Harvard researchers suggest new Alzheimer’s theory

A new theory by Harvard researchers could radically change our understanding of the disease and suggest new routes for treatment and prevention.

The researchers think that the immune system might play a key role in the development of Alzheimer's, which leads to progressive loss of memory and is eventually fatal.

A protein called beta amyloid, long held as the villain in  Alzheimer's, actually has a positive role to play in fighting off bacteria and fungus in mice, worms and cells, the researchers showed in a new paper in Science Translational Medicine.

Assuming that also held true in people, it suggests that getting rid of amyloid, as some drug trials had tried could be dangerous, while  approaches that stimulated the immune system could be safer and more effective.

According to the researchers, Rudy Tanzi and Robert Moir, both of Harvard Medical School and Massachusetts General Hospital, Alzheimer's could  be triggered by a normal immune response gone astray or into over-drive in response to bacteria or other pathogens.

Amyloid ''lights the fire,'' said Tanzi, whose work has been supported by a grant from the Cure Alzheimer's Fund. ''We think it's meant to be beneficial, but it can turn against you and cause problems.''

In their study, cultured human and hamster cells that were infected with the fungus Candida albicans and had a high expression of amyloid beta doubled the number of cells that were not infected, Scientific American reported.

The researchers found that beta amyloid had a similar protective effect in roundworms, or nematodes, which usually die within two to three days after fungal infection.

Those worms with overexpression of amyloid beta continued to live five to six days after infection. Scientific American further reported that mice genetically engineered to overproduce human amyloid beta lived about twice as long as mice without the protein.