Amyloid beta-induced microvasculature dysfunction
2014
Phoenix Veterans Affairs Health Care System, Phoenix, USA
Alzheimer's disease is the most prevalent neurodegenerative disorder and is characterized by progressive brain degeneration that leads to cognitive decline and death. Amyloid beta has been extensively proposed to be the driving cause of the disease and, currently, there is growing evidence that it may also lead to vascular dysfunction and hypoperfusion during the progression of the disease. Thus, there is a need to investigate the mechanisms of amyloid beta-induced endothelial dysfunction and oxidative stress in human microvasculature. Here, abdominal subcutaneous arterioles from living humans and post-mortem leptomeningeal arterioles are used to study how amyloid beta affects vascular dilatation and the production of reactive oxygen species. The results showed that exposure to amyloid beta impaired dilatation of adipose and leptomeningeal arterioles, which could be reversed with the use of an antioxidant. Moreover, amyloid beta also induced increased oxidative stress in adipose arterioles. The researchers propose a model based on easily accessible tissue that can be obtained from living patients to study the mechanisms of amyloid beta-driven microvasculature dysfunction and opens the door to study new therapeutical approaches to counteract the pathological effects of amyloid beta in Alzheimer's disease.
Adipose and leptomeningeal arteriole endothelial dysfunction induced by β-amyloid peptide: A practical human model to study Alzheimer's disease vasculopathy
Raymond Q Migrino
Added on: 10-01-2021
[1] https://www.sciencedirect.com/science/article/abs/pii/S016502701400226X[2] https://data.jrc.ec.europa.eu/dataset/a8fd26ef-b113-47ab-92ba-fd2be449c7eb
