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

Familial Alzheimer's disease mutations in amyloid precursor protein impair calcineurin signaling to NMDA receptors.

The Journal of biological chemistry - 1 Feb 2025

Tavalin Steven J

Abstract excerpt

Familial Alzheimer's disease (FAD) is frequently associated with mutations in the amyloid precursor protein (APP), which are thought to lead to cognitive deficits by impairing NMDA receptor (NMDAR)-dependent forms of synaptic plasticity. Given the reliance of synaptic plasticity on NMDAR-mediated Ca2+ entry, shaping of NMDAR activity by APP and/or its disease-causing variants could provide a basis for...

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
Share to Calcineurin

Methodology Data sources Editorial policy Privacy About Contact Helena Bioinformatics

Share to HEK293 Cells

Share to Mutation

Share to Neuronal Plasticity

Share to Receptors, N-Methyl-D-Aspartate

Share to Signal Transduction

Source

Open in PubMed Open full text

Identifiers

PMID: 39732167
DOI: 10.1016/j.jbc.2024.108147
PMCID: PMC11910330

Genes

APP
APLP1
APLP2

Provenance

PubMed metadata and Literature Corpus relationships. Corpus snapshot updated 6 Sept 2026.

Related research

Semantic proximity does not establish scientific evidence.

Research trail→

Click a neighbor to travelStep 1 · 12 closest

Familial Alzheimer's disease mutations in amyloid precursor protein impair calcineurin signaling to NMDA receptors.PMID 39732167Read ↗

Presenilins and APP in neuritic and synaptic plasticity: implications for the pathogenesis of Alzheimer's disease.Semantic proximity Read ↗

Calmodulin and Amyloid Beta as Coregulators of Critical Events during the Onset and Progression of Alzheimer’s DiseaseSemantic proximity Read ↗

Tau Protein Mediates APP Intracellular Domain (AICD)-Induced Alzheimer's-Like Pathological Features in Mice.Semantic proximity Read ↗

Amyloidogenic proteolysis of APP regulates glutamatergic presynaptic functionSemantic proximity Read ↗

Presenilins function in ER calcium leak and Alzheimer's disease pathogenesis.Semantic proximity Read ↗

The amyloid precursor family of proteins in excitatory neurons are essential for regulating cortico-hippocampal circuit dynamics in vivoSemantic proximity Read ↗

Tau phosphorylation and tau mislocalization mediate soluble Aβ oligomer-induced AMPA glutamate receptor signaling deficits.Semantic proximity Read ↗

The dysregulation of intracellular calcium in Alzheimer disease.Semantic proximity Read ↗

Cellular functions of the amyloid precursor protein from development to dementia.Semantic proximity Read ↗

Alzheimer's disease: a dysfunction of the amyloid precursor protein(1).Semantic proximity Read ↗

The pathological hallmarks of Alzheimer’s disease derive from compensatory responses to NMDA receptor insufficiencySemantic proximity Read ↗

Presenilins as endoplasmic reticulum calcium leak channels and Alzheimer's disease pathogenesis.Semantic proximity Read ↗

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