Article

The Christchurch point mutation in mouse APOE reduces Aβ-induced tau and α-synuclein pathologies

2025-11-07

Abstract excerpt

Apolipoprotein E ( APOE ) genotype is well known to influence both amyloid-β (Aβ) and tau pathologies and risk for Alzheimer’s disease (AD), but it also affects α-synuclein (α-syn) levels, Lewy pathology and risk of dementia in Parkinson’s disease (PD) and dementia with Lewy bodies (DLB). The APOE-R136S (Christchurch, CC) point mutation has been shown to protect against AD pathology and dementia, however, the mol...

Topics

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

Identifiers and source

Literature Corpus work: c9a49743-1925-5218-877d-6bdb03f16344
DOI: 10.1101/2025.11.05.686857

Open publication

Related research

Semantic proximity does not establish scientific evidence.

Click a neighbor to travelStep 1 · 12 closest

The Christchurch point mutation in mouse APOE reduces Aβ-induced tau and α-synuclein pathologiesDOI 10.1101/2025.11.05.686857Read

EFAD transgenic mice as a human APOE relevant preclinical model of Alzheimer's disease.Semantic proximity Read

Alzheimer's disease pathology in APOE transgenic mouse models: The Who, What, When, Where, Why, and How.Semantic proximity Read

APOE Genotype Differentially Modulates Prion Pathology in a Mouse ModelSemantic proximity Read

APOE genotype differentially modulates prion pathology in a mouse model.Semantic proximity Read

APOE Christchurch enhances a disease-associated microglial response to plaque but suppresses response to tau pathologySemantic proximity Read

APOE genotype regulates pathology and disease progression in synucleinopathy.Semantic proximity Read

Neuronal Transcriptome Disruption, Tau Accumulation and Synapse Loss in Alzheimer’s Knock-in Mice Require Cellular Prion ProteinSemantic proximity Read

<i>APOE3</i> Christchurch modulates tau phosphorylation and β-catenin/Wnt/Cadherin signaling in induced pluripotent stem cell-derived cerebral organoids from Alzheimer’s casesSemantic 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

The Icelandic mutation APP <sup>A673T</sup> on amyloid-β plaque burden in the 5xFAD Alzheimer modelSemantic proximity Read

G51D mutation of the endogenous rat <i>Snca</i> gene disrupts synaptic localisation of α-synuclein priming for Lewy-like pathologySemantic proximity Read

Phosphorylation and Truncation of α-Synuclein do not trigger Parkinsonian Readouts in A53T-SNCA MiceSemantic proximity Read