Researchers at Mount Sinai School of Medicine say Alzheimer's pathology originates in amyloid-beta oligomers in the brain, rather than the amyloid plaques previously thought by many researchers to cause the disease."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 lonstanding debate over whether plaques are toxic, protective or inert," lead author Dr. Sam Gandy says in a news release. A professor of neurology and psychiatry, he serves as Associate Director of the Alzheimer's Disease Research Center at Mount Sinai.
The study, paid for by the "Oligomer Research Consortium" of the Cure Alzheimer Fund and a MERIT Award from the Veterans Administration, appears in the journal Annals of Neurology.
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.
"These findings may enable the development of neuroimaging agents and drugs that visualize or detoxify oligomers," Gandy says. That could lead to breakthroughs in managing, slowing, stopping--or even preventing Alzheimer's.
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