Article

Aβ43 levels determine the onset of pathological amyloid deposition

2022-12-12

Abstract excerpt

<title>Abstract</title> <p>Background While most Alzheimer’s disease cases are sporadic with late onset (LOAD), ~ 2% of cases are inherited, have an early onset, and are caused by mutations in <italic>Presenilin</italic>s <italic>(PSEN1/2)</italic> or <italic>Amyloid-β Precursor Protein (APP</italic>) genes (familial AD, FAD). PSEN1/2 are the catalytic component of γ-secretase, a protease that generates Aβ pepti...

Topics

Open a Topic to create a Post that cites this publication.

Identifiers and source

Literature Corpus work: f2d488ad-910b-5710-845f-ab7945bc864a
DOI: 10.21203/rs.3.rs-2272441/v1

Open publication

Related research

Semantic proximity does not establish scientific evidence.

Click a neighbor to travelStep 1 · 12 closest

Aβ43 levels determine the onset of pathological amyloid depositionDOI 10.21203/rs.3.rs-2272441/v1Read

Aβ43 levels determine the onset of pathological amyloid deposition.Semantic proximity Read

Aβ profiles generated by Alzheimer's disease causing PSEN1 variants determine the pathogenicity of the mutation and predict age at disease onset.Semantic proximity Read

Knock-in rats with homozygous PSEN1 Alzheimer mutation are viable and show selective γ-secretase activity loss causing low Aβ40/42 and high Aβ43Semantic proximity Read

A Transgenic Alzheimer Rat with Plaques, Tau Pathology, Behavioral Impairment, Oligomeric Aβ, and Frank Neuronal LossSemantic proximity Read

Opposite changes in APP processing and human Aβ levels in rats carrying either a protective or a pathogenic APP mutation.Semantic proximity Read

Molecular consequences of amyloid precursor protein and presenilin mutations causing autosomal-dominant Alzheimer's diseaseSemantic proximity Read

An App knock-in rat model for Alzheimer’s disease exhibiting Aβ and tau pathologies, neuronal death and cognitive impairmentsSemantic proximity Read

Novel aspects of accumulation dynamics and A beta composition in transgenic models of AD.Semantic proximity Read

New <i>App</i> knock-in mice that accumulate wild-type human Aβ as rapidly as <i> App <sup>NL-G-F</sup> </i> mice exhibit intensive cored plaque pathology and neuroinflammationSemantic proximity Read

A third-generation mouse model of Alzheimer's disease shows early and increased cored plaque pathology composed of wild-type human amyloid β peptide.Semantic proximity Read

Deposition of C-terminally truncated Aβ species Aβ37 and Aβ39 in Alzheimer's disease and transgenic mouse models.Semantic proximity Read

Intraneuronal beta-amyloid aggregates, neurodegeneration, and neuron loss in transgenic mice with five familial Alzheimer's disease mutations: potential factors in amyloid plaque formation.Semantic proximity Read