{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,11,10]],"date-time":"2026-11-10T16:42:58Z","timestamp":1794328978686,"version":"4.9.0"},"reference-count":187,"publisher":"Frontiers Media SA","license":[{"start":{"date-parts":[[2023,9,19]],"date-time":"2023-09-19T00:00:00Z","timestamp":1695081600000},"content-version":"vor","delay-in-days":0,"URL":"https:\/\/creativecommons.org\/licenses\/by\/4.0\/"}],"content-domain":{"domain":["frontiersin.org"],"crossmark-restriction":true},"short-container-title":["Front. Neurosci."],"abstract":"<jats:p>Epidemiological studies have shown that traumatic brain injury (TBI) increases the risk for developing neurodegenerative diseases (NDs). However, molecular mechanisms that underlie this risk are largely unidentified. TBI triggers widespread epigenetic modifications. Similarly, NDs such as Alzheimer\u2019s or Parkinson\u2019s are associated with numerous epigenetic changes. Although epigenetic changes can persist after TBI, it is unresolved if these modifications increase the risk of later ND development and\/or dementia. We briefly review TBI-related epigenetic changes, and point out putative feedback loops that might contribute to long-term persistence of some modifications. We then focus on evidence suggesting persistent TBI-associated epigenetic changes may contribute to pathological processes (e.g., neuroinflammation) which may facilitate the development of specific NDs \u2013 Alzheimer\u2019s disease, Parkinson\u2019s disease, or chronic traumatic encephalopathy. Finally, we discuss possible directions for TBI therapies that may help prevent or delay development of NDs.<\/jats:p>","DOI":"10.3389\/fnins.2023.1259405","type":"journal-article","created":{"date-parts":[[2023,9,19]],"date-time":"2023-09-19T12:49:22Z","timestamp":1695127762000},"update-policy":"https:\/\/doi.org\/10.3389\/crossmark-policy","source":"Crossref","is-referenced-by-count":28,"title":["Traumatic brain injury-associated epigenetic changes and the risk for neurodegenerative diseases"],"prefix":"10.3389","volume":"17","author":[{"given":"Paul","family":"Smolen","sequence":"first","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Pramod K.","family":"Dash","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"John B.","family":"Redell","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"1965","published-online":{"date-parts":[[2023,9,19]]},"reference":[{"key":"ref1","doi-asserted-by":"publisher","first-page":"214","DOI":"10.1186\/s13568-017-0513-z","article-title":"Considering choline as methionine precursor, lipoproteins transporter, hepatic promoter and antioxidant agent in dairy cows","volume":"7","author":"Abbasi","year":"2017","journal-title":"AMB Express"},{"key":"ref2","doi-asserted-by":"publisher","first-page":"1679","DOI":"10.1089\/neu.2020.7283","article-title":"Differential DNA methylation of the genes for amyloid precursor protein, tau, and neurofilaments in human traumatic brain injury","volume":"38","author":"Abu Hamdeh","year":"2021","journal-title":"J. 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