amyloid-beta peptide

amyloid-β peptide

major neurotoxic component of extracellular deposits found in patients with Alzheimer disease.
References in periodicals archive ?
2009) Amyloid seeds formed by cellular uptake, concentration, and aggregation of the amyloid-beta peptide.
ACU-193 selectively binds to and captures soluble oligomers of the amyloid-beta peptide.
Amyloid-beta peptide, particularly the 42-amino-acid peptide (Abeta(1-42)), is a principal component of senile plaques and is thought to be central to the pathogenesis of the disease.
The progression of Alzheimer's disease, the most common form of adult onset dementia worldwide, is marked by a rise in the body's level of amyloid-beta peptide.
This drug is a modulator of gamma-secretase, which is a protease that cleaves amyloid precursor protein to produce the amyloid-beta peptide that consists of amyloid plaques, a defining feature of Alzheimer's disease.
This drug is a modulator of gamma-secretase, a protease that cleaves amyloid precursor protein to produce the amyloid-beta peptide that consists of amyloid plaques, a defining feature of Alzheimer's disease.
Psychologists, immunologists, neurologists, genetics researchers, and others from the US and Europe discuss the effects of healthy aging on emotional memory and the neurocognitive changes that occur with Alzheimer's; amyloid-beta peptide mechanisms and antibodies for treatment; the need for a new paradigm of drug development; etiology; the role of chronic inflammation; and the role of gelsolin.
Current research suggests that an intermediate (Abeta protofibril) in the aggregation process of the amyloid-beta peptide (Abeta) initiates and drives the neurodegenerative process in Alzheimer's disease.
Intracellular amyloid-beta 1-42, but not extracellular soluble amyloid-beta peptide, induces neuronal apoptosis.
The drug works by hampering the activity of gamma secretase, an enzyme that cleaves a precursor compound to form amyloid-beta peptide.
Injecting the mice with the amyloid-beta peptide triggered an immune response which prevented new plaques forming and significantly slowed the progression of existing ones.
Rao said that ApoE4 favored the formation of the amyloid-beta peptide that is associated with the sticky plaques that are one of the hallmarks of the disease.