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

Amyloid beta induces neuronal cell death through ROS-mediated ASK1 activation.

H Kadowaki1, H Nishitoh, F Urano

  • 1Laboratory of Cell Signaling, Graduate School of Pharmaceutical Sciences, University of Tokyo, 7-3-1 Hongo, Bunkyo-ku, Tokyo 113-0033, Japan.

Cell Death and Differentiation
|December 14, 2004
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

Erratum: Quadrupole Order in the Frustrated Pyrochlore Tb_{2+x}Ti_{2-x}O_{7+y} [Phys. Rev. Lett. 116, 217201 (2016)].

Physical review letters·2021
Same author

Five subtypes of benign paroxysmal positional vertigo.

The Journal of laryngology and otology·2021
Same author

The risk of rabies spread in Japan: a mathematical modelling assessment.

Epidemiology and infection·2018
Same author

Quadrupole Order in the Frustrated Pyrochlore Tb_{2+x}Ti_{2-x}O_{7+y}.

Physical review letters·2016
Same author

PO-16 - ASK1 regulates tumor lung metastasis and platelet functions.

Thrombosis research·2016
Same author

Mental and physical distress of field veterinarians during and soon after the 2010 foot and mouth disease outbreak in Miyazaki, Japan.

Revue scientifique et technique (International Office of Epizootics)·2016
Same journal

A planar dimer of bovine ATP synthase.

Cell death and differentiation·2026
Same journal

GCN5 and TADA2B constitutively regulate XRCC1 function during DNA repair to maintain cell survival.

Cell death and differentiation·2026
Same journal

MEGF8 controls osteogenic differentiation through post-transcriptional regulation of BMP-SMAD signaling in craniosynostosis.

Cell death and differentiation·2026
Same journal

Macrophage-secreted brain-derived neurotrophic factor promotes tumor growth in triple-negative breast cancer by inducing axonogenesis.

Cell death and differentiation·2026
Same journal

Species-specific regulation of necroptosis by STK38-dependent RIPK1 phosphorylation.

Cell death and differentiation·2026
Same journal

Ssu72 phosphatase orchestrates obesogenic adipogenesis and metabolic homeostasis during nutrient excess.

Cell death and differentiation·2026
See all related articles

Amyloid beta triggers neuronal death in Alzheimer's disease by activating ASK1 through reactive oxygen species. This finding highlights a key mechanism in neurotoxicity and suggests ASK1 as a potential therapeutic target.

Area of Science:

  • Neuroscience
  • Molecular Biology
  • Cellular Biology

Background:

  • Alzheimer's disease (AD) is characterized by amyloid beta (Abeta) plaques, which induce neuronal cell death.
  • Reactive oxygen species (ROS), nitric oxide, and endoplasmic reticulum (ER) stress are implicated in Abeta neurotoxicity.
  • Apoptosis signal-regulating kinase 1 (ASK1) mediates ROS- and ER stress-induced JNK activation and apoptosis.

Purpose of the Study:

  • To investigate the role of ASK1 in Abeta-induced neuronal cell death.
  • To elucidate the signaling pathways involved in Abeta neurotoxicity.

Main Methods:

  • Utilized cultured neuronal cells to study Abeta-induced neurotoxicity.
  • Examined ASK1 activation in response to Abeta exposure.
  • Assessed JNK activation and cell death in wild-type and ASK1 knockout (ASK1-/-) neurons.

Related Experiment Videos

Main Results:

  • Abeta activated ASK1 primarily through ROS production, not ER stress, in neuronal cells.
  • ASK1-/- neurons exhibited impaired JNK activation and reduced cell death upon Abeta exposure.
  • Demonstrated the crucial role of ROS-mediated ASK1 activation in Abeta neurotoxicity.

Conclusions:

  • ROS-mediated ASK1 activation is a central mechanism underlying Abeta-induced neurotoxicity in Alzheimer's disease.
  • Targeting the ASK1 pathway may offer a therapeutic strategy for Alzheimer's disease.