Researchers are one step closer to understanding why Alzheimer's Disease develops. A team led by Dr. Ganesh M. Shankar and Dr. Dennis J. Selkoe of Harvard Medical School has found that a particular form of beta-amyloid, extracted from brains of dead humans, causes Alzheimer's in rats.

The research was published in Sunday's online edition of the journal Nature Medicine and details experiments carried out on rats injected with various forms of the beta-amyloid proteins known to make up plaques in the brains of Alzheimer's patients.

Whereas soluble one-molecule or three-molecule forms of the beta-amyloid proteins caused no damage to the rats' brains, the two-molecule solution triggered symptoms which are characteristic of Alzheimer's patients. The density brain cells were also reduced by 47 percent, researchers claim.

This partly solves a medical dillema which surrounded the fact that although some people develop beta-amyloid plaques they do not have Alzheimer's symptoms. The new experiment points out the area where future research needs to focus, which might eventually lead to developing a cure or means to prevent Alzheimer's altogether.

Earlier this month, Myriad Genetics, Inc. has announced its upcoming Alzheimer drug Flurizan (tarenflurbil) which the company alleges that it works in two different ways to stop the disease. Tarenflurbil is part of a class called gamma-secretase modulators (GSM), whose exact way of action was still unclear.

Alzheimer’s causes a progressive loss of memory and mental faculties, which can be devastating for the patients concerned and those around them. According to the World Health Organization, there are about 18 million people worldwide with Alzheimer’s disease. By 2025, that number is expected to reach 34 million, as existing drugs can ease symptoms but do not stop the disease.