Jove
Visualize
Contact Us
JoVE
x logofacebook logolinkedin logoyoutube logo
ABOUT JoVE
OverviewLeadershipBlogJoVE Help Center
AUTHORS
Publishing ProcessEditorial BoardScope & PoliciesPeer ReviewFAQSubmit
LIBRARIANS
TestimonialsSubscriptionsAccessResourcesLibrary Advisory BoardFAQ
RESEARCH
JoVE JournalMethods CollectionsJoVE Encyclopedia of ExperimentsArchive
EDUCATION
JoVE CoreJoVE BusinessJoVE Science EducationJoVE Lab ManualFaculty Resource CenterFaculty Site
Terms & Conditions of Use
Privacy Policy
Policies

Related Experiment Videos

Presenilin-mediated signal transduction.

Richard F Cowburn1, Bogdan O Popescu, Maria Ankarcrona

  • 1Karolinska Institutet, Department of Neurobiology, Care Sciences and Society, KI-Alzheimer's Disease Research Center, Novum, plan 5, S-141 57 Huddinge, Sweden. richard.cowburn@astrazeneca.com

Physiology & Behavior
|June 15, 2007
PubMed
Summary
This summary is machine-generated.

Related Concept Videos

You might also read

Related Articles

Articles linked to this work by shared authors, journal, and citation graph.

Sort by
Same author

Cognition at the core of metabolic syndrome: linking metabolic load to behavioural impairment in a longitudinal high-fat diet rat model.

Brain, behavior, & immunity - health·2026
Same author

Mitochondria serve as a holdout compartment for aggregation-prone proteins hindering efficient degradation.

Nature communications·2026
Same author

Integrating simulated and experimental data to identify mitochondrial bioenergetic defects in Parkinson's Disease models.

PloS one·2026
Same author

Pharmacogenetics in advanced Parkinson's disease.

Journal of neural transmission (Vienna, Austria : 1996)·2025
Same author

Bioenergetics and lipid metabolism in Alzheimer's disease: From cell biology to systemic health.

Journal of internal medicine·2025
Same author

GRK-biased adrenergic agonists for the treatment of type 2 diabetes and obesity.

Cell·2025

Presenilin proteins influence Alzheimer's disease by altering calcium signaling pathways. Mutations disrupt calcium release and entry, impacting cell function and disease progression.

Area of Science:

  • Neuroscience
  • Cell Biology
  • Biochemistry

Background:

  • Presenilin proteins are implicated in early-onset familial Alzheimer's disease.
  • Mutated presenilins affect cell signal transduction, particularly intracellular calcium signaling.
  • Previous research focused on endoplasmic reticulum calcium release and capacitative calcium entry.

Purpose of the Study:

  • To review how presenilins modulate intracellular calcium signaling.
  • To explore the role of deregulated calcium homeostasis in Alzheimer's disease pathogenesis.
  • To highlight a novel function of presenilins in regulating phospholipase C activity.

Main Methods:

  • Literature review of presenilin function in calcium signaling.
  • Analysis of mechanisms involving inositol(1,4,5)trisphosphate (InsP3) mediated calcium release.

Related Experiment Videos

  • Investigation of presenilin regulation of acetylcholine muscarinic receptor-stimulated phospholipase C.
  • Main Results:

    • Presenilin mutations can potentiate InsP3-mediated calcium release from the endoplasmic reticulum.
    • Mutations may also attenuate capacitative calcium entry.
    • Presenilins regulate phospholipase C activity upstream of InsP3-mediated calcium release.

    Conclusions:

    • Presenilins play a critical role in modulating intracellular calcium homeostasis.
    • Dysregulation of calcium signaling by presenilins is a potential contributor to Alzheimer's disease.
    • Further research into presenilin-mediated calcium signaling is crucial for understanding Alzheimer's disease.