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.
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They also used mouse models of each disease to analyze the combined effects of high blood sugar and beta-amyloid protein in living animals.
Alzheimer's is marked by deposits of beta-amyloid protein in the brain, and knotty protein structures in the nerves called tau tangles.
Now, using new research techniques, scientists have shown that a two-molecule aggregate (or dimer) of beta-amyloid protein fragments may play a role in initiating the disease.
Today, the beta-amyloid protein is what most researchers believe is the cause of Alzheimer's disease.
Researchers used mice genetically engineered to accumulate waxy plaques of beta-amyloid protein in their brains, a symptom of Alzheimer's disease in people.
Besides the Company's Synuclere[TM] program, in late pre-clinical development for the treatment of Parkinson's disease, ProteoTech is developing Exebryl-1[R] for the treatment of diseases caused by beta-amyloid protein and tau protein aggregates and fibrils; and is in early human clinical studies with Systebryl[TM] for the treatment of Systemic AA Amyloidosis.
With Alzheimer's disease, for example, it's thought that an amino acid called lysine, part of the beta-amyloid protein believed to cause Alzheimer's, was the key to its transition from a regular component of every cell's normal biological function, to a toxin that kills brain cells and causes dementia.
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.
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.