Prosperous populations live longer and old age carries an increased risk of dementia, a condition that is so far neither preventable nor curable. The trend of incidence of Alzheimer’s Disease (AD), the most common form of dementia, is increasing all over the world. AD is widely thought to be driven by amyloid pathology, in which peptides of amyloid-β are generated in the brain and clump together into plaques triggering neuroinflammation and neurodegeneration.
This seminar will present a quick overview of AD neuropathology, followed by a presentation of ongoing preclinical research done at my laboratory using animal models of AD, and how several AD manifestations can be alleviated in these models by manipulation of the gene encoding p75 neurotrophin receptor (p75NTR).
p75NTR is a “death receptor”, i.e. a transmembrane protein present on the surface of a variety of cells, including neurons, that mediates the elimination of defective cells by instigation of so-called “cell death” pathways. p75NTR expression and activity is induced after lesions and neural damage, thus contributing to neuropathological effects in a variety of conditions. Interest in p75NTR biology stems from the possibility of blocking p75NTR activity as a strategy to combat neurodegenerative diseases, including AD.