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A gene on chromosome 21q21.3 that encodes a cell surface receptor and transmembrane precursor protein which is cleaved by secretases to form various peptides.

Molecular pathology
APP mutations are implicated in autosomal dominant Alzheimer’s disease and cerebroarterial amyloidosis (cerebral amyloid angiopathy).


Amyloid beta peptide. It is the toxic peptide that causes damage to neurons in patients having Alzheimer disease.
References in periodicals archive ?
Amyloid beta plaque accumulated first in parts of the brain associated with smell, well before accumulating in areas associated with cognition and coordination.
The data from our pivotal Phase III and Phase IIB amyloid beta trials, currently ongoing in Europe, will potentially add much value to the research data base on Alzheimer's treatments.
In healthy people, levels of amyloid beta drop to their lowest point about six hours after sleep, and return to their highest point six hours after maximum wakefulness," said Randall Bateman, MD, associate professor of neurology.
Washington, June 21 (ANI): Scientists have shown a molecular chaperone is working like a waste management company to collect and detoxify high levels of toxic amyloid beta peptide found in Alzheimer's disease.
The ongoing Phase IIB clinical study is designed to evaluate Phenserine's ability to lower the levels of the beta-amyloid precursor protein ((beta)-APP) and Amyloid beta (A-(beta)) in the plasma and cerebrospinal fluid of mild-to-moderate AD patients.
PHILADELPHIA, July 20, 2015 /PRNewswire/ -- Treventis Corporation announced today that the Company's pre-clinical candidate TRV 101 has successfully demonstrated significant reduction in the toxic aggregates/ oligomers of both amyloid beta and tau protein in multiple transgenic mouse models of Alzheimer's Disease (AD).
Dravid, the research team developed an MRI (magnetic resonance imaging) probe that pairs a magnetic nanostructure (MNS) with an antibody that seeks out the amyloid beta brain toxins responsible for onset of the disease.
AZD3293 is an oral, potent and selective small molecule inhibitor of BACE that has been shown in Phase I studies to significantly and dose-dependently reduce levels of amyloid beta in the cerebro-spinal fluid of Alzheimer s patients and healthy volunteers.
In this case, OL-1 blocks the translation of RNA, which triggers a process that keeps excess amyloid beta protein from being produced.
For the latest study in the Proceedings of the National Academy of Sciences, researchers looked at how copper in the capillaries may cause a breakdown in the blood-brain barrier, leading to a build-up of the protein amyloid beta, or plaques that are a hallmark of Alzheimer's.
The study showed that copper accumulating in the brain disrupted the natural removal of toxic amyloid beta protein, which is strongly implicated in Alzheimer's.
It is expected that developing a new treatment for Alzheimer's disease which reduces amyloid beta will not only improve symptoms, but also help slow down the progression of the disease.