THE SEARCH is on for a new type of drug to fight Alzheimer’s disease following an important discovery about how the condition takes hold. Scientists believe they can target a specific part of this process and halt the disease.
Alzheimer’s is a very common disease, but is also on the increase as better healthcare allows people to live longer according to the Alzheimer’s Society of Ireland.
It is the most frequently seen form of a general condition known as dementia, something that affects one in 20 of those over 65. There are currently 44,000 dementia patients in Ireland but this is expected to exceed 100,000 within the next 20 years, the society said.
For some years researchers have known that Alzheimer’s disease is associated with the build-up in the brain of a material known as plaque. It causes nerve cells to weaken and die, gradually destroying normal brain activity.
Research published this morning in the journal Natureby a Nobel prize-winning scientist from Rockefeller University in New York describes a potential way to block the disease however.
Prof Paul Greenard and colleagues at centres in New York, Massachusetts and Connecticut have discovered a protein, GSAP, that is central to the build-up of plaques. GSAP increases plaque production in the brain.
“Reducing GSAP concentrations in cell lines decreases [plaque] concentrations,” Prof Greenard writes.
The researchers already know of a drug that can block the action of GSAP without affecting any other tissues or processes in the brain. Called imatinib (Gleevec), the drug is usually used for cancer treatments, but it connects directly to GSAP and blocks its activity, the authors write.
The drug cannot be used immediately to treat Alzheimer’s however because it can’t easily reach the brain. It cannot cross the “blood-brain barrier”, which protects the brain from chemicals that get into the blood.
Yet identifying the role of GSAP and knowing about the action of imatinib opens the way for the discovery of a new drug that can pass the blood-brain barrier, the authors state.
They have evidence from mouse models for Alzheimer’s disease to show it should work. Knocking out GSAP caused plaque levels in mice to fall almost 40-fold, they found.
The goal now is to develop a drug that can pass the barrier and accumulate in the brain to block GSAP.