A new perspective on ischemic brain damage?
The last 20-30 years of research has brought detailed information on the pathophysiology and the neurochemistry of anoxic/ischemic brain damage. On the basis of this information, important mediators of such damage have been identified, notably loss of calcium homeostasis, excessive acidosis and enhanced production of free radicals. At present, the tools of basic neuroscience are being employed to unravel the cellular and molecular mechanisms involved. The results suggest that the second and third messengers expressed as a result of a calcium transient may be instrumental in triggering cell damage. These encompass excessive activation of protein kinases and phosphatases, and expression of new genes. The new data emerging in this field herald the advent of new concepts which can explain the causes of ischemic/anoxic brain damage in molecular terms.
Siesjö
B K
BK
University of Lund, Laboratory for Experimental Brain Research, Sweden.
D000818:Animals; D001921:Brain / Q000378:metabolism / Q000473:pathology; D002545:Brain Ischemia / Q000209:etiology*; D002118:Calcium / Q000378:metabolism; D004734:Energy Metabolism; D005609:Free Radicals; D006801:Humans
D005609:Free Radicals; D002118:Calcium