Contrary to what the scientific world has believed up until now, researchers at the Mount Sinai School of Medicine have deemed the Amyloid-Beta (Abeta) oligomers in the brain as the real culprits behind Alzheimer's disease, and not the Amyloid-Beta plaques as many believed.
"The buildup of amyloid plaques was described over 100 years ago and has received the bulk of the attention in Alzheimer's pathology. But there has been a longstanding debate over whether plaques are toxic, protective, or inert," said lead author Sam Gandy, Professor of Neurology and Psychiatry, and Associate Director of the Alzheimer's Disease Research Center, Mount Sinai School of Medicine.
Several research groups had previously proposed that rather than plaques, floating clumps of amyloid (called oligomers) are the key components that impede brain cell function in Alzheimer's patients.
To study this, the Mount Sinai team developed a mouse that forms only these oligomers, and never any plaques, throughout their lives.
The researchers found that the mice that never develop plaques were just as impaired by the disease as mice with both plaques and oligomers.
Moreover, when a gene that converted oligomers into plaques was added to the mice, the mice were no more impaired than they had been before.
"These findings may enable the development of neuroimaging agents and drugs that visualize or detoxify oligomers. New neuroimaging agents that could monitor changes in Abeta oligomer presence would be a major advance," said Dr. Gandy.
"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," Dr. Gandy added.
The study appears in the journal Annals of Neurology.