Molecular mechanisms of chronic traumatic encephalopathy

被引:11
作者
van den Bedem, Henry [1 ]
Kuhl, Ellen [2 ,3 ]
机构
[1] Stanford Univ, Biosci Div, SLAC Natl Accelerator Lab, Stanford, CA 94305 USA
[2] Stanford Univ, Dept Mech Engn, Stanford, CA 94305 USA
[3] Stanford Univ, Dept Bioengn, Stanford, CA 94305 USA
关键词
Chronic traumatic encephalopathy; Neurodegeneration; Diffuse axonal injury; Tau protein; Neurofibrillary tangles; REPETITIVE BRAIN TRAUMA; ALZHEIMERS-DISEASE; TAU; INJURY; MICROTUBULES; SPECTRUM; SPORT; NEURODEGENERATION; NEUROPATHOLOGY; ORGANIZATION;
D O I
10.1016/j.cobme.2017.02.003
中图分类号
R318 [生物医学工程];
学科分类号
0831 ;
摘要
The prevalence of neurodegenerative disorders is rapidly increasing. While Alzheimer's disease and dementia generally correlate with longer lifespans, neurodegenerative disorders like chronic traumatic encephalopathy often affect individuals at young age. Historically, the underlying disease mechanisms of these chronic disorders-the slowly changing biochemical composition during aging and the repeated, rapidly changing biomechanical environment during head impact-have been viewed as distinct events. Recent studies suggest that Alzheimer's disease and chronic traumatic encephalopathy share common degenerative pathways on the molecular and cellular levels. Here we examine this current trend and explore the molecular, cellular, tissue, and organ level mechanisms of neurodegeneration through the lens of biomedical engineering. Understanding the underlying disease mechanisms across the spatio-temporal scales of neuro-degeneration provides new opportunities to modulate, slow down, and possibly revert molecular dysfunction, axonal death, tissue atrophy, and loss of brain function.
引用
收藏
页码:23 / 30
页数:8
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