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

Physiological roles for amyloid beta peptides.

Hugh A Pearson1, Chris Peers

  • 1Faculty of Biological Sciences, University of Leeds, Leeds LS2 9JT, UK. h.a.pearson@leeds.ac.uk

The Journal of Physiology
|July 1, 2006
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

The thienopyridine A-769662 and benzimidazole 991 inhibit human TASK-3 potassium channels in an AMPK-independent manner.

Biochemical pharmacology·2024
Same author

Inhibition of the voltage-gated potassium channel Kv1.5 by hydrogen sulfide attenuates remodeling through S-nitrosylation-mediated signaling.

Communications biology·2023
Same author

Publisher Correction: LKB1 is the gatekeeper of carotid body chemosensing and the hypoxic ventilatory response.

Communications biology·2022
Same author

LKB1 is the gatekeeper of carotid body chemosensing and the hypoxic ventilatory response.

Communications biology·2022
Same author

Hydrogen sulfide regulates hippocampal neuron excitability via S-sulfhydration of Kv2.1.

Scientific reports·2021
Same author

Kv1.3 voltage-gated potassium channels link cellular respiration to proliferation through a non-conducting mechanism.

Cell death & disease·2021
Same journal

Who are you, ketamine? Good, evil, or dose- and context-dependent?

The Journal of physiology·2026
Same journal

Nuances in explaining the blunted erythropoietic response at altitude following recombinant human erythropoietin treatment at sea level.

The Journal of physiology·2026
Same journal

Sex-dependent responses to glucagon agonist therapies in obesity: Mechanistic insights and broader pharmacological implications.

The Journal of physiology·2026
Same journal

Brain sparing in fetal growth restriction: The double-edged sword of fetal hypoxaemia.

The Journal of physiology·2026
Same journal

Protein kinase Cδ and pharmacomechanical coupling: Re-envisioning cerebral vascular control.

The Journal of physiology·2026
Same journal

Improved subjective sleep quality in older adults by enhancing the GABAergic system in the sensorimotor cortex.

The Journal of physiology·2026
See all related articles

Alzheimer's disease pathology involves amyloid beta peptide (Abeta) plaques. Emerging research suggests Abeta has vital physiological roles, challenging its purely toxic nature when levels are balanced.

Area of Science:

  • Neuroscience
  • Biochemistry

Background:

  • Alzheimer's disease (AD) is characterized by amyloid beta peptide (Abeta) plaques.
  • Abeta is traditionally viewed as the primary neurotoxic agent in AD pathogenesis.
  • Research has focused on Abeta's production, activity, and degradation pathways.

Purpose of the Study:

  • To review current data on amyloid beta peptide's physiological functions.
  • To re-evaluate the toxicological profile of Abeta in the context of its production and degradation balance.
  • To explore the potential beneficial roles of Abeta in neuronal health.

Main Methods:

  • Literature review of studies on amyloid beta peptide formation, degradation, and function.
  • Analysis of emerging data suggesting physiological roles for Abeta.

Related Experiment Videos

  • Synthesis of evidence regarding the balance between Abeta production and degradation.

    • Main Results:

    • Significant progress has been made in understanding Abeta's formation from amyloid precursor protein and its degradation by enzymes like neprilysin.
    • Growing evidence indicates that Abeta possesses important physiological functions.
    • Abeta may be toxic only when its production and degradation are imbalanced.

    Conclusions:

    • Physiological levels of amyloid beta peptide may play crucial roles in normal brain function and neuronal survival.
    • The perception of Abeta as solely a toxic peptide requires re-evaluation based on its potential beneficial physiological roles.
    • Understanding the balance of Abeta metabolism is key to comprehending its role in both health and disease.