{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,7,27]],"date-time":"2026-07-27T19:09:52Z","timestamp":1785179392874,"version":"3.55.0"},"reference-count":88,"publisher":"Portland Press Ltd.","issue":"3","content-domain":{"domain":["portlandpress.com"],"crossmark-restriction":true},"short-container-title":[],"published-print":{"date-parts":[[2024,6,26]]},"abstract":"<jats:p>In the United States, it is now estimated that 6.7 million people over the age of 65 are afflicted by Alzheimer's disease (AD), over 1 million people are living with Parkinson's disease (PD), and over 200\u2009000 have or are at risk for developing Huntington's disease (HD). All three of these neurodegenerative diseases result in the ultimate death of distinct neuronal subtypes, and it is widely thought that age-related damage is the single biggest contributing factor to this neuronal death. However, recent studies are now suggesting that developmental defects during early neurogenesis could also play a role in the pathology of neurodegenerative diseases. Loss or overexpression of proteins associated with HD, PD, and AD also result in embryonic phenotypes but whether these developmental defects slowly unmask over time and contribute to age-related neurodegeneration remains highly debated. Here, we discuss known links between embryonic neurogenesis and neurodegenerative disorders (including common signaling pathways), potential compensatory mechanisms that could delay presentation of neurodegenerative disorders, and the types of model systems that could be used to study these links in vivo.<\/jats:p>","DOI":"10.1042\/bst20230422","type":"journal-article","created":{"date-parts":[[2024,4,25]],"date-time":"2024-04-25T12:08:20Z","timestamp":1714046900000},"page":"1035-1044","update-policy":"https:\/\/doi.org\/10.1042\/crossmark_policy","source":"Crossref","is-referenced-by-count":11,"title":["Exploring potential developmental origins of common neurodegenerative disorders"],"prefix":"10.1042","volume":"52","author":[{"given":"James P.","family":"Catlin","sequence":"first","affiliation":[{"name":"Department of Biochemistry, Jacobs School of Medicine and Biomedical Sciences, State University of New York at Buffalo, Buffalo, NY 14203, U.S.A."}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0001-9133-5583","authenticated-orcid":false,"given":"Christine E.","family":"Schaner Tooley","sequence":"additional","affiliation":[{"name":"Department of Biochemistry, Jacobs School of Medicine and Biomedical Sciences, State University of New York at Buffalo, Buffalo, NY 14203, U.S.A."}],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"288","published-online":{"date-parts":[[2024,4,25]]},"reference":[{"key":"2024062609205121500_BST-2023-0422CC1","doi-asserted-by":"publisher","first-page":"70","DOI":"10.3389\/fncom.2017.00070","article-title":"Striatal network models of Huntington's disease dysfunction phenotypes","volume":"11","year":"2017","journal-title":"Front. 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