A team of researchers at Harvard Medical School have just come up with a new hypothesis that could have major implications for preventing and treating Alzheimer’s disease. The study was published yesterday in the AAAS journal, Science Translational Medicine.
The research looks at a specific protein called amyloid-β peptide (Aβ) that is considered a key player in Alzheimer’s disease and originally thought to cause neuronal death. However, the new study suggests that the Aβ protein acts as a natural antibiotic to prevent bacteria from getting into the brain and that the remnants of this defense lead to the development of Alzheimer’s.
Shortly after the Harvard research was published, the New York Times published an article featuring members of the investigating team and Dana Alliance members who specialize in neurodegenerative disorders: Rudolph Tanzi, Ph.D.; Berislav Zlokovic, M.D., Ph.D.; and David Holtzman, M.D.
So far, the group has confirmed this hypothesis in neurons growing in petri dishes as well as in yeast, roundworms, fruit flies, and mice. There is much more work to be done to determine if a similar sequence happens in humans, but plans—and funding—are in place to start those studies, involving a multicenter project that will examine human brains.
The idea about this function of amyloid proteins started with Robert D. Moir, Ph.D., whose research focuses specifically on Alzheimer’s disease. Moir and Tanzi soon began collaborating on a study funded by the National Institutes of Health and the Cure Alzheimer’s Fund. But the new hypothesis is just that, a hypothesis; so there is still a long road of research that lies ahead.
Researchers will soon begin to look for microbes in plaques found in human brains, which Tanzi says is a big second step. “First, we need to ask whether there are microbes that may sneak into the brain as we age and trigger amyloid deposition. Then we can aim at stopping them,” he told the Times.
For more information on this study, read the full article by the New York Times.