{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,6,30]],"date-time":"2026-06-30T05:46:42Z","timestamp":1782798402786,"version":"3.54.5"},"reference-count":76,"publisher":"Frontiers Media SA","license":[{"start":{"date-parts":[[2026,6,30]],"date-time":"2026-06-30T00:00:00Z","timestamp":1782777600000},"content-version":"vor","delay-in-days":0,"URL":"https:\/\/creativecommons.org\/licenses\/by\/4.0\/"}],"funder":[{"DOI":"10.13039\/100000002","name":"National Institutes of Health","doi-asserted-by":"publisher","award":["HL153120 , UM1TR004929"],"award-info":[{"award-number":["HL153120 , UM1TR004929"]}],"id":[{"id":"10.13039\/100000002","id-type":"DOI","asserted-by":"publisher"}]}],"content-domain":{"domain":["frontiersin.org"],"crossmark-restriction":true},"short-container-title":["Front. Immunol."],"abstract":"<jats:sec>\n                    <jats:title>Introduction<\/jats:title>\n                    <jats:p>Monoamine oxidase A (Mao A) is a mitochondrial enzyme responsible for the degradation of monoaminergic neurotransmitters. While pharmacological inhibition of Mao A has been reported to improve outcomes in experimental autoimmune encephalomyelitis (EAE), the role of Mao A in immune cells on disease progression was unknown.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Methods<\/jats:title>\n                    <jats:p>\n                      To address this question, we generated mice with conditional Mao A deletion restricted to hematopoietic cells (Mao A\n                      <jats:sub>Leuko<\/jats:sub>\n                      <jats:sup>-\/-<\/jats:sup>\n                      ), including circulating immune cells, and induced EAE by immunizing the mice with the MOG35-55 peptide. Disease severity, ataxia, inflammation, and demyelination were assessed.\n                    <\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Results and discussion<\/jats:title>\n                    <jats:p>\n                      Mao A\n                      <jats:sub>Leuko<\/jats:sub>\n                      <jats:sup>-\/-<\/jats:sup>\n                      female mice exhibited significantly accelerated weight loss, worsened ataxia, and a 2.2-fold increase in EAE severity compared with controls. Histological analyses revealed increased inflammation and enhanced demyelination in the lumbar spinal cords of Mao A\n                      <jats:sub>Leuko<\/jats:sub>\n                      <jats:sup>-\/-<\/jats:sup>\n                      mice. Immunohistochemistry revealed increased IBA-1\n                      <jats:sup>+<\/jats:sup>\n                      and CD68\n                      <jats:sup>+<\/jats:sup>\n                      staining in the spinal cord, consistent with enhanced microglia and macrophage accumulation and activation and exacerbated neuroinflammation. However, no differences in CD3\n                      <jats:sup>+<\/jats:sup>\n                      T-cells levels were observed between female Mao A\n                      <jats:sub>Leuko<\/jats:sub>\n                      <jats:sup>-\/-<\/jats:sup>\n                      and Vav-i Cretg\/wt EAE mice. These effects were restricted to female mice. No significant differences were observed in disease course or pathology between male Mao A\n                      <jats:sub>Leuko<\/jats:sub>\n                      <jats:sup>-\/-<\/jats:sup>\n                      and control mice. This study identified hematopoietic Mao A as a novel critical regulator of neuroimmune crosstalk, with loss of Mao A function exacerbating inflammation, demyelination, and neurological deficits in female but not male EAE mice.\n                    <\/jats:p>\n                  <\/jats:sec>","DOI":"10.3389\/fimmu.2026.1829375","type":"journal-article","created":{"date-parts":[[2026,6,30]],"date-time":"2026-06-30T05:38:09Z","timestamp":1782797889000},"update-policy":"https:\/\/doi.org\/10.3389\/crossmark-policy","source":"Crossref","is-referenced-by-count":0,"title":["Hematopoietic monoamine oxidase A deficiency exacerbates neuroinflammation and demyelination in female but not male mice with experimental autoimmune encephalomyelitis"],"prefix":"10.3389","volume":"17","author":[{"given":"Alessandro G.","family":"Salerno","sequence":"first","affiliation":[{"name":"Department of Internal Medicine, Wake Forest School of Medicine","place":["Winston-Salem, NC, United States"]}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Amarylis C. B. A.","family":"Wanschel","sequence":"additional","affiliation":[{"name":"Department of Basic Pharmaceutical Sciences, Fred Wilson School of Pharmacy, High Point University","place":["High Point, NC, United States"]}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Giovana Y. 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