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

2. See: Application Program.


Shorthand for appreciation.
References in periodicals archive ?
While resulting plaques occupy prime real estate in the brain, it's still better than toxic Abeta killing neurons, Cashikar said.
It could very well be that releasing Abeta is good, and that's why drugs that lower it are ineffective, or even damaging," Dr.
They found an increased level of Abeta in SorCS1-deficient mice, and low levels of Abeta in the cells overexpressing SorCS1.
Mechanism of action of PBT2 in AD PBT2 prevents formation and toxicity of pathological ABeta species (primarily soluble oligomers) and promotes their clearance.
When Abeta is released, it can form plaque, a contributing factor in AD.
Small molecule drugs that directly target the binding and pathogenic signaling of soluble oligomers of the Abeta protein represent a potentially important clinical tool to address both the symptoms and disease progression in patients diagnosed with Alzheimer's disease," said Dr.
Pasinetti said his findings supported the conclusion that "NIC5-15 is a safe and tolerable natural compound that may alleviate Alzheimer's disease dementia through multiple mechanisms including Abeta lowering activities.
1], we looked at levels of unaggregated soluble Abeta peptides in spinal fluid, and they were significantly reduced with PBT2 treatment.
Lycopene may prevent Alzheimer's by inhibiting formation of oxidant-producing Abeta proteins.
Louis, Missouri, observed during tehs tudy that these Abeta dynamics rely on the hormone orexin, and that forcing animals to sleep or stay awake decreases or increases Abeta plaque formation accordingly in a mouse model for Alzheimer disease.
Though this long-term follow-up data is limited and must be assessed cautiously, we believe that the data support the hypothesis that ABeta immunotherapy has the potential for long-term functional benefits.
They found that elevated ABeta leads to widespread activation of calcium-dependent signaling molecules that contribute to neuronal degeneration.