New research from the University of Eastern Finland explores the role of diabetes in the cellular and molecular changes underlying Alzheimer’s disease (AD). In an AD mouse model, diabetes induced through a diet rich in fats and sugars weakened the accumulation of microglial cells around amyloid plaques and increased the formation of neuritic plaques with prominent tau pathology. Besides the mouse model, a similar observation was also made in hydrocephalus patients with type 2 diabetes, who had fewer microglia around amyloid plaques than patients without diabetes. The findings provide valuable new insight into the cellular mechanisms by which type 2 diabetes contributes to the risk and development of AD.
Alzheimer’s disease is the most common form of dementia, with no cure to date. AD is characterised by the accumulation of beta-amyloid peptides and phosphorylated tau proteins in the brain, leading to the activation of the immune cells in brain: microglia and astrocytes. AD also causes damage to axons and dendrites and, ultimately, leads to neuronal cell death. Recent genetic studies suggest that microglia play a key role in the development of AD. In addition to genetics, environmental and lifestyle factors, and diseases associated with them, such as type 2 diabetes, affect the risk of AD. Type 2 diabetes has long been known to increase the risk of AD and to influence the disease course, but the underlying cellular and molecular events are still elusive.
Release date: 16 November 2020
Source: University of Eastern Finland