{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,9,16]],"date-time":"2026-09-16T12:08:47Z","timestamp":1789560527775,"version":"build-2803163510"},"reference-count":38,"publisher":"Wiley","issue":"2","license":[{"start":{"date-parts":[[2025,1,8]],"date-time":"2025-01-08T00:00:00Z","timestamp":1736294400000},"content-version":"vor","delay-in-days":0,"URL":"http:\/\/creativecommons.org\/licenses\/by-nc-nd\/4.0\/"},{"start":{"date-parts":[[2025,1,8]],"date-time":"2025-01-08T00:00:00Z","timestamp":1736294400000},"content-version":"tdm","delay-in-days":0,"URL":"http:\/\/doi.wiley.com\/10.1002\/tdm_license_1.1"}],"funder":[{"DOI":"10.13039\/100000002","name":"National Institutes of Health","doi-asserted-by":"publisher","award":["R21 AG071269\u201001"],"award-info":[{"award-number":["R21 AG071269\u201001"]}],"id":[{"id":"10.13039\/100000002","id-type":"DOI","asserted-by":"publisher"}]},{"DOI":"10.13039\/100000060","name":"National Institute of Allergy and Infectious Diseases","doi-asserted-by":"publisher","award":["T32\u2010AI\u2010060519"],"award-info":[{"award-number":["T32\u2010AI\u2010060519"]}],"id":[{"id":"10.13039\/100000060","id-type":"DOI","asserted-by":"publisher"}]}],"content-domain":{"domain":["alz-journals.onlinelibrary.wiley.com"],"crossmark-restriction":true},"short-container-title":["Alzheimer's &amp;amp; Dementia"],"published-print":{"date-parts":[[2025,2]]},"abstract":"<jats:title>Abstract<\/jats:title>\n                  <jats:sec>\n                    <jats:title>INTRODUCTION<\/jats:title>\n                    <jats:p>Plaques are a hallmark feature of Alzheimer's disease (AD). We found that the loss of mucosal\u2010associated invariant T (MAIT) cells and their antigen\u2010presenting molecule MR1 caused a delay in plaque pathology development in AD mouse models. However, it remains unknown how this axis is impacting dystrophic neurites.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>METHODS<\/jats:title>\n                    <jats:p>Brain tissue from 5XFAD mice and those that are MR1 deficient (MR1 KO), were analyzed for dystrophic neurites, amyloid plaques, and synapses via immunofluorescence, RNA sequencing, enzyme\u2010linked immunosorbent assay, and western blot.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>RESULTS<\/jats:title>\n                    <jats:p>\n                      In 8\u2010month\u2010old 5XFAD\/MR1 KO mice, there was reduced expression of lysosomal\u2010associated membrane protein 1, ubiquitin, and\n                      <jats:italic>n<\/jats:italic>\n                      \u2010terminal amyloid precursor protein in the hippocampus compared to 5XFAD mice (\n                      <jats:italic>P<\/jats:italic>\n                      \u00a0&lt;\u00a00.05). 5XFAD\/MR1 KO mice also had less insoluble amyloid beta 40 (\n                      <jats:italic>P<\/jats:italic>\n                      \u00a0&lt;\u00a00.001) and higher levels of postsynaptic density protein 95 (\n                      <jats:italic>P<\/jats:italic>\n                      \u00a0&lt;\u00a00.01) in the hippocampus.\n                    <\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>DISCUSSION<\/jats:title>\n                    <jats:p>Our data contribute additional mechanistic insight into the detrimental role of the MR1\/MAIT cell axis in AD pathology development.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Highlights<\/jats:title>\n                    <jats:p>\n                      <jats:list list-type=\"bullet\">\n                        <jats:list-item>\n                          <jats:p>5XFAD mice lacking the innate immune MR1\/MAIT (mucosal\u2010associated invariant T) cell axis (5XFAD\/MR1 KO) have reduced numbers of dystrophic neurite markers in the hippocampus at 8 months of age.<\/jats:p>\n                        <\/jats:list-item>\n                        <jats:list-item>\n                          <jats:p>Hippocampal tissue transcriptional analyses showed reduced expression of genes encoding classical dystrophic neurite markers in 5XFAD\/MR1 KO mice.<\/jats:p>\n                        <\/jats:list-item>\n                        <jats:list-item>\n                          <jats:p>5XFAD\/MR1 KO mice had less insoluble amyloid beta 40 and increased levels of the post\u2010synaptic marker, postsynaptic density protein 95, in the hippocampus than did MR1+ 5XFAD mice.<\/jats:p>\n                        <\/jats:list-item>\n                      <\/jats:list>\n                    <\/jats:p>\n                  <\/jats:sec>","DOI":"10.1002\/alz.14480","type":"journal-article","created":{"date-parts":[[2025,1,8]],"date-time":"2025-01-08T09:24:35Z","timestamp":1736328275000},"update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":5,"title":["The MR1\/MAIT cell axis enhances dystrophic neurite development in Alzheimer's disease"],"prefix":"10.1002","volume":"21","author":[{"given":"Season K.","family":"Wyatt\u2010Johnson","sequence":"first","affiliation":[{"name":"Department of Microbiology and Immunology Indiana University School of Medicine  Indianapolis Indiana USA"},{"name":"Stark Neurosciences Research Institute Indiana University School of Medicine  Indianapolis Indiana USA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Samantha","family":"Ackley","sequence":"additional","affiliation":[{"name":"Department of Microbiology and Immunology Indiana University School of Medicine  Indianapolis Indiana USA"},{"name":"Stark 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