Loading publication...

Noodle always counts identifier-free feature events for service operation. With your permission, Google Analytics can also estimate audience and engagement. Search text, publication identifiers, cookies, IP addresses and browser fingerprints are never included in Noodle's first-party event counters.

Privacy details

Article

Genetic determinants of white matter hyperintensities and amyloid angiopathy in familial Alzheimer's disease.

Neurobiology of aging - 1 Dec 2015

Ryan Natalie S, Biessels Geert-Jan, Kim Lois, Nicholas Jennifer M, Barber Philip A, Walsh Phoebe, Gami Priya, Morris Huw R, Bastos-Leite António J, Schott Jonathan M, Beck Jon, Mead Simon, Chavez-Gutierrez Lucia, de Strooper Bart, Rossor Martin N, Revesz Tamas, Lashley Tammaryn, Fox Nick C

Abstract excerpt

Familial Alzheimer's disease (FAD) treatment trials raise interest in the variable occurrence of cerebral amyloid angiopathy (CAA); an emerging important factor in amyloid-modifying therapy. Previous pathological studies reported particularly severe CAA with postcodon 200 PSEN1 mutations and amyloid beta coding domain APP mutations. As CAA may manifest as white matter hyperintensities (WMH) on magnetic resonance...

Read the complete abstract on PubMed

Topics

Share this publication in a Topic to start or enrich a Post.

Share to Alzheimer Disease
Share to Amyloid beta-Protein Precursor

Methodology Data sources Editorial policy Privacy About Contact Helena Bioinformatics

Share to Apolipoproteins E

Share to Cerebral Amyloid Angiopathy

Share to Magnetic Resonance Imaging

Share to Presenilin-1

Share to White Matter

Source

Identifiers

PMID: 26410308
DOI: 10.1016/j.neurobiolaging.2015.08.026

Genes

PSEN1
APP

Variants

Provenance

PubMed metadata and Literature Corpus relationships. Corpus snapshot updated 2 Sept 2026.

Related research

Semantic proximity does not establish scientific evidence.

Research trail→

Click a neighbor to travelStep 1 · 12 closest

Genetic determinants of white matter hyperintensities and amyloid angiopathy in familial Alzheimer's disease.PMID 26410308Read ↗

White matter hyperintensities are a core feature of Alzheimer's disease: Evidence from the dominantly inherited Alzheimer network.Semantic proximity Read ↗

Variability in the type and layer distribution of cortical Aβ pathology in familial Alzheimer's disease.Semantic proximity Read ↗

Presenile Alzheimer dementia characterized by amyloid angiopathy and large amyloid core type senile plaques in the APP 692Ala-->Gly mutation.Semantic proximity Read ↗

White matter hyperintensities and patterns of atrophy in early onset Alzheimer's disease with causative gene mutations.Semantic proximity Read ↗

White matter hyperintensities and the mediating role of cerebral amyloid angiopathy in dominantly-inherited Alzheimer's disease.Semantic proximity Read ↗

Presenilin-1 mutation position influences amyloidosis, small vessel disease, and dementia with disease stage.Semantic proximity Read ↗

Prominent amyloid plaque pathology and cerebral amyloid angiopathy in APP V717I (London) carrier - phenotypic variability in autosomal dominant Alzheimer's disease.Semantic proximity Read ↗

An APP mutation family exhibiting white matter hyperintensities and cortical calcification in East China.Semantic proximity Read ↗

Hereditary cerebral amyloid angiopathy, Piedmont-type mutationSemantic proximity Read ↗

Amyloid angiopathy in a Volga German family with Alzheimer's disease and a presenilin-2 mutation (N141I).Semantic proximity Read ↗

Understanding the roles of mutations in the amyloid precursor protein in Alzheimer disease.Semantic proximity Read ↗

Senile dementia associated with amyloid beta protein angiopathy and tau perivascular pathology but not neuritic plaques in patients homozygous for the APOE-epsilon4 allele.Semantic proximity Read ↗

⌁Select a neighboring publication to make it the new centre.