Discover Community Create You

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

A familial Alzheimer's disease associated mutation in presenilin-1 mediates amyloid-beta independent cell specific neurodegeneration.

PloS one - 1 Jan 2024

Parvand Mahraz, Liang Joseph J H, Bozorgmehr Tahereh, Born Dawson, Luna Cortes Alvaro, Rankin Catharine H

Abstract excerpt

Mutations in the presenilin (PS) genes are a predominant cause of familial Alzheimer's disease (fAD). An ortholog of PS in the genetic model organism Caenorhabditis elegans (C. elegans) is sel-12. Mutations in the presenilin genes are commonly thought to lead to fAD by upregulating the expression of amyloid beta (Aβ), however this hypothesis has been challenged by recent evidence. As C. elegans lack amyloid beta...

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-Peptides

Methodology Data sources Editorial policy Privacy About Contact Helena Bioinformatics

Share to Animals, Genetically Modified

Share to Caenorhabditis elegans

Share to Caenorhabditis elegans Proteins

Share to Chemotaxis

Share to Presenilin-1

Share to Sensory Receptor Cells

Source

Open in PubMed Open full text

Identifiers

PMID: 39240956
DOI: 10.1371/journal.pone.0289435
PMCID: PMC11379242

Provenance

PubMed metadata and Literature Corpus relationships. Corpus snapshot updated 4 Sept 2026.

Related research

Semantic proximity does not establish scientific evidence.

Research trail→

Click a neighbor to travelStep 1 · 12 closest

A familial Alzheimer's disease associated mutation in presenilin-1 mediates amyloid-beta independent cell specific neurodegeneration.PMID 39240956Read ↗

A Familial Alzheimer’s Disease Associated Mutation in Presenilin-1 Mediates Amyloid-Beta Independent Cell Specific NeurodegenerationSemantic proximity Read ↗

Presenilin is required for proper morphology and function of neurons in C. elegans.Semantic proximity Read ↗

Levels of Amyloid Beta (Aβ) Expression in the Caenorhabditis elegans Neurons Influence the Onset and Severity of Neuronally Mediated Phenotypes.Semantic proximity Read ↗

Use of Caenorhabditis elegans as a model to study Alzheimer’s disease and other neurodegenerative diseasesSemantic proximity Read ↗

APL-1, a <i>Caenorhabditis elegans</i> protein related to the human β-amyloid precursor protein, is essential for viabilitySemantic proximity Read ↗

Behavioral phenotyping of a transgenic Caenorhabditis elegans expressing neuronal amyloid-beta.Semantic proximity Read ↗

The presenilin 1 C92S mutation increases abeta 42 production.Semantic proximity Read ↗

Reverse genetic analysis of Caenorhabditis elegans presenilins reveals redundant but unequal roles for sel-12 and hop-1 in Notch-pathway signaling.Semantic proximity Read ↗

Identification of presenilin mutations that have sufficient gamma-secretase proteolytic activity to mediate Notch signaling but disrupt organelle and neuronal healthSemantic proximity Read ↗

Human presenilin-1, but not familial Alzheimer's disease (FAD) mutants, facilitate Caenorhabditis elegans Notch signalling independently of proteolytic processing.Semantic proximity Read ↗

Loss of endogenous tau suppresses APOE4-induced patterned behavioral decline and axon dysmorphia in a model of Alzheimer's disease.Semantic proximity Read ↗

HOP-1, a Caenorhabditis elegans presenilin, appears to be functionally redundant with SEL-12 presenilin and to facilitate LIN-12 and GLP-1 signaling.Semantic proximity Read ↗

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