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Beta-protein immunoreactivity in the human brain after cardiac arrest.
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1996
Year
Total Brain IschemiaSocial SciencesCerebral Vascular RegulationNeuroinflammationThrombosisAlzheimer's DiseaseBrain InjuryNeurologyNeuropathologyIschemic SyndromeBeta PpNeuroprotectionCerebral Blood FlowReperfusion InjuryTotal IschemiaCardiac ArrestNeurophysiologyNeuroscienceConcussionMedicine
Brain of twelve, 44-78 years old non-demented patients affected by total ischemia after cardiac arrest, were used in the study. All of them were resuscitated within a few minutes after cardiac arrest and they survived for 3 to 36 days afterward. In all cases, after cardiac arrest, beta PP overexpression was found by immunocytochemical methods in many cortical and subcortical neurons as well as in ependymal and choroid plexus cells. This overexpression of beta PP, was concomitant with formation of many A beta nonfibrillar (thioflavine-negative) plaques in the neuropil. Because of a break in the blood-brain barrier around many vessels, weakly A beta-immunoreactive material was also found. The data presented provided strong evidence that the total brain ischemia resulting from cardiac arrest is a risk factor for beta-amyloidosis.