Oligodendrocytes are crucial for the formation and maintenance of myelin, the protective sheath that insulates axons in the central nervous system (CNS). In Alzheimer's disease (AD), the health of oligodendrocytes is compromised, leading to myelin degradation and subsequent cognitive decline. This degradation is often exacerbated by neuroinflammation, which is a hallmark of AD pathology.
Research indicates that myelin loss is associated with cognitive impairment in AD. Oligodendrocytes not only provide structural support but also play a role in metabolic support for neurons. When oligodendrocytes are damaged, the resulting myelin loss can lead to impaired neuronal communication and increased neuroinflammation, further contributing to cognitive decline
Neuroinflammation is a significant contributor to oligodendrocyte dysfunction in AD. Amyloid-beta (Aβ) accumulation can activate inflammatory pathways that lead to oligodendrocyte apoptosis and myelin breakdown . This creates a vicious cycle where inflammation leads to further oligodendrocyte damage, exacerbating cognitive decline.
Targeting oligodendrocyte health could potentially reverse cognitive decline in AD. Strategies may include:
In conclusion, targeting oligodendrocyte health presents a promising avenue for reversing cognitive decline in Alzheimer's disease. By restoring myelin integrity and reducing neuroinflammation, it may be possible to enhance cognitive resilience and improve outcomes for individuals affected by this devastating condition.