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TWEAK and the central nervous system

Manuel Yepes1

  • 1Department of Neurology and Center for Neurodegenerative Disease, Emory University School of Medicine, Atlanta, GA, USA. myepes@emory.edu

Molecular Neurobiology
|October 6, 2007
PubMed

Insights

Tumor necrosis factor-like weak inducer of apoptosis (TWEAK) and its receptor Fn14 are implicated in central nervous system injury. Inhibiting TWEAK shows therapeutic promise for conditions like ischemic stroke and multiple sclerosis.

Area of Science:

  • Neuroscience
  • Immunology
  • Molecular Biology

Background:

  • Tumor necrosis factor-like weak inducer of apoptosis (TWEAK) is a TNF superfamily member.
  • TWEAK interacts with its receptor fibroblast growth factor-inducible 14 (Fn14).
  • Both TWEAK and Fn14 are expressed in the central nervous system (CNS).

Purpose of the Study:

  • To investigate the role of TWEAK/Fn14 signaling in CNS pathologies.
  • To evaluate the therapeutic potential of inhibiting TWEAK activity in neurological disorders.

Main Methods:

  • Analysis of TWEAK and Fn14 expression in CNS tissues.
  • Investigating TWEAK-induced cellular responses, including NF-kappaB activation and cytokine release.
  • Evaluating the efficacy of Fn14-Fc fusion protein and anti-TWEAK antibodies in animal models.

Main Results:

  • TWEAK and Fn14 expression increases in the CNS following stimuli like cerebral ischemia.
  • TWEAK signaling contributes to blood-brain barrier permeability and cell death.
  • TWEAK activation of NF-kappaB leads to the release of proinflammatory mediators.
  • Inhibition of TWEAK demonstrated therapeutic effects in models of ischemic stroke, cerebral edema, and multiple sclerosis.

Conclusions:

  • TWEAK/Fn14 signaling plays a significant role in CNS injury.
  • Targeting TWEAK represents a potential therapeutic strategy for various neurological diseases.

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