Abstract Title

Neuronal injury from cardiac arrest: aging years in minutes

Presenter Name

Brandon H Cherry

Abstract

Cardiac arrest is a leading cause of death and permanent disability. Most victims succumb to the oxidative and inflammatory damage sustained during arrest/resuscitation, but even survivors typically battle long-term neurocognitive impairment. Although extensive research has delineated the complex mechanisms that culminate in neuronal damage and death, no effective treatments have been developed to interrupt these mechanisms. Of importance, many of these injury cascades are also active in the aging brain. In the aged brain, neurons and other cells are under persistent oxidative and inflammatory stress which eventually damages or kills the cells. With respect to these similarities, it is reasonable to propose that the brain essentially ages the equivalent of several years within the few minutes taken to resuscitate a patient from cardiac arrest. Accordingly, cardiac arrest-resuscitation models may afford an opportunity to study the deleterious mechanisms underlying the aging process, on an accelerated time course. The purpose of this presentation is to highlight parallel mechanisms of brain damage and neuronal death that ensue following cardiac arrest and in the aging brain. Despite their different time courses, mechanistic information gained from studying the two conditions could be harnessed to synergistically advance both fields. Ultimately this could lead to the development of treatments targeting specific components in these neurodegenerative pathways, in order to provide more robust protection of patients from neurocognitive impairment and/or death.

Presentation Type

Oral

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Neuronal injury from cardiac arrest: aging years in minutes

Cardiac arrest is a leading cause of death and permanent disability. Most victims succumb to the oxidative and inflammatory damage sustained during arrest/resuscitation, but even survivors typically battle long-term neurocognitive impairment. Although extensive research has delineated the complex mechanisms that culminate in neuronal damage and death, no effective treatments have been developed to interrupt these mechanisms. Of importance, many of these injury cascades are also active in the aging brain. In the aged brain, neurons and other cells are under persistent oxidative and inflammatory stress which eventually damages or kills the cells. With respect to these similarities, it is reasonable to propose that the brain essentially ages the equivalent of several years within the few minutes taken to resuscitate a patient from cardiac arrest. Accordingly, cardiac arrest-resuscitation models may afford an opportunity to study the deleterious mechanisms underlying the aging process, on an accelerated time course. The purpose of this presentation is to highlight parallel mechanisms of brain damage and neuronal death that ensue following cardiac arrest and in the aging brain. Despite their different time courses, mechanistic information gained from studying the two conditions could be harnessed to synergistically advance both fields. Ultimately this could lead to the development of treatments targeting specific components in these neurodegenerative pathways, in order to provide more robust protection of patients from neurocognitive impairment and/or death.