journal-article","created":{"date-parts":[[2024,9,27]],"date-time":"2024-09-27T12:01:42Z","timestamp":1727438502000},"update-policy":"https:\/\/doi.org\/10.1007\/springer_crossmark_policy","source":"Crossref","is-referenced-by-count":9,"title":["Knockdown of microglial iron import gene, Slc11a2, worsens cognitive function and alters microglial transcriptional landscape in a sex-specific manner in the APP\/PS1 model of Alzheimer\u2019s disease"],"prefix":"10.1186","volume":"21","author":[{"given":"Katrina Volk","family":"Robertson","sequence":"first","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Alec S.","family":"Rodriguez","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Jean-Philippe","family":"Cartailler","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Shristi","family":"Shrestha","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Michael W.","family":"Schleh","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Kyle R.","family":"Schroeder","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Arianna M.","family":"Valenti","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Alec T.","family":"Kramer","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Fiona E.","family":"Harrison","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Alyssa H.","family":"Hasty","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"297","published-online":{"date-parts":[[2024,9,27]]},"reference":[{"issue":"4","key":"3238_CR1","doi-asserted-by":"publisher","first-page":"1598","DOI":"10.1002\/alz.13016","volume":"19","author":"A As","year":"2023","unstructured":"As A. 2023 Alzheimer\u2019s disease facts and figures. 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