[Proteic marker of hypoxic-ischemic damage]

Ann Ist Super Sanita. 2001;37(4):581-91.
[Article in Italian]

Abstract

Perinatal hypoxic injury is the major cause of normal neural developmental alterations. Recent studies concerning animal models show that an hypoxic/ischaemic event triggers a process taking to a synaptic architecture reorganization which induces a transient change in the synaptic (synapsin 1, SNAP 25, APP) and neuronal (MAP2, N-CAM, GAP-43 and presenilins) protein expression. Here we review the post-translational modifications of some proteins after hypoxic-ischaemic events. A deeper study on synaptic proteins plasticity could give an important key for the understanding of the recovery mechanisms of the nervous system.

Publication types

  • English Abstract
  • Review

MeSH terms

  • Amyloid beta-Peptides / physiology
  • Disease Models, Animal
  • GAP-43 Protein / physiology
  • Humans
  • Hypoxia-Ischemia, Brain / etiology*
  • Membrane Proteins / physiology
  • Microtubule-Associated Proteins / physiology
  • Nerve Tissue Proteins / physiology*
  • Neural Cell Adhesion Molecules / physiology
  • Presenilin-1
  • Presenilin-2
  • Synapsins / physiology
  • Synaptosomal-Associated Protein 25

Substances

  • Amyloid beta-Peptides
  • GAP-43 Protein
  • Membrane Proteins
  • Microtubule-Associated Proteins
  • Nerve Tissue Proteins
  • Neural Cell Adhesion Molecules
  • PSEN1 protein, human
  • PSEN2 protein, human
  • Presenilin-1
  • Presenilin-2
  • SNAP25 protein, human
  • Synapsins
  • Synaptosomal-Associated Protein 25