Journal
INTERNATIONAL JOURNAL OF NEUROSCIENCE
Volume 126, Issue 2, Pages 97-104Publisher
TAYLOR & FRANCIS LTD
DOI: 10.3109/00207454.2015.1025778
Keywords
Alzheimer's disease; oligodendrocyte; myelin
Categories
Funding
- Hubei Province Health and Family Planning Scientific Research Project [WJ2015MB219]
- Hubei Provincial Nature Science Foundation [2105CFB260]
- Nature Science Foundation of Shiyan Renmin Hospital
Ask authors/readers for more resources
Extensive evidence has indicated that the breakdown of myelin is associated with Alzheimer's disease (AD) since the vulnerability of oligodendrocytes under Alzheimer's pathology easily induces the myelin breakdown and the loss of the myelin sheath which might be the initiating step in the changes of the earliest stage of AD prior to appearance of amyloid and tau pathology. Considerable research implicated that beta-amyloid (A)-mediated oligodendrocyte dysfunction and myelin breakdown may be via neuroinflammation, oxidative stress and/or apoptosis. It also seems that the oligodendrocyte dysfunction is triggered by the formation of neurofibrillary tangles (NFTs) through inflammation and oxidative stress as the common pathophysiological base. Impaired repair of oligodendrocyte precursor cells (OPCs) might possibly enhance the disease progress under decreased self-healing ability from aging process and pathological factors including A pathology and/or NFTs. Thus, these results have suggested that targeting oligodendrocytes may be a novel therapeutic intervention for the prevention and treatment of AD.
Authors
I am an author on this paper
Click your name to claim this paper and add it to your profile.
Reviews
Recommended
No Data Available