Sentences with phrase «of amyloid precursor protein»

Amyloid beta (Aβ) is a small peptide molecule generated from cleavage of amyloid precursor protein (APP).

That's because the boosted mice produced normal — rather than high — levels of the amyloid precursor proteins from which plaques are made.

Previously, researchers have shown that treating cells with neuregulin - 1, for example, dampens levels of amyloid precursor protein, a molecule that generates amyloid beta, which aggregate and form plaques in the brains of Alzheimer's patients.

Abstract: Overexpression of the amyloid precursor protein (APP) gene on chromosome 21 in Down syndrome (DS) has been linked to increased brain amyloid levels and early - onset Alzheimer's disease (AD).

Role of amyloid precursor protein (APP) in brain development and implications for Down syndrome

Increasing evidence suggests that the synaptic functions of the amyloid precursor protein (APP), that is key to Alzheimer (AD) pathogenesis, may be carried out by its secreted ectodomain.

These studies revealed that loss of NEU1 activity was associated with a build - up in lysosomes of the amyloid precursor protein (APP), which they identified as a natural target of the enzyme.

The production of neurotoxic Aβ peptide results from the specific proteolytic processing of the amyloid precursor protein (APP).

Suh was involved in the identification of novel mutations from late - onset AD families in the prodomain of ADAM10, a major a-secretase that cleaves B - amyloid (AB region of amyloid precursor protein (APP).

Beta amyloid plaques can form when particular fragments of the amyloid precursor protein (APP), cleaved by the enzyme gamma secretase, clump together.

One hypothesis is that as a regulator of Amyloid Precursor Protein (APP), a gene that may be partly responsible for inducing Alzheimer's, TSH levels may have a direct impact on the prevalence of Alzheimer's.

Exploiting this compartmentalization, the team developed an endosomally - targeted β - secretase inhibitor that specifically blocked cleavage of amyloid precursor protein but not non-amyloid proteins.

Overexpression of the amyloid precursor protein (APP) gene on chromosome 21 in Down syndrome (DS) has been linked to increased brain amyloid levels and early - onset Alzheimer's disease (AD).

Specifically, that aggregates of A-beta peptides, which are formed following cleavage of the Amyloid Precursor Protein (APP), instigate a series of events that leads to neurodegeneration and, eventually, AD.

Our microscopy studies with quantitative co-localization analysis revealed the presence of intraneuronal Aβ in transgenic rats, with an immunological signal that was clearly distinguished from that of the amyloid precursor protein (APP) and its C - terminal fragments (CTFs).