{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,8,18]],"date-time":"2026-08-18T04:04:52Z","timestamp":1787025892081,"version":"build-2736575974"},"reference-count":60,"publisher":"SAGE Publications","issue":"4","license":[{"start":{"date-parts":[[2024,2,3]],"date-time":"2024-02-03T00:00:00Z","timestamp":1706918400000},"content-version":"unspecified","delay-in-days":0,"URL":"https:\/\/creativecommons.org\/licenses\/by-nc\/4.0\/"}],"content-domain":{"domain":["journals.sagepub.com"],"crossmark-restriction":true},"short-container-title":["Journal of Alzheimer\u2019s Disease"],"published-print":{"date-parts":[[2024,2,13]]},"abstract":"<jats:sec>\n                    <jats:title>Background:<\/jats:title>\n                    <jats:p>Vitamin D has neuroprotective and immunomodulating functions that may impact glial cell function in the brain. Previously, we reported molecular and behavioral changes caused by deficiency and supplementation of vitamin D in an Alzheimer\u2019s disease (AD) mouse model. Recent studies have highlighted reactive astrocytes as a new therapeutic target for AD treatment. However, the mechanisms underlying the therapeutic effects of vitamin D on the glial cells of AD remain unclear.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Objective:<\/jats:title>\n                    <jats:p>To investigate the potential association between vitamin D deficiency\/supplementation and the pathological progression of AD, including amyloid-\u03b2 (A\u03b2) pathology and reactive astrogliosis.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Methods:<\/jats:title>\n                    <jats:p>Transgenic hemizygous 5XFAD male mice were subjected to different dietary interventions and intraperitoneal vitamin D injections to examine the effects of vitamin D deficiency and supplementation on AD. Brain tissue was then analyzed using immunohistochemistry for A\u03b2 plaques, microglia, and astrocytes, with quantifications performed via ImageJ software.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Results:<\/jats:title>\n                    <jats:p>Our results demonstrated that vitamin D deficiency exacerbated A\u03b2 plaque formation and increased GABA-positive reactive astrocytes in AD model mice, while vitamin D supplementation ameliorated these effects, leading to a reduction in A\u03b2 plaques and GABA-positive astrocytes.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Conclusions:<\/jats:title>\n                    <jats:p>Our findings highlight the significant impact of vitamin D status on A\u03b2 pathology and reactive astrogliosis, underscoring its potential role in the prevention and treatment of AD. This study provides the first in vivo evidence of the association between vitamin D and reactive astrogliosis in AD model mice, indicating the potential for targeting vitamin D levels as a novel therapeutic approach for AD.<\/jats:p>\n                  <\/jats:sec>","DOI":"10.3233\/jad-231033","type":"journal-article","created":{"date-parts":[[2024,2,6]],"date-time":"2024-02-06T13:28:07Z","timestamp":1707226087000},"page":"1939-1950","update-policy":"https:\/\/doi.org\/10.1177\/sage-journals-update-policy","source":"Crossref","is-referenced-by-count":11,"title":["Vitamin D Reduces GABA-Positive Astrocytes in the 5xFAD Mouse Model of Alzheimer\u2019s Disease"],"prefix":"10.1177","volume":"97","author":[{"given":"Jiseung","family":"Kang","sequence":"first","affiliation":[{"name":"Department of Biomedical Science and Engineering, Gwangju Institute of Science and Technology, Gwangju, South Korea"},{"name":"Division of Sleep Medicine, Harvard Medical School, Boston, MA, 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