A Queensland Brain Institute neuroscientist at UQ is working on ways to reduce neuronal loss in the brain of a person with Alzheimer's disease.
Dr Elizabeth Coulson and her Cell Survival Laboratory have been awarded an $80,000 UQ Foundation Research Excellence Award to study what causes healthy nerve cells to "switch off" and die - a characteristic associated with many neurodegenerative conditions including Alzheimer's disease.
The UQ Foundation Research Excellence Awards have been run for 10 years and are an initiative of UQ to recognise outstanding performance and leadership potential in early career researchers.
As one of the most common forms of dementia, Alzheimer's disease affects about 10 percent of the population aged over 65, and an estimated 40 percent of people aged 80 or above.
Dr Coulson said that while memory loss in people with Alzheimer's disease could be attributed to several factors, researchers were starting to pinpoint some of the specific mechanisms thought to be responsible.
"These include a build-up of the neuro-toxin beta-amyloid - the major component of amyloid plaques found in brains of patients with Alzheimer's - and corresponding degeneration of a specific population of nerve cells in the basal forebrain," she said.
Her laboratory has established the molecule known as p75 neurotrophin receptor was necessary for the beta-amyloid to cause nerve cell degeneration in the basal forebrain.
"Discovering how beta-amyloid triggers neuronal degeneration has been a question bugging neuroscientists for decades, and we have identified an important piece of the puzzle," Dr Coulson said.
These results provide a novel mechanism to explain the early and characteristic loss of brain cells that occurs in Alzheimer's disease, which are known to be important for memory formation.
Dr Coulson will use her grant money to continue this promising line of research.
Together with researchers at Aarhus University in Denmark, she will study the sortilin family of p75 interacting proteins, some of which are down-regulated in Alzheimer's disease.
This will shed further light on the regulation of the p75 neurotrophin receptor cell death "switch" in beta-amyloid toxicity, and its role in cognitive decline.