NZ researchers find Alzheimer's clue

By GEOFF CUMMING

New Zealand scientists have opened a new frontier in the search for a cure for Alzheimer's disease by pinpointing a mutant protein similar to the one known to cause Huntington's disease.

Auckland University researchers working with British counterparts have found that an insoluble form of a protein known as TBP is present in large amounts in the brains of Alzheimer's patients.

Their findings, after five years of research, have just been published in the American journal Molecular Brain Research and are expected to prompt a worldwide rethink about the likely causes of the degenerative brain disease.

But lack of funding is frustrating the New Zealand team's effort to take the research to the next stage, to try to prove a causative link between TBP and Alzheimer's.

About 30,000 New Zealanders live with the disease, the most prevalent form of dementia, which typically begins with memory loss and leads to near-total loss of function.

There is no known cure and the brain cell-destroying illness, which can strike in early middle age, takes a slow, destructive toll on patients and caregivers, who are usually close family members.

The disease that killed former US President Ronald Reagan has long been associated with a build-up of insoluble deposits of another group of proteins, amyloids.

TBP belongs to the polyglutamine group of proteins. When it mutates it produces insoluble deposits known to cause neurodegenerative diseases similar to Huntington's.

Polyglutamines had not been directly associated with Alzheimer's before, says PhD student Suzanne Reid, of the university's department of pharma-cology.

"We have made the connection between the two."

Her supervisor, Dr Russell Snell, was part of the international group that discovered the mutation that causes Huntington's.

Dr Snell says the finding is spectacular.

"In effect we've opened a field of new research with a new protein. Labs around the world will be seizing on it. It may give us a clue as to how the majority of these diseases function and may give us a target for further therapeutic intervention."

Further research is needed to determine what role TBP has in Alzheimer's, but Dr Snell says the research team has yet to secure funding.

"As a contributing pathway to the disease it's a pretty good candidate," he says.

"It's in all of us, it's ubiquitously expressed in every cell, it can cause a degenerative disease and the mutation is similar to a number of degenerative diseases."

Miss Reid said research already suggested that similar types of structures formed in the brains of both Huntington's and Alzheimer's patients.

"Now we have found that this protein is playing a part. Until now it has not been seen in a pathological form in an Alzheimer's brain."

Alzheimer's New Zealand, which provides support and services nationwide for sufferers and caregivers, said research was pivotal to finding ways either to slow down or intervene in Alzheimer's and other dementias.

"We are very aware of how difficult it can be to have research funded," said the manager of communications and funding, Florence Leota.

"If New Zealand is given the opportunity to lead new research in an area that includes Alzheimer's, particularly with international interest growing, it would be short-sighted on our part to show a lack of support for that research."