Mount Sinai Medical Makes Important Finding In Alzheimer's Disease Causation

Researchers at the Mount Sinai School of Medicine have discovered that the real culprit in Alzheimer's disease is the Amyloid-Beta (Abeta) oligomers in the brain, and not the Amyloid-Beta plaques as many believed.  Though this is not the first finding that supports Abeta oligomers as the cause of Alzheimer's, the Mount Sinai results are hard to dispute because of the methodology used.

Beta-ameloid oligomers: Health & Human Services via Kleinlab.org

Abeta oligomers are protein clumps in the brain (see above image) that have been identified as toxic in previous studies.  But Sam Gandy, MD, PhD, Professor of Neurology and Psychiatry, and Associate Director of the Alzheimer's Disease Research Center, Mount Sinai School of Medicine said there had been a longstanding debate among researchers over whether the Beta-amyloid plaques are toxic, protective, or inert.  That is why we often read of the plaques as being causative of Alzheimer's. 

The approach that Gandy's team took was to develop mice that form only the oligomers, never the plaques, throughout their lives. Once accomplished, the researchers compared the mice to those with plaques and oligomers and found that both groups of mice were equally impaired.  Then, working with the oligomer mice, the researchers converted the oligomers to plaques, and the mice had no impairments.

"These findings may enable the development of neuroimaging agents and drugs that visualize or detoxify oligomers," said Dr. Gandy. "New neuroimaging agents that could monitor changes in Abeta oligomer presence would be a major advance. Innovative neuroimaging agents that will allow visualization of brain oligomer accumulation, in tandem with careful clinical observations, could lead to breakthroughs in managing, slowing, stopping or even preventing Alzheimer's.

"This is especially important in light of research reported in March showing that 70 weeks of infusion of the Abeta immunotherapeutic Bapineuzumab® cleared away 25 percent of the Abeta plaque, yet no clinical benefit was evident."

via press release