{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,10,6]],"date-time":"2026-10-06T00:58:15Z","timestamp":1791248295848,"version":"4.1.0"},"reference-count":59,"publisher":"Rockefeller University Press","issue":"8","content-domain":{"domain":["rupress.org"],"crossmark-restriction":true},"short-container-title":[],"published-print":{"date-parts":[[2010,8,2]]},"abstract":"<jats:p>TDP-43 is a multifunctional DNA\/RNA-binding factor that has been implicated in the regulation of neuronal plasticity. TDP-43 has also been identified as the major constituent of the neuronal cytoplasmic inclusions (NCIs) that are characteristic of a range of neurodegenerative diseases, including the frontotemporal lobar degeneration with ubiquitin+ inclusions (FTLD-U) and amyotrophic lateral sclerosis (ALS). We have generated a FTLD-U mouse model (CaMKII-TDP-43 Tg) in which TDP-43 is transgenically overexpressed in the forebrain resulting in phenotypic characteristics mimicking those of FTLD-U. In particular, the transgenic (Tg) mice exhibit impaired learning\/memory, progressive motor dysfunction, and hippocampal atrophy. The cognitive and motor impairments are accompanied by reduced levels of the neuronal regulators phospho\u2013extracellular signal-regulated kinase and phosphorylated cAMP response element-binding protein and increased levels of gliosis in the brains of the Tg mice. Moreover, cells with TDP-43+, ubiquitin+ NCIs and TDP-43\u2013deleted nuclei appear in the Tg mouse brains in an age-dependent manner. Our data provide direct evidence that increased levels of TDP-43 protein in the forebrain is sufficient to lead to the formation of TDP-43+, ubiquitin+ NCIs and neurodegeneration. This FTLD-U mouse model should be valuable for the mechanistic analysis of the role of TDP-43 in the pathogenesis of FTLD-U and for the design of effective therapeutic approaches of the disease.<\/jats:p>","DOI":"10.1084\/jem.20092164","type":"journal-article","created":{"date-parts":[[2010,7,27]],"date-time":"2010-07-27T03:17:55Z","timestamp":1280200675000},"page":"1661-1673","update-policy":"https:\/\/doi.org\/10.1084\/jem.crossmarkpolicy","source":"Crossref","is-referenced-by-count":194,"title":["Elevated expression of TDP-43 in the forebrain of mice is sufficient to cause neurological and pathological phenotypes mimicking FTLD-U"],"prefix":"10.1084","volume":"207","author":[{"given":"Kuen-Jer","family":"Tsai","sequence":"first","affiliation":[{"name":"Institute of Clinical Medicine, National Cheng Kung University, Tainan 704, Taiwan 1"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Chun-Hung","family":"Yang","sequence":"additional","affiliation":[{"name":"Institute of Molecular Biology, Academia Sinica, Taipei 115, Taiwan 2"},{"name":"Institute of Genome Sciences 3 , 4"},{"name":"Institute of Neuroscience, National Yang-Ming University, Taipei 112, Taiwan 3 , 4"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Yen-Hsin","family":"Fang","sequence":"additional","affiliation":[{"name":"Institute of Molecular Biology, Academia Sinica, Taipei 115, Taiwan 2"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Kuan-Hung","family":"Cho","sequence":"additional","affiliation":[{"name":"Institute of Genome Sciences 3 , 4"},{"name":"Institute of Neuroscience, National Yang-Ming University, Taipei 112, Taiwan 3 , 4"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Wei-Lin","family":"Chien","sequence":"additional","affiliation":[{"name":"Institute of Pharmacology, National Taiwan University, Taipei 100, Taiwan 5"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Wei-Ting","family":"Wang","sequence":"additional","affiliation":[{"name":"Institute of Molecular Biology, Academia Sinica, Taipei 115, Taiwan 2"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Tzu-Wei","family":"Wu","sequence":"additional","affiliation":[{"name":"Institute of Molecular Biology, Academia Sinica, Taipei 115, Taiwan 2"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Ching-Po","family":"Lin","sequence":"additional","affiliation":[{"name":"Institute of Genome Sciences 3 , 4"},{"name":"Institute of Neuroscience, National Yang-Ming University, Taipei 112, Taiwan 3 , 4"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Wen-Mei","family":"Fu","sequence":"additional","affiliation":[{"name":"Institute of Pharmacology, National Taiwan University, Taipei 100, Taiwan 5"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Che-Kun James","family":"Shen","sequence":"additional","affiliation":[{"name":"Institute of Molecular Biology, Academia Sinica, Taipei 115, Taiwan 2"},{"name":"Institute of Genome Sciences 3 , 4"},{"name":"Institute of Neuroscience, National Yang-Ming University, Taipei 112, Taiwan 3 , 4"}],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"291","published-online":{"date-parts":[[2010,7,26]]},"reference":[{"key":"2023072522241077600_bib1","doi-asserted-by":"publisher","first-page":"2315","DOI":"10.1093\/hmg\/ddm185","article-title":"Cell-specific expression of wild-type MeCP2 in mouse models of Rett syndrome yields insight about pathogenesis","volume":"16","author":"Alvarez-Saavedra","year":"2007","journal-title":"Hum. 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