Model of acute injury to study neuroprotection.
A major causative factor in the paralysis that often follows an acute injury to the central nervous system (CNS) is the paradoxical inability of the CNS to tolerate its own mechanism of self-repair. The dismal result is often a wider spread of damage (part of the inevitable "secondary" or "delayed" degeneration) rather than contribution toward a cure. Ever since the phenomenon of posttraumatic damage spread in the CNS was first recognized, neuroscientists have attempted to identify the players in this destructive process and have sought ways to neutralize or bypass them with the object of rescuing any neurons that are still viable. This approach is collectively termed neuroprotection. In this chapter, we present a view of experimental paradigms used to study neuroprotection.
Schwartz
Michal
M
Department of Neurobiology, The Weizmann Institute of Science, Rehovot, Israel.
Kipnis
Jonathan
J
D000818:Animals; D015551:Autoimmunity; D002490:Central Nervous System / Q000276:immunology* / Q000473:pathology / Q000503:physiopathology; D002493:Central Nervous System Diseases / Q000276:immunology* / Q000473:pathology / Q000503:physiopathology; D004195:Disease Models, Animal; D006801:Humans; D007108:Immune Tolerance; D051379:Mice; D009410:Nerve Degeneration / Q000378:metabolism* / Q000473:pathology / Q000503:physiopathology; D020221:Optic Nerve Injuries / Q000276:immunology* / Q000473:pathology / Q000503:physiopathology; D051381:Rats; D012038:Regeneration / Q000276:immunology*