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PNNs play a role in neuroprotection against oxidative stress. Oxidative stress within motor neurons can trigger neuronal death, which has been implicated in amyotrophic lateral sclerosis (ALS). We investigated the spatio\u2010temporal timeline of PNN breakdown and the contributing cellular factors in the SOD1\n                      <jats:sup>G93A<\/jats:sup>\n                      strain, a fast\u2010onset ALS mouse model.\n                    <\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Methods<\/jats:title>\n                    <jats:p>\n                      This was conducted at the presymptomatic (P30), onset (P70), mid\u2010stage (P130), and end\u2010stage disease (P150) using immunofluorescent microscopy, as this characterisation has not been conducted in the SOD1\n                      <jats:sup>G93A<\/jats:sup>\n                      strain.\n                    <\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Results<\/jats:title>\n                    <jats:p>\n                      We observed a significant breakdown of PNNs around \u03b1\u2010motor neurons in the ventral horn of onset and mid\u2010stage disease SOD1\n                      <jats:sup>G93A<\/jats:sup>\n                      mice compared with wild\u2010type controls. This was observed with increased numbers of microglia expressing matrix metallopeptidase\u20109 (MMP\u20109), an endopeptidase that degrades PNNs. Microglia also engulfed PNN components in the SOD1\n                      <jats:sup>G93A<\/jats:sup>\n                      mouse. Further increases in microglia and astrocyte number, MMP\u20109 expression, and engulfment of PNN components by glia were observed in mid\u2010stage SOD1\n                      <jats:sup>G93A<\/jats:sup>\n                      mice. This was observed with increased expression of fractalkine, a signal for microglia engulfment, within \u03b1\u2010motor neurons of SOD1\n                      <jats:sup>G93A<\/jats:sup>\n                      mice. Following PNN breakdown, \u03b1\u2010motor neurons of onset and mid\u2010stage SOD1\n                      <jats:sup>G93A<\/jats:sup>\n                      mice showed increased expression of 3\u2010nitrotyrosine, a marker for protein oxidation, which could render them vulnerable to death.\n                    <\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Conclusions<\/jats:title>\n                    <jats:p>\n                      Our observations suggest that increased numbers of MMP\u20109 expressing glia and their subsequent engulfment of PNNs around \u03b1\u2010motor neurons render these neurons sensitive to oxidative damage and eventual death in the SOD1\n                      <jats:sup>G93A<\/jats:sup>\n                      ALS model mouse.\n                    <\/jats:p>\n                  <\/jats:sec>","DOI":"10.1111\/nan.12982","type":"journal-article","created":{"date-parts":[[2024,5,14]],"date-time":"2024-05-14T03:45:49Z","timestamp":1715658349000},"update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":38,"title":["Perineuronal nets are phagocytosed by MMP\u20109 expressing microglia and astrocytes in the SOD1\n                    <sup>G93A<\/sup>\n                    ALS mouse model"],"prefix":"10.1111","volume":"50","author":[{"given":"Sang Won","family":"Cheung","sequence":"first","affiliation":[{"name":"School of Biomedical Sciences The University of Queensland  St. Lucia Australia"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Ekta","family":"Bhavnani","sequence":"additional","affiliation":[{"name":"School of Biomedical Sciences The University of Queensland  St. Lucia Australia"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"David 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