Glial biology and disorders

Curr Opin Neurol Neurosurg. 1993 Feb;6(1):27-33.

Abstract

Much work has been devoted this year to the localization and mode of expression of growth factors and cytokines. Although it is not possible to extrapolate directly from in vitro to in vivo conditions, the plasticity of glial cells seems to be very influenced by growth factors. Astrocytes in vivo do not express many growth factors during normal conditions, but a pathologic event can lift these restrictions. Cytokines and their receptors have been localized on neuronal or glial cell types. The programmed cell death, well identified in neurons, seems to occur also in oligodendrocytes and may be influenced by survival factors. In the adult brain, glial progenitors are present and may be a potential source to generate myelinating oligodendrocytes for myelin repair. In the peripheral nervous system, axonal-Schwann cell signaling may function in both directions during development. Some animal neurologic mutants are models for human diseases; one of them, the Trembler mouse, has effectively led to the genetic characterization of Charcot-Marie-Tooth disease type 1a. As for myelin destruction, the relationship between demyelination and inflammation is still not very clear.

Publication types

  • Review

MeSH terms

  • Cell Death / genetics
  • Central Nervous System Diseases / genetics
  • Central Nervous System Diseases / physiopathology*
  • Charcot-Marie-Tooth Disease / genetics
  • Demyelinating Diseases*
  • Diffuse Cerebral Sclerosis of Schilder / genetics
  • Diffuse Cerebral Sclerosis of Schilder / physiopathology
  • Female
  • Fibroblast Growth Factor 2 / genetics*
  • Humans
  • Male
  • Oligodendroglia / physiology*
  • Platelet-Derived Growth Factor / genetics*
  • RNA, Messenger
  • Schwann Cells / physiology
  • Stem Cells / physiology*
  • Tumor Necrosis Factor-alpha / genetics

Substances

  • Platelet-Derived Growth Factor
  • RNA, Messenger
  • Tumor Necrosis Factor-alpha
  • Fibroblast Growth Factor 2