Caspase-3 in the central nervous system: beyond apoptosis

被引:214
作者
D'Amelio, Marcello [1 ,2 ]
Sheng, Morgan [3 ]
Cecconi, Francesco [1 ,4 ]
机构
[1] S Lucia Fdn, IRCCS, I-00143 Rome, Italy
[2] Univ Campus Biomed, I-00128 Rome, Italy
[3] Genentech Inc, Dept Neurosci, San Francisco, CA 94080 USA
[4] Univ Roma Tor Vergata, Dept Biol, Dulbecco Telethon Inst, I-00133 Rome, Italy
关键词
Alzheimer's disease; neuronal differentiation; synaptic plasticity; long-term potentiation; long-term depression; synaptic loss; PROGRAMMED CELL-DEATH; LONG-TERM DEPRESSION; MITOCHONDRIAL-MEMBRANE PERMEABILIZATION; MILD COGNITIVE IMPAIRMENT; ALZHEIMERS-DISEASE; NEURODEGENERATIVE DISEASES; HUNTINGTONS-DISEASE; PARKINSONS-DISEASE; PRECURSOR PROTEIN; SYNAPTIC PLASTICITY;
D O I
10.1016/j.tins.2012.06.004
中图分类号
Q189 [神经科学];
学科分类号
071006 ;
摘要
Caspase-3 has been identified as a key mediator of neuronal programmed cell death. This protease plays a central role in the developing nervous system and its activation is observed early in neural tube formation and persists during postnatal differentiation of the neural network. Caspase-3 activation, a crucial event of neuronal cell death program, is also a feature of many chronic neurodegenerative diseases. This traditional apoptotic function of caspase-3 is challenged by recent studies that reveal new cell death-independent roles for mitochondrial-activated caspase-3 in neurite pruning and synaptic plasticity. These findings underscore the need for further research into the mechanism of action and functions of caspase-3 that may prove useful in the development of novel pharmacological treatments for a diverse range of neurological disorders.
引用
收藏
页码:700 / 709
页数:10
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