An international team of researchers from the University of Melbourne and the Polish Academy of Sciences have discovered a rather helpful role of a protein associated with the progression of Alzheimer’s disease in humans. These findings could help scientists comprehend the intricate brain mechanisms involved in the development of Alzheimer’s – a neurodegenerative condition affecting thousands of Australians.

The Novel Beta-Amyloid Protein

Scientists have been keenly interested in the functioning of beta-amyloid and its association with the progression of Alzheimer’s disease. Clumps of this protein are formed in brain tissue of people suffering from the illness.

In the late 90’s, the presence of large quantities of copper was detected in these clumps. Copper – as a micronutrient – is important; however excessive amounts can produce dangerous free radicals. Many scientists contemplated that copper played an integral role in the development of Alzheimer’s – beta-amyloid could randomly bind to the metal and allow it to form free radicals

Upon further investigation, it was seen that beta-amyloid existed in various sizes. Researchers led by Dr Simon Drew (University of Melbourne) and Prof Wojciech Bal (Polish Academy of Sciences) have now discovered that a shorter form of the beta-amyloid – missing three links at the beginning of the protein’s chain-like structure – is involved in safely binding copper that damages brain tissue. The protein acts like a ‘sponge’, trapping the extra metal, and has been overlooked since the discovery of beta-amyloid over 30 years ago.

Significance Of The Findings

“We know that the shorter form of beta-amyloid is present in the diseased brain, but we now know that it is abundantly present in healthy brains as well”, claims Dr Drew.

The minute changes in the length of this protein cause significant alterations in its ability to bind copper. Dr Drew explained that this form of beta-amyloid could bind copper about a 1000 times more powerfully than the longer forms. Moreover, it wraps around the metal in such a way that it cannot produce free radicals.

According to these properties, and its relative abundance in healthy brains, the shorter beta-amyloid suggests a protective function.

Future Prospects: Development Of Alzheimer’s Disease Re-evaluated

Currently, therapies designed to lower beta-amyloid production have only been modestly successful at slowing down cognitive deterioration – Alzheimer’s continues to affect people at large.

Dr Drew, along with his team has started work on developing a method that identifies the copper-bound form of short beta-amyloid in the body. This will allow researchers to screen for levels of copper in the brain, and whether the short form can safely transport excessive amounts of the metal from one point to another. These findings may change what scientists currently know about aging and Alzheimer’s.

“If a beneficial role in copper balance can be established, it’s still possible to have too much of a good thing”, stated Dr Drew.