ALZHEIMER'S CURE COMES STEP CLOSER; Irish & US scientists in breakthrough.

Byline: BY SENAN HOGAN AND JOHN VON RADOWITZ

A LANDMARK discovery about the way Alzheimer's triggers memory loss could pave the way for a possible cure for the disease, it emerged yesterday.

Researchers conducted experiments using brain material from dead patients to show how a tiny protein building block disrupts communication between nerve cells.

The findings from Irish and US scientists provide the starting block for developing more effective drugs for the devastating disease, which affects more than 40,000 people in Ireland.

Professor Dominic Walsh from University College of Dublin's Conway Institute said: "The onset of the disease is insidious with the earliest symptoms often manifested as subtle and intermittent deficits of episodic memory.

"Our findings support the growing theory that Alzheimer's disease memory deficits may result from loss of dendritic spines and that this process is mediated by amyloid-beta protein." Scientists know Alzheimer's is known to be associated with deposits of a protein called amyloid-beta that build up in the brain.

But precisely how the protein is linked to the disease and its symptoms of progressive memory loss and mental confusion is still a mystery.

The new research involved extracting amyloid-beta material from dead Alzheimer's patients and injecting it into the brains of mice and rats.

Through a series of experiments, the scientists homed in an amyloid-beta subunit consisting of two molecules bonded together.

Known as "dimers", these protein elements were found to interfere with the transmission of signals at synapses, the junction points where nerve cells "talk" to each other. The effects were seen in the hippocampus, a part of the brain essential to short-term memory.

And the rodent experiments showed amyloid-beta dimers weakened these connections and reduced the density of dendritic spines - specialised "receivers" on neurons that pick up brain cell signals. Dendritic spines are believed to be vital to memory.

In another part of the study, researchers found injecting rats with amyloidbeta from human patients disrupted their memory of learned behaviour.

The research is reported in the latest issue of the journal Nature Medicine.

The scientists, led by Dr Dennis Selkoe from Harvard Medical School in Boston, Massachusetts, wrote: "Our findings support the emerging concept that the effects of amyloid-beta in Alzheimer's disease initially centre on subtly altered synapse function."

Scientists from UCD also took part in the study, together with colleagues from Trinity College and the Royal College of Surgeons in Ireland.

British author Terry Pratchett, who recently revealed he had Alzheimer's, has condemned the 'shameful' lack of funding to help fight the disease.