neurolove:

Infection Defense May Spur Alzheimer’s

The new hypothesis got its start late one Friday evening in the summer of 2007 in a laboratory at Harvard Medical School. The lead researcher, Rudolph E. Tanzi, a neurology professor who is also director of the genetics and aging unit at Massachusetts General Hospital, said he had been looking at a list of genes that seemed to be associated with Alzheimer’s disease.

To his surprise, many looked just like genes associated with the so-called innate immune system, a set of proteins the body uses to fight infections. The system is particularly important in the brain, because antibodies cannot get through the blood-brain barrier, the membrane that protects the brain. When the brain is infected, it relies on the innate immune system to protect it.

For more information about amyloid beta and Alzheimer’s, go to my post here.  If this is true (that amyloid beta is a defense mechanism and not part of the problem), it would really change the way we study and try to treat Alzheimer’s.  There was a “vaccine” against amyloid beta plaques that would have been the vaccine against Alzheimer’s, but in clinical trials, it did not significantly help those that received it in the early stages as far as cognitive decline or time to death went.  If these researchers are right about their new theory, that could help explain why.