Related Experiment Video

Updated: Feb 2, 2026

Characterization of MLKL-mediated Plasma Membrane Rupture in Necroptosis
08:55

Characterization of MLKL-mediated Plasma Membrane Rupture in Necroptosis

Published on: August 7, 2018

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Necroptosis and RIPK1-mediated neuroinflammation in CNS diseases

Junying Yuan1, Palak Amin2, Dimitry Ofengeim3

  • 1Department of Cell Biology, Harvard Medical School, Boston, MA, USA. junying_yuan@hms.harvard.edu.

Nature Reviews. Neuroscience
|November 24, 2018
PubMed

Insights

Necroptosis, a regulated cell death pathway, contributes to neuroinflammation in diseases like Alzheimer's. Targeting receptor-interacting protein kinase 1 (RIPK1) may inhibit cell death and reduce neuroinflammation.

Area of Science:

  • Neuroscience
  • Cell Biology
  • Immunology

Background:

  • Apoptosis is vital for nervous system development, but adult CNS neurons resist it.
  • Pathological conditions can trigger necroptosis, a regulated necrotic cell death pathway, in the CNS.
  • Necroptosis involves key mediators like RIPK1, RIPK3, and MLKL, and promotes neuroinflammation.

Purpose of the Study:

  • To review the role of necroptosis in neurodegenerative diseases.
  • To highlight the involvement of necroptosis in conditions such as multiple sclerosis, amyotrophic lateral sclerosis, Parkinson disease, and Alzheimer disease.
  • To explore the therapeutic potential of targeting RIPK1.

Main Methods:

  • Review of existing scientific literature on necroptosis and neurodegeneration.
  • Analysis of evidence implicating necroptosis in the pathogenesis of various neurological disorders.
  • Discussion of potential therapeutic strategies targeting necroptosis pathways.

Main Results:

  • Necroptosis is implicated in the pathogenesis of several neurodegenerative diseases.
  • Upregulation of death receptor ligands can sensitize CNS cells to necroptosis.
  • Necroptosis exacerbates cell death and neuroinflammation in affected neurological conditions.

Conclusions:

  • Targeting RIPK1 presents a potential strategy to inhibit multiple cell death pathways.
  • Inhibiting RIPK1 may offer a therapeutic approach to ameliorate neuroinflammation in neurodegenerative diseases.
  • Further research into necroptosis inhibitors could lead to novel treatments for neurological disorders.

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