< Back to previous page

Project

Microglia and neuroinflammation: transducers of amyloid beta toxicity in human Alzheimer’s disease

Alzheimer’s disease (AD) is a chronic neurodegenerative disease and is the most common form of dementia worldwide. AD is characterized by the build up of abnormal protein, in the form of amyloid beta plaques and tau tangles. AD is accompanied by changes in the immune cells of the brain, the microglia. This inflammation in the brain is referred to as neuroinflammation, which may be a simple consequence of damage to nerve cells or may contribute to disease progression. Recent genetic studies reveal a link between neuroinflammation and susceptibility to develop AD, suggesting that inflammation might be a driver of the disease opposed to just a consequence. The current proposal has two complementary approaches aimed at determining the role of neuroinflammation in human AD by generating novel models where human derived cells are injected into AD mice, in order to expose those cells to the environment they would find in the pathological brain. By doing this both with neural and microglial cells, we will be able to dissect the contribution of neuroinflammation in the AD brain in two crucial human cell types. These findings would have major implications for our understanding of the progression of human AD and would allow tailored treatments to slow down or arrest AD progression. This approach addresses a critical component of the pathology in the AD brain and might yield novel drug targets with the potential to change the disease trajectory and patients’ quality of life

Date:1 Jan 2019 →  31 Dec 2022
Keywords:Medical cell biology, Medical immunology
Disciplines:Neurological and neuromuscular diseases