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Limiting Apoptosis as a Strategy for CNS Neuroprotection

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CNS Neuroprotection

Part of the book series: Handbook of Experimental Pharmacology ((HEP,volume 155))

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Abstract

The term necrosis is a Greek word meaning “deadness.” A contemporary definition of necrosis is the sum of morphological changes indicative of cell death (Majno and Joris 1995). Necrosis usually applies to cell death that occurs to a group of cells or part of an organ in vivo, but the term has more recently been applied to cells in culture. Necrosis is the form of cell death which usually occurs when cells were injured by extreme physical stress or chemical challenges to the point that is beyond repair. As a result of the presence of massive ion influx (e.g., Na+, Ca2+), early and marked mitochondria swelling and cell swelling (oncosis) characterize necrosis (Majno and Joris 1995; Trump et al. 1997) (Fig. 1). Nonspecific DNA breakage results in the formation of chromatin fragments (in a punctuate fashion) all over the nuclei. Eventually, the nuclei become leaky and ultimately the plasma membrane ruptures. At least under in vitro conditions, necrosis is rapid and the time course of cell death is usually within 1–5-h death (Majno and Joris 1995).

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Wang, K.K.W. (2002). Limiting Apoptosis as a Strategy for CNS Neuroprotection. In: Marcoux, F.W., Choi, D.W. (eds) CNS Neuroprotection. Handbook of Experimental Pharmacology, vol 155. Springer, Berlin, Heidelberg. https://doi.org/10.1007/978-3-662-06274-6_2

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