Abeta


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APP

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).

Abeta

Amyloid beta peptide. It is the toxic peptide that causes damage to neurons in patients having Alzheimer disease.
References in periodicals archive ?
By inhibiting BACE, a key enzyme in the production of Abeta peptides, elenbecestat reduces Abeta production, and by reducing amyloid plaque formations in the brain, exerts disease modifying effects of potentially slowing the progression of AD.
Nilsson et al., "Cell surface expression of the major amyloid-beta peptide (Abeta)-degrading enzyme, neprilysin, depends on phosphorylation by mitogen-activated protein kinase/extracellular signal-regulated kinase kinase (MEK) and dephosphorylation by protein phosphatase 1a," The Journal of Biological Chemistry, vol.
Increased amount of APP might lead to heightened levels of Abeta generation, whereas lower levels of APP could also bear certain risks, such as impaired muscular function and spatial working memory (Senechal et al.
Preclinical results show die treatment reduces the amount of plaque as much as the best drug candidates to manage Abeta amyloidosis, the company said, and did not lead to side effects.
Preclinical results show the treatment reduces the amount of plaque as much as the best drug candidates to manage Abeta amyloidosis, the company said, and did not lead to side effects.
Alpha motor neurons are responsible for conducting motor impulses at 70 to 120 m/s and Abeta or A-alpha fibers with a similar conduction speed are used in the afferent pathway of vibration sense and proprioception.
[30.] Benilova I, Karran E, De Strooper B (2012) The toxic Abeta oligomer and Alzheimer's disease: an emperor in need of clothes.
Presenilin-1 280Glu-->Ala mutation alters C-terminal APP processing yielding longer abeta peptides: implications for Alzheimer's disease.
The problem with older mouse models is that they overexpress a protein called amyloid precursor protein, or APP, which gives rise to the amyloid-beta (Abeta) peptides that accumulate in the brain, eventually leading to the neurodegeneration that characterizes Alzheimer's disease.
The mice showed early accumulation of Abeta peptides, and importantly, were found to undergo cognitive dysfunction similar to the progression of AD seen in human patients.
Neither bapineuzumab, which targets soluble and aggregated amyloid-beta (Abeta), nor solanezumab, which targets soluble Abeta, achieved the primary endpoints in their overall cohorts, investigators wrote.
Solanezum-ab increased Abeta in plasma and CSF, a sign that the protein had stopped clumping in the brain.