{"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":1791248295972,"version":"4.1.0"},"reference-count":219,"publisher":"Wiley","issue":"1","license":[{"start":{"date-parts":[[2014,12,30]],"date-time":"2014-12-30T00:00:00Z","timestamp":1419897600000},"content-version":"vor","delay-in-days":0,"URL":"http:\/\/onlinelibrary.wiley.com\/termsAndConditions#vor"}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["Annals of the New York Academy of Sciences"],"published-print":{"date-parts":[[2015,3]]},"abstract":"<jats:p>\n                    The concept that frontotemporal dementia (FTD) is a purely cortical dementia has largely been refuted by the recognition of its close association with motor neuron disease, and the identification of transactive response DNA\u2010binding protein 43 (TDP\u201043) as a major pathological substrate underlying both diseases. Genetic findings have transformed this field and revealed connections between disorders that were previous thought clinically unrelated. The discovery that the\n                    <jats:italic>C9ORF72<\/jats:italic>\n                    locus is responsible for the majority of hereditary FTD, amyotrophic lateral sclerosis (ALS), and FTD\u2013ALS cases and the understanding that repeat\u2010containing RNA plays a crucial role in pathogenesis of both disorders has paved the way for the development of potential biomarkers and therapeutic targets for these devastating diseases. In this review, we summarize the historical aspects leading up to our current understanding of the genetic, clinical, and neuropathological overlap between FTD and ALS, and include brief discussions on chronic traumatic encephalopathy (CTE), given its association with TDP\u201043 pathology, its associated increased dementia risk, and reports of ALS in CTE patients. In addition, we describe other genetic associations between dementia and neuromuscular disease, such as inclusion body myositis with Paget's disease and FTD.\n                  <\/jats:p>","DOI":"10.1111\/nyas.12638","type":"journal-article","created":{"date-parts":[[2014,12,30]],"date-time":"2014-12-30T10:18:52Z","timestamp":1419934732000},"page":"71-93","source":"Crossref","is-referenced-by-count":111,"title":["Frontotemporal dementia: a bridge between dementia and neuromuscular disease"],"prefix":"10.1111","volume":"1338","author":[{"given":"Adeline S.L.","family":"Ng","sequence":"first","affiliation":[{"name":"Department of Neurology National Neuroscience Institute Tan Tock Seng Hospital  Novena Singapore"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Rosa","family":"Rademakers","sequence":"additional","affiliation":[{"name":"Department of Neurology Mayo Clinics  Jacksonville Florida"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Bruce L.","family":"Miller","sequence":"additional","affiliation":[{"name":"Memory and Aging Centre Department of Neurology University of California  San Francisco, San Francisco California"}],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"311","published-online":{"date-parts":[[2014,12,30]]},"reference":[{"key":"e_1_2_14_2_1","doi-asserted-by":"publisher","DOI":"10.1212\/WNL.59.7.1077"},{"key":"e_1_2_14_3_1","doi-asserted-by":"publisher","DOI":"10.1038\/ng1332"},{"key":"e_1_2_14_4_1","doi-asserted-by":"publisher","DOI":"10.1002\/ajmg.a.31862"},{"key":"e_1_2_14_5_1","first-page":"165","article-title":"\u00dcber die Beziehungen der senilen Hirnatrophie zur Aphasie","volume":"17","author":"Pick A.","year":"1892","journal-title":"Prag. 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