{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,8,24]],"date-time":"2026-08-24T08:22:05Z","timestamp":1787559725280,"version":"build-2736575974"},"reference-count":33,"publisher":"Wiley","issue":"8","license":[{"start":{"date-parts":[[2026,8,11]],"date-time":"2026-08-11T00:00:00Z","timestamp":1786406400000},"content-version":"vor","delay-in-days":10,"URL":"http:\/\/creativecommons.org\/licenses\/by-nc-nd\/4.0\/"},{"start":{"date-parts":[[2026,8,1]],"date-time":"2026-08-01T00:00:00Z","timestamp":1785542400000},"content-version":"tdm","delay-in-days":0,"URL":"http:\/\/doi.wiley.com\/10.1002\/tdm_license_1.1"}],"funder":[{"DOI":"10.13039\/501100014188","name":"Ministry of Science and ICT, South Korea","doi-asserted-by":"publisher","award":["RS\u20102025\u201000516274"],"award-info":[{"award-number":["RS\u20102025\u201000516274"]}],"id":[{"id":"10.13039\/501100014188","id-type":"DOI","asserted-by":"publisher"}]},{"DOI":"10.13039\/501100014188","name":"Ministry of Science and ICT, South Korea","doi-asserted-by":"publisher","award":["RS\u20102025\u201000559259"],"award-info":[{"award-number":["RS\u20102025\u201000559259"]}],"id":[{"id":"10.13039\/501100014188","id-type":"DOI","asserted-by":"publisher"}]}],"content-domain":{"domain":["onlinelibrary.wiley.com"],"crossmark-restriction":true},"short-container-title":["Parasite Immunology"],"published-print":{"date-parts":[[2026,8]]},"abstract":"<jats:title>ABSTRACT<\/jats:title>\n                  <jats:p>\n                    Alzheimer's disease (AD) is characterized by amyloid\u2010\u03b2 (A\u03b2) peptide accumulation and tau protein\u2010mediated neurodegeneration, and neuroinflammation is increasingly recognized as a major process associated with tau pathology. Chronic\n                    <jats:italic>Toxoplasma gondii<\/jats:italic>\n                    infection reduces amyloid accumulation in AD models through immune modulation, but its stage\u2010specific associations with tau\u2010related pathology remain unclear. Here, we investigated how chronic\n                    <jats:italic>T<\/jats:italic>\n                    .\n                    <jats:italic>gondii<\/jats:italic>\n                    infection is associated with tau\u2010related molecular and neuropathological changes in the 5XFAD AD mouse model. At 40\u2009weeks post\u2010infection, we profiled transcriptomic changes and evaluated A\u03b2\u2010associated (21 genes), A\u03b2\/tau\u2010shared (22 genes), and tau\u2010associated (21 genes) pathological programs together with p\u2010tau immunoreactivity in brain sections. Chronic infection was associated with selective modulation of molecular networks linked to neuroimmune signalling and tau\u2010related pathways rather than broad suppression of AD\u2010related gene expression. Among tau\u2010related pathological stages, the neuroinflammation\u2010related amplification module linking A\u03b2 and tau exhibited the most prominent transcriptomic change in\n                    <jats:italic>T. gondii\u2010<\/jats:italic>\n                    infected AD mice, whereas upstream kinase\u2010related initiation pathways and downstream toxin conversion or accumulation\u2010related processes changed relatively minimally. These transcriptomic changes were accompanied by a marked reduction in phosphorylated tau load at the tissue level. Collectively, these findings suggest that chronic\n                    <jats:italic>T. gondii<\/jats:italic>\n                    infection is associated with selective modulation of tau\u2010related pathogenic programs and reduced p\u2010tau burden in the 5XFAD brain.\n                  <\/jats:p>","DOI":"10.1111\/pim.70096","type":"journal-article","created":{"date-parts":[[2026,8,11]],"date-time":"2026-08-11T11:14:41Z","timestamp":1786446881000},"update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":0,"title":["Attenuation of Tau Hyperphosphorylation by Chronic\n                    <i>Toxoplasma gondii<\/i>\n                    Infection in a Mouse Model of Alzheimer's Disease"],"prefix":"10.1111","volume":"48","author":[{"ORCID":"https:\/\/orcid.org\/0000-0002-8645-1966","authenticated-orcid":false,"given":"Seung\u2010Hwan","family":"Seo","sequence":"first","affiliation":[{"name":"Department of Tropical Medicine and Parasitology Seoul National University College of Medicine  Seoul Republic of Korea"},{"name":"Institute of Endemic Diseases, Medical Research Center Seoul National University  Seoul Republic of Korea"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Ji\u2010Eun","family":"Lee","sequence":"additional","affiliation":[{"name":"Department of Tropical Medicine and Parasitology Seoul National University College of Medicine  Seoul Republic of Korea"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Eun\u2010Ji","family":"Cho","sequence":"additional","affiliation":[{"name":"Department of Tropical Medicine and Parasitology Seoul National University College of Medicine  Seoul Republic of Korea"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0003-1215-1079","authenticated-orcid":false,"given":"Eun\u2010Hee","family":"Shin","sequence":"additional","affiliation":[{"name":"Department of Tropical Medicine and Parasitology Seoul National University College of Medicine  Seoul Republic of Korea"},{"name":"Institute of Endemic Diseases, Medical Research Center Seoul National University  Seoul Republic of Korea"},{"name":"Seoul National University Bundang Hospital  Seongnam Republic of Korea"}],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"311","published-online":{"date-parts":[[2026,8,11]]},"reference":[{"key":"e_1_2_10_2_1","doi-asserted-by":"publisher","DOI":"10.1186\/s40035-024-00432-x"},{"key":"e_1_2_10_3_1","doi-asserted-by":"publisher","DOI":"10.1016\/j.cell.2025.11.033"},{"key":"e_1_2_10_4_1","doi-asserted-by":"publisher","DOI":"10.1093\/procel\/pwae026"},{"key":"e_1_2_10_5_1","doi-asserted-by":"publisher","DOI":"10.1016\/bs.acc.2025.06.002"},{"key":"e_1_2_10_6_1","doi-asserted-by":"publisher","DOI":"10.1016\/j.tjpad.2024.100013"},{"key":"e_1_2_10_7_1","article-title":"Beyond Amyloid and Tau: The Critical Role of Microglia in Alzheimer's Disease Therapeutics","volume":"13","author":"Dias 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