beta-amyloid protein


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beta-amyloid protein (BAP),

n a protein found in excess in the brains of Alzheimer's disease sufferers; aggregates into dense plaques on the exterior of brain cells, which in turn destroy the synapses and conduction of nerve impulses.
References in periodicals archive ?
The other type of investigational drug is called a beta-amyloid antibody, which targets the removal of the beta-amyloid protein.
As the aggregation of the beta-amyloid protein in the brain is also a key target for new therapeutic treatments under development, 18F-Florbetaben might also be able to support the development of these new treatment approaches.
A traditional vaccine -- an injection of beta-amyloid protein itself into the arm -- has been shown in other research to trigger an immune response, including the production of antibodies and other bodily defenses against beta-amyloid.
It decreases the amount of plaque-forming beta-amyloid protein by changing the point at which gamma secretase cleaves the amyloid precursor protein.
New agents called luminescent conjugated oligothiophenes (LCOs) are beginning to reveal to scientists how APOE status affects the way in which beta-amyloid protein aggregates in the brain of Alzheimer's patients.
Like other experimental vaccines, AN-1792 targeted the destructive beta-amyloid protein that typically accumulates in the brains of Alzheimer's patients.
Deposits of beta-amyloid protein, called plaques, build up in the brains of sufferers and destroy neuro ne s.
The idea was to create a peptide that would "interrupt or change the assembly of beta-amyloid protein," says Hammer.
Alzheimer's disease is characterized by the brain accumulation of aggregates and insoluble fibrillar deposits that contain a specific protein known as the beta-amyloid protein.
Most neuroscientists believe AD is caused by the accumulating assemblies of beta-amyloid protein triggering a sequence of events that leads to impaired cell function and death.
In the hypothetical model of Alzheimer's progression over time, now refined with several years of clinical evidence, biological markers of changes in beta-amyloid protein become abnormal first, then biomarkers of the degeneration and death of brain cells, followed by dementia symptoms.
Exebryl-1(R) has been shown to inhibit beta-amyloid protein aggregate formation in brain, as well as disaggregate amyloid plaques that are already present.