[Proteic marker of hypoxic-ischemic damage].
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.
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Laboratorio di Metabolismo e Biochimica Patologica, Istituto Superiore di Sanità, Roma.
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D016229:Amyloid beta-Peptides / Q000502:physiology; D004195:Disease Models, Animal; D019922:GAP-43 Protein / Q000502:physiology; D006801:Humans; D020925:Hypoxia-Ischemia, Brain / Q000209:etiology*; D008565:Membrane Proteins / Q000502:physiology; D008869:Microtubule-Associated Proteins / Q000502:physiology; D009419:Nerve Tissue Proteins / Q000502:physiology*; D019006:Neural Cell Adhesion Molecules / Q000502:physiology; D053764:Presenilin-1; D053766:Presenilin-2; D016704:Synapsins / Q000502:physiology; D050825:Synaptosomal-Associated Protein 25
D016229:Amyloid beta-Peptides; D019922:GAP-43 Protein; D008565:Membrane Proteins; D008869:Microtubule-Associated Proteins; D009419:Nerve Tissue Proteins; D019006:Neural Cell Adhesion Molecules; C508853:PSEN1 protein, human; C508861:PSEN2 protein, human; D053764:Presenilin-1; D053766:Presenilin-2; C494208:SNAP25 protein, human; D016704:Synapsins; D050825:Synaptosomal-Associated Protein 25
Marker proteici del danno ipossico-ischemico.