Traumatic brain injury-associated epigenetic changes and the risk for neurodegenerative diseases

被引:3
|
作者
Smolen, Paul [1 ]
Dash, Pramod K. [1 ]
Redell, John B. [1 ]
机构
[1] Univ Texas Hlth Sci Ctr Houston, McGovern Med Sch, Dept Neurobiol & Anat, Houston, TX 77054 USA
关键词
acetylation; Alzheimer's disease; dementia; feedback loop; epigenetics; methylation; Parkinson's disease; encephalopathy; AMYLOID PROTEIN DEPOSITION; EXACERBATES TAU PATHOLOGY; HISTONE H3 ACETYLATION; ALZHEIMERS-DISEASE; DNA METHYLATION; HEAD-INJURY; PARKINSONS-DISEASE; ALPHA-SYNUCLEIN; MICROGLIAL ACTIVATION; INFLAMMATORY RESPONSE;
D O I
10.3389/fnins.2023.1259405
中图分类号
Q189 [神经科学];
学科分类号
071006 ;
摘要
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's or Parkinson's 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 - Alzheimer's disease, Parkinson's disease, or chronic traumatic encephalopathy. Finally, we discuss possible directions for TBI therapies that may help prevent or delay development of NDs.
引用
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页数:10
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