{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,2,26]],"date-time":"2026-02-26T15:12:34Z","timestamp":1772118754967,"version":"3.50.1"},"reference-count":58,"publisher":"Wiley","issue":"11","license":[{"start":{"date-parts":[[2025,10,30]],"date-time":"2025-10-30T00:00:00Z","timestamp":1761782400000},"content-version":"vor","delay-in-days":0,"URL":"http:\/\/onlinelibrary.wiley.com\/termsAndConditions#vor"}],"funder":[{"DOI":"10.13039\/501100012166","name":"National Key Research and Development Program of China","doi-asserted-by":"publisher","id":[{"id":"10.13039\/501100012166","id-type":"DOI","asserted-by":"publisher"}]}],"content-domain":{"domain":["onlinelibrary.wiley.com"],"crossmark-restriction":true},"short-container-title":["J of Neuroscience Research"],"published-print":{"date-parts":[[2025,11]]},"abstract":"<jats:title>ABSTRACT<\/jats:title>\n                  <jats:p>\n                    Primary familial brain calcification (PFBC) is a rare inherited neurodegenerative disorder characterized by abnormal brain calcium\u2010phosphate (Ca\u2010Pi) deposits along microvessels or inside neuronal cells. Eight genes have been linked to PFBC, with the\n                    <jats:italic>SLC20A2<\/jats:italic>\n                    being the earliest identified.\n                    <jats:italic>SLC20A2<\/jats:italic>\n                    encodes PiT\u20102, which is crucial for Pi homeostasis in the cerebrospinal fluid (CSF). In\n                    <jats:italic>Slc20a2<\/jats:italic>\n                    homozygous knockout (HO) mice, the neurotoxic effects resulting from pathological CSF\u2010Pi accumulation and the unique brain transcriptome suggested that the absence of PiT\u20102 might lead to myelin abnormalities. However, the myelin morphology and content under\n                    <jats:italic>Slc20a2<\/jats:italic>\n                    deficiency remained largely unknown, and these were quantitatively investigated in this study. The results indicated no direct demyelination in the brains of\n                    <jats:italic>Slc20a2<\/jats:italic>\n                    \u2010HO mice, but an increased susceptibility to demyelination under the induction of oligodendrocyte\u2010toxic cuprizone (CPZ). The enhanced susceptibility was related to a greater infiltration of Th17 cells in the brain parenchyma, accompanying an exacerbation of brain calcification in\n                    <jats:italic>Slc20a2<\/jats:italic>\n                    deficiency.\n                  <\/jats:p>","DOI":"10.1002\/jnr.70088","type":"journal-article","created":{"date-parts":[[2025,10,30]],"date-time":"2025-10-30T07:51:28Z","timestamp":1761810688000},"update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":0,"title":["<i>Slc20a2<\/i>\n                    Deficiency Increases Susceptibility to\n                    <scp>CNS<\/scp>\n                    Demyelination Possibly Through Th17 Cells"],"prefix":"10.1002","volume":"103","author":[{"given":"Yueni","family":"Zhang","sequence":"first","affiliation":[{"name":"National Health Commission Key Laboratory of Molecular Probes and Targeted Diagnosis and Therapy The Fourth Hospital of Harbin Medical University  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