amyloid beta protein

amyloid beta protein

[¦am·ə‚lȯid ¦bād·ə ′prō‚tēn]
(biochemistry)
A 42-amino-acid proteolytic product of the amyloid precursor protein that accumulates in the brains (frontal cortex and hippocampus) of persons with Alzheimer's disease.
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References in periodicals archive ?
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.
The Pitt researchers postulate that the drug works through a different biological process, perhaps by reducing soluble oligomers which, like the plaques, are composed of the toxic amyloid beta protein fragments.
In this case, OL-1 blocks the translation of RNA, which triggers a process that keeps excess amyloid beta protein from being produced.
This research stemmed from a previous cell culture study that highlighted the protective effects of walnut extract against the oxidative damage caused by amyloid beta protein.
New Data from Phase 1b Study of Aducanumab (Biogen) in Prodromal or Mild Alzheimer's Aducanumab (BIIB037) is a monoclonal antibody targeting aggregated forms of amyloid beta protein -- a hallmark of Alzheimer's disease progression is the accumulation of beta amyloid in the brain.
the amyloid beta protein thought to be present only in amyloid plaques was
Large sticky plaques of amyloid beta protein are a hallmark of Alzheimer's, which causes memory loss, confusion, the inability to care for oneself and eventually death.
Among the topics discussed are the amyloid beta protein cascade hypothesis, mechanisms of toxicity of these proteins, the possible role of prions, tau (protein)-based therapies, animal models of AD after repetitive brain trauma, imaging biomarkers, and suggestions for improving assessment of function and clinical trials.
The drug had no effect on an Alzheimer's hallmark - the build up of amyloid beta protein in the brain.
Major Finding: Non-plaque forming fragments of the amyloid beta protein, once thought to be non-neurotoxic, may be more dangerous to the brain than the full-length, plaque-forming amyloid.
These questions are important and timely as a number of approaches for reducing brain amyloid beta protein levels are currently being tested, including antibodies that might bind to and promote the clearance of amyloid beta protein as well as drugs that inhibit amyloid beta protein synthesis.
GSMs reduce the production of long pieces of amyloid beta protein (Abeta) that stick together and for mclumps in the brain.