White Matter Damage in Alzheimer's Disease: Contribution of Oligodendrocytes
作者全名:"Zhou, Jinyu; Zhang, Peng; Zhang, Bo; Kong, Yuhan"
作者地址:"[Zhou, Jinyu; Kong, Yuhan] Chongqing Med Univ, Affiliated Hosp 1, Dept Rehabil Med, Chongqing 400042, Peoples R China; [Zhang, Peng] Chongqing Med Univ, Dept Neurol, Affiliated Hosp 2, Chongqing 400010, Peoples R China; [Zhang, Bo] Chongqing Med & Pharmaceut Coll, Dept Basic Med, Chongqing 401331, Peoples R China"
通信作者:"Kong, YH (通讯作者),Chongqing Med Univ, Affiliated Hosp 1, Dept Rehabil Med, 1 Youyi Rd, Chongqing 400042, Peoples R China."
来源:CURRENT ALZHEIMER RESEARCH
ESI学科分类:NEUROSCIENCE & BEHAVIOR
WOS号:WOS:000921237700001
JCR分区:Q4
影响因子:2.1
年份:2022
卷号:19
期号:9
开始页:629
结束页:640
文献类型:Review
关键词:Alzheimer's disease; signaling pathways; oligodendrocytes; myelin sheath; central nervous system; white matter
摘要:"Alzheimer's disease (AD) is an age-related neurodegenerative disease seriously influencing the quality of life and is a global health problem. Many factors affect the onset and development of AD, but specific mechanisms underlying the disease are unclear. Most studies investigating AD have focused on neurons and the gray matter in the central nervous system (CNS) but have not led to effective treatments. Recently, an increasing number of studies have focused on white matter (WM). Magnetic resonance imaging and pathology studies have shown different degrees of WM abnormality during the progression of AD. Myelin sheaths, the main component of WM in the CNS, wrap and insulate axons to ensure conduction of the rapid action potential and axonal integrity. WM damage is characterized by progressive degeneration of axons, oligodendrocytes (OLs), and myelin in one or more areas of the CNS. The contributions of OLs to AD progression have, until recently, been largely overlooked. OLs are integral to myelin production, and the proliferation and differentiation of OLs, an early characteristic of AD, provide a promising target for preclinical diagnosis and treatment. However, despite some progress, the key mechanisms underlying the contributions of OLs to AD remain unclear. Given the heavy burden of medical treatment, a better understanding of the pathophysiological mechanisms underlying AD is vital. This review comprehensively summarizes the results on WM abnormalities in AD and explores the relationship between OL progenitor cells and the pathogenesis of AD. Finally, the underlying molecular mechanisms and potential future research directions are discussed."
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