Summary

There is a high level of neuro-inflammation in the brains of Alzheimer's patients. These inflammatory factors are secreted by stressed cells and lead to deterioration of other cell types (e.g. neurons) present in the brain. This proposal intends to study the molecular pathways that govern this inflammatory response inside the brain and target them to limit the neuronal damage that leads to cognitive deficits and memory loss in Alzheimer's disease.

Project Details

This research aims to study the molecular pathways that govern senescence and inflammation in Alzheimer’s disease (AD). Cellular senescence is a state of growth arrest in response to stress. Cells in the body can become senescent in aging and many disease conditions. These cells induce chronic inflammation which damages their surrounding tissue. There is evidence that senescent cells increase in AD brains. Importantly, treatment of AD mouse models with drugs that selectively kill senescent cells has been shown to ameliorate the neurological and cognitive deficits in these mice. These promising preliminary results underline the need to study the mechanisms of senescence and inflammation in human post-mortem AD brains and mouse models. My research will focus on specific inflammatory pathways that are activated during senescence and cause tissue damage. I hope that my work will lead to a better understanding of the biology of AD and identify novel therapeutic targets to limit brain cell damage in humans suffering from AD.