APP

(redirected from beta-amyloid peptide)
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Application

1. A formal request. Generally, one must fill out an application form as part of the application process.

2. See: Application Program.

APP

Shorthand for appreciation.
References in periodicals archive ?
Studies in AD transgenic mice show that the binding of beta-amyloid peptides to ABAD prevents the normal function of ABAD and leads to enhanced production of free radicals followed by increased apoptosis.
Hock and his team took an additional step by calculating the ratio of tau protein to beta-amyloid peptide and found that Alzheimer's patients averaged 147 times as much of the protein as the peptide, whereas healthy people averaged only 39 times as much.
In addition, unpublished work by this team suggests that apo E-IV leads to denser deposits of the beta-amyloid peptide implicated in Alzheimer's disease.
Like the beta-amyloid peptide, this 37-amino-acid particle, called amylin, aggregates; but instead of forming plaques in the brain, as beta-amyloid does, amylin accumulates near insulin-producing beta cells located in the pancreas.
Caprospinol binds to the Beta-Amyloid peptide, preventing its aggregation into more neurotoxic entities and entry into neurons, as well as protecting neuronal mitochondria from Beta-Amyloid induced damage, and maintaining neuronal cell energy levels.
Central to the development of Alzheimer's disease is beta-amyloid peptide, a substance normally produced in the brain but which in Alzheimer's is deposited abnormally.
The beta-amyloid peptide Ass-42 (the main component of amyloid plaques in AD patients) is the AD target that has received the most attention from drug developers, and drugs targeting amyloid are the disease-modifying therapies furthest along in development.
Excessive accumulation in the brain of the beta-amyloid peptide, due either to overproduction and/or decreased clearance and the formation of senile plaques, is one of the hallmarks of Alzheimer disease.
Elan has been at the forefront of Alzheimer's disease research for almost two decades, in particular in advancing the understanding of the beta-amyloid peptide - A-beta - that is the main building block of amyloid plaques, which are a hallmark of Alzheimer's disease neuropathology.
The first is active immunization with a segment of the beta-amyloid peptide, which triggers an immune response and the generation of antibodies, with the goal of reducing the level of beta-amyloid in the brain, and second, passive immunization (antibody administration) specific to the beta-amyloid peptide.
A family of molecular pumps found in cells throughout the body, ABC transporter substrates and associated diseases rank among the key prizes in the pharmaceutical industry: the beta-amyloid peptide which aggregates in the brain to cause Alzheimer's disease, all-trans retinal whose inefficient removal from the retina causes macular degeneration, and cholesterol which deposits in the vasculature to cause atherosclerosis.
Reiner, President & CEO stated, "Recent advances in understanding the role of the beta-amyloid peptide in Alzheimer's disease strongly validate the direction we took several years ago.