Project Overview

Alzheimer’s Disease (AD) affects many people and leads to memory loss and cognitive decline. It is linked to brain inflammation and changes in proteins like GFAP, which is usually found in support cells called astrocytes. Recent research has discovered that GFAP can also appear in neurons, potentially making these cells more vulnerable to damage. Understanding this abnormal GFAP presence could lead to new treatment options for AD.

This study aims to explore why GFAP appears in neurons in Alzheimer’s Disease when it normally should not be present in these cells. We will try to understand its effects on neuron health, and test whether reducing GFAP can improve brain function. We believe that stopping GFAP buildup in neurons could prevent damage and enhance memory and cognition, leading to potential new treatments for AD.

The project will use mouse models of Alzheimer’s Disease to study GFAP in neurons. We will use advanced imaging to find and track GFAP, then test whether reducing GFAP with specific gene treatments can protect neurons. We will also observe behavioural changes to measure how well these treatments improve memory and learning.

We expect that reducing GFAP in neurons will improve their health and boost memory in AD models. This could reveal a new treatment target to slow down or stop the damage caused by AD. The findings may also provide insights into other conditions involving brain inflammation and neuron damage. Approved treatments to reduce GFAP already exist for other disease. If we are successful, it may be possible to apply these treatments for AD patients.

This study could help develop new treatments for Alzheimer’s by focusing on preventing damage to neurons. If successful, the research may lead to new therapies that protect brain cells in AD and other related diseases, giving hope for better outcomes for people affected by neurodegeneration.

Principal Investigator

Jonathan Epp , University of Calgary

Partners and Donors

Alzheimer Society of Canada