Acute cerebral ischemia inflammation

Apoptosis is programed cell death and differs from necrosis in that it results in minimal inflammation and release of genetic material. Although necrosis is the predominant process that follows acute ischemia, apoptosis is important after more minor injury, particularly within the ischemic penumbra. Apoptosis is executed by the production, activation and action of caspases, which are protein-cleaving enzymes that dismantle cytoskeleton proteins and enzymes responsible for cellular repair (Zhang et al. 2004). Neurons are particularly susceptible to caspase-mediated cell death after cerebral ischemia, as demonstrated by the reduction in infarct size by caspase inhibitors in experimental models. 

Bemeur C, Ste-Marie L, Desjardins P, Vachon L, Butterworth RE, HazeU AS, Montgomery J (2005) Dehydroascorbic acid normalizes several markers of oxidative stress and inflammation in acute hyperglycemic focal cerebral ischemia in the rat. Neurochem Int 46(5) 399 07... 

Many events occuring during and after cerebral ischemia are well known, but they are not known enough to fully elucidate the mechanisms of brain damage. Factors responsible for the extension of infarction into the penumbral zone include acidosis, edema formation, acute local inflammation, dissipative ion fluxes, calcium overload, glutamate excitotoxicity, free radical formation, nitric oxide overproduction and programmed cell death [2,13-16]. 

An understanding of the role of leukocytes and the mediators of inflammation in cerebral ischemia may have a very great impact on therapy. An increasing number of molecules are currently being investigated in animals for their possible effectiveness in human acute stroke. Treatments to induce neutropenia, to reduce infarct volume and improve functional outcome are under heavy study. One group of studies has focused on... 

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