β-Amyloid FragmentsPharmaceutical InformationUpdated on May 30, 2019 View more like this | Visit SHIRLEY, NY | Contact Cathy Miller |
Beta-amyloid and the amyloid hypothesis
In Alzheimer’s disease, brain cells that process, store and retrieve information degenerate and die. Although scientists do not yet know the underlying cause of this destruction, they have identified several possible culprits.
One prime suspect is a microscopic brain protein fragment called beta-amyloid, a sticky compound that accumulates in the brain, disrupting communication between brain cells and eventually killing them. Some researchers believe that flaws in the processes governing production, accumulation or disposal of beta-amyloid are the primary cause of Alzheimer’s. This theory is called “the amyloid hypothesis.”
Although early studies suggested that amyloid plaques — large accumulations of beta-amyloid — were the cause of nerve cell toxicity in Alzheimer’s, researchers now believe that small, soluble aggregates of beta-amyloid may be more toxic.
In Alzheimer’s disease, brain cells that process, store and retrieve information degenerate and die. Although scientists do not yet know the underlying cause of this destruction, they have identified several possible culprits.
One prime suspect is a microscopic brain protein fragment called beta-amyloid, a sticky compound that accumulates in the brain, disrupting communication between brain cells and eventually killing them. Some researchers believe that flaws in the processes governing production, accumulation or disposal of beta-amyloid are the primary cause of Alzheimer’s. This theory is called “the amyloid hypothesis.”
Although early studies suggested that amyloid plaques — large accumulations of beta-amyloid — were the cause of nerve cell toxicity in Alzheimer’s, researchers now believe that small, soluble aggregates of beta-amyloid may be more toxic.
