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

Calcium signaling, excitability, and synaptic plasticity defects in a mouse model of Alzheimer's disease.

Journal of Alzheimer's disease : JAD - 1 Jan 2015

Zhang Hua, Liu Jie, Sun Suya, Pchitskaya Ekaterina, Popugaeva Elena, Bezprozvanny Ilya

Abstract excerpt

Alzheimer's disease (AD) and aging result in impaired ability to store memories, but the cellular mechanisms responsible for these defects are poorly understood. Presenilin 1 (PS1) mutations are responsible for many early-onset familial AD (FAD) cases. The phenomenon of hippocampal long-term potentiation (LTP) is widely used in studies of memory formation and storage. Recent data revealed long-term LTP...

Read the complete abstract on PubMed

Topics

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

Share to Calcium Channel Blockers
Share to Calcium Signaling

Methodology Data sources Editorial policy Privacy About Contact Helena Bioinformatics

Share to Central Nervous System Stimulants

Share to Dendritic Spines

Share to Hippocampus

Share to Neuronal Plasticity

Share to Neurons

Share to Presenilin-1

Source

Open in PubMed Open full text

Identifiers

PMID: 25589721
DOI: 10.3233/JAD-142427
PMCID: PMC4814213

Provenance

PubMed metadata and Literature Corpus relationships. Corpus snapshot updated 7 Sept 2026. Manifest publication-graph-cohort-2026-09-08.1.

Source receipt: pubmed, retrieved 7 Sept 2026.

Related research

Semantic proximity does not establish scientific evidence.

Research trail→

Click a neighbor to travelStep 1 · 12 closest

Calcium signaling, excitability, and synaptic plasticity defects in a mouse model of Alzheimer's disease.PMID 25589721Read ↗

Reduced synaptic STIM2 expression and impaired store-operated calcium entry cause destabilization of mature spines in mutant presenilin mice.Semantic proximity Read ↗

Synaptic function of nicastrin in hippocampal neurons.Semantic proximity Read ↗

Intracellular Ca 2+ stores control in vivo neuronal hyperactivity in a mouse model of Alzheimer’s diseaseSemantic proximity Read ↗

Hippocampal synaptic plasticity in Alzheimer’s disease: what have we learned so far from transgenic models?Semantic proximity Read ↗

Presenilin-1 mutation impairs cholinergic modulation of synaptic plasticity and suppresses NMDA currents in hippocampus slices.Semantic proximity Read ↗

Dysregulation of Intracellular Calcium Signaling in Alzheimer's DiseaseSemantic proximity Read ↗

Reduction of increased calcineurin activity rescues impaired homeostatic synaptic plasticity in presenilin 1 M146V mutant.Semantic proximity Read ↗

Impaired neurotransmitter release in Alzheimer's and Parkinson's diseases.Semantic proximity Read ↗

Aberrant miR-339-5p/neuronatin signaling causes prodromal neuronal calcium dyshomeostasis in mutant presenilin miceSemantic proximity Read ↗

Restoration of Olfactory Memory in Drosophila Overexpressing Human Alzheimer’s Disease Associated Tau by Manipulation of L-Type Ca2+ ChannelsSemantic proximity Read ↗

Aβ/APP-induced hyperexcitability and dysregulation of homeostatic synaptic plasticity in models of Alzheimer’s diseaseSemantic proximity Read ↗

Mutant presenilins disturb neuronal calcium homeostasis in the brain of transgenic mice, decreasing the threshold for excitotoxicity and facilitating long-term potentiation.Semantic proximity Read ↗

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