Protein may hold key to cure for Alzheimer’s

A PROTEIN that acts as a “master regulator” of nerve signalling in the brain may hold the key to curing or controlling Alzheimer’s disease, research suggests.

Artificially boosting its levels completely removed the symptoms of Alzheimer’s affected mice.

The US findings hold out the promise of an entirely new approach to tackling the disease in humans.

However, experts pointed out that achieving the same result in humans might still be a long way off.

The protein is an enzyme called EphB2 that plays a crucial role in neurotransmission, the passing of nerve messages between neurons by means of chemical signals.

“We thought it might be involved in memory problems of AD (Alzheimer’s disease) because it is a master regulator of neurotransmission and its brain levels are decreased in the disease,” said study leader Dr Moustapha Cisse, from the Gladstone Institute of Neurological Disease in San Francisco.

Dr Cisse’s team tested the theory by using gene therapy to manipulate EphB2 levels in the brains of laboratory mice. A virus was used to “infect” the mice with genetic material that either boosted or reduced production of the enzyme.

Lowered levels of the protein disrupted neurotransmission in healthy mice and generated memory problems similar to those caused by Alzheimer’s. This suggested a lack of EphB2 contributed to Alzheimer’s symptoms.

But the big discovery came when levels of the enzyme were increased in mice genetically modified to suffer a condition that mimicked human Alzheimer’s disease. The animals’ memory problems were “completely fixed”, said the scientists, whose results appear in an online edition of the journal Nature.

They also found that beta-amyloid protein, which accumulates in lumps and damages the brains of Alzheimer’s patients, became attached to EphB2 and destroyed it.

Dr Lennart Mucke, director of the Gladstone Institute and one of the study authors, said: “What we were most curious about ... was whether normalising EphB2 levels could fix memory problems caused by amyloid proteins. We were absolutely thrilled to discover that it did.

“Based on our results, we think that blocking amyloid proteins from binding to EPhB2 and enhancing EphB2 levels or functions with drugs might be of benefit in AD. We are excited about these possibilities and look forward to pursuing them in future studies.”