We had reported sometime back that brain plaques could explain higher risk of Alzheimer’s disease. By means of a mouse model of Alzheimer’s disease, scientists at Mount Sinai School of Medicine have discovered that Alzheimer’s pathology seemingly originates in Amyloid-Beta (Abeta) oligomers in the brain as opposed to the amyloid plaques formerly believed by several researchers to cause the disease.
Numerous research groups had formerly suggested that rather than plaques, floating clumps of amyloid known as oligomers appear to be the vital components that slow down brain cell role in Alzheimer’s patients. To examine this, the Mount Sinai team crafted a mouse that is said to form only these oligomers, and never any plaques, all through their lives.
“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,” commented, Lead author Sam Gandy, MD, PhD, Professor of Neurology and Psychiatry, and Associate Director of the Alzheimer’s Disease Research Center, Mount Sinai School of Medicine.
The study authors discovered that the mice that seemingly never develop plaques were just as damaged by the disease as mice with both plaques and oligomers. Furthermore, when a gene that transformed oligomers into plaques was apparently added to the mice, the mice were no more injured than they had been before.
Dr. Gandy remarked, “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. 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.”
The researcher mentioned that 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.
The research was published in the journal Annals of Neurology.