Are Oligodendrocytes the Culprits or Victims in Alzheimer’s Disease

TL;DR

This paper reviews the role of oligodendrocytes and myelin in Alzheimer’s disease, exploring whether they contribute to or are affected by the disease.

Contribution

The paper provides a comprehensive review of oligodendrocyte functions and their evolving role in Alzheimer’s disease.

Findings

Oligodendrocytes and myelin have roles beyond insulation, including axon support and neuroprotection.

Myelin damage is linked to neurological disorders, including Alzheimer’s disease.

Oligodendrocyte changes during Alzheimer’s suggest a complex interaction between myelin and disease progression.

Abstract

Oligodendrocytes are vital for the functioning of the nervous system. Oligodendrocyte-created myelin sheaths work as dynamic partners which play a substantial role in the myelination of axons. In addition to its well-known functions of providing insulation and enhancing conduction velocity, myelination controls axons’ maturity, longevity, and regenerative ability via trophic support and signalling molecules. Myelination also regulates ion concentration and offers neuroprotection. Myelin is generated via complex procedures including cell differentiation, specialised lipids, and protein synthesis. Understanding the physiology of myelin sheath formation is required to understand various neurological disorders associated with myelin sheath damage. This review focuses on our growing understanding of the intricate actions and changes in oligodendrocytes during the course of evolution and in Alzheimer’s disease.

Figures