QBI neuroscientists make Alzheimer's disease advance

June 10, 2008

Queensland Brain Institute (QBI) neuroscientists at UQ have discovered a new way to reduce neuronal loss in the brain of a person with Alzheimer's disease. Memory loss in people with Alzheimer's disease can be attributed to several factors.

These include a build-up of the neuro-toxin Amyloid beta – the major component of amyloid plaques found in patients with Alzheimer's – and corresponding degeneration of a specific population of nerve cells in the basal forebrain.

QBI neuroscientist Dr Elizabeth Coulson's research was recently published in the Journal of Neuroscience.

She said the research had established that the molecule known as p75 neurotrophin receptor was necessary for the Amyloid beta to cause nerve cell degeneration in the basal forebrain.

During her research, Dr Coulson's team found – both in cultured cells and in an animal model of Alzheimer's disease – that it was possible to completely prevent Amyloid beta toxicity by removing the p75 cell death receptor.

"Discovering how Amyloid beta 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 already has patented molecules that can block p75 and is ready to begin testing them in animal models of Alzheimer's disease.

"If such therapy is successful, it probably wouldn't cure this multifaceted disease," Dr Coulson said.

"But it would be a significant improvement on what is currently available for Alzheimer's disease patients."

The World Health Organisation predicts that by 2040, neurodegenerative conditions will become the world's leading cause of death, overtaking cancer.

Alzheimer's disease is the most common dementia affecting 10 per cent of people over 65 and 40 per cent over 80 years of age.

Significant advances in determining the molecular regulation of nerve cell function and survival have major impact on our understanding of more complex areas such as behaviour, cognition, aging and neurological diseases.

Source: Research Australia

Explore further: Early signs of Alzheimer's disease identified

Related Stories

Alzheimer's protein plaques may also harm the heart

November 28, 2016

(HealthDay)—Protein fragments that form plaques in the brains of Alzheimer's patients might also stiffen their heart muscle and increase their risk of heart failure, a new study reports.

Recommended for you

Researchers question lifelong immunity to toxoplasmosis

December 8, 2016

Medical students are taught that once infected with Toxoplasma gondii—the "cat parasite"—then you're protected from reinfection for the rest of your life. This dogma should be questioned, argue researchers in an Opinion ...

Key regulator of bone development identified

December 8, 2016

Loss of a key protein leads to defects in skeletal development including reduced bone density and a shortening of the fingers and toes—a condition known as brachydactyly. The discovery was made by researchers at Penn State ...

TET proteins drive early neurogenesis

December 7, 2016

The fate of stem cells is determined by series of choices that sequentially narrow their available options until stem cells' offspring have found their station and purpose in the body. Their decisions are guided in part by ...

0 comments

Please sign in to add a comment. Registration is free, and takes less than a minute. Read more

Click here to reset your password.
Sign in to get notified via email when new comments are made.