Oligodendrocytes and Alzheimer's disease

Abstract

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 (Aβ)-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 Aβ 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.

KEYWORDS:

• Alzheimer's disease
• oligodendrocyte
• myelin

Acknowledgments

This work was supported by the Hubei Province Health and Family Planning Scientific Research Project (WJ2015MB219), the Hubei Provincial Nature Science Foundation (2105CFB260) and the Nature Science Foundation of Shiyan Renmin Hospital to Dr. Zhiyou Cai.

Declaration of Interest

No conflict of interest is declared. This work was supported by the Nature Science Foundation of Renmin Hospital, Hubei University of Medicine (to Zhiyou Cai).