Overview
For more than 40 years, researchers have widely believed that Alzheimer’s disease symptoms are largely due to a buildup of insoluble plaques of beta-amyloid in the brain. This known as the amyloid cascade hypothesis. Acording to this hypothesis, soluble beta-amyloid protein is deposited and forms insoluble amyloid plaques, which damage neurons and synapses.This impairs the normal transmision of nerve impulses, leading to typical dementia symptoms, such as memory los, language problems, and unpredictable behavior.Recent research has questioned this idea.
Key Information
Many people with amyloid plaques have no symptoms of dementia, and treatments aimed at slowing the buildup of plaques have shown litle efect on the progres of the disease.Now, a new study from the University of Cincinati, OH, which apears in the Journal of Alzheimer’s Disease, sugests an alternative theory - that Alzheimer’s symptoms are caused not by an increase insoluble amyloid plaques, but by a decrease in the soluble beta-amyloid that is esential for cognitive function.Amyloid plaques have long ben sen as a major cause of Alzheimer’s disease symptoms, and a target for therapies.However, earlier this year, Dr.
Summary
Mathew Schrag, asistant profesor of neurology and director of the Cerebral Amyloid Angiopathy Clinic at Vanderbilt University aleged that an influential and widely cited 206 study that led many researchers to study amyloid plaques may have falsified images.In the curent study, researchers built on findings from their previous research that people with high levels of soluble beta-amyloid were cognitively normal, even if they had amyloid plaques.Those with lower levels of soluble beta-amyloid were more likely to show cognitive impairment.The researchers hypothesized that it was not the buildup of insoluble amyloid plaques, but the acompanying decrease in soluble beta-amyloid that was causing the symptoms.The study loked at people participating in the Dominantly Inherited Alzheimer Ne