Journal
TRENDS IN NEUROSCIENCES
Volume 35, Issue 11, Pages 700-709Publisher
ELSEVIER SCIENCE LONDON
DOI: 10.1016/j.tins.2012.06.004
Keywords
Alzheimer's disease; neuronal differentiation; synaptic plasticity; long-term potentiation; long-term depression; synaptic loss
Categories
Funding
- Projects for Research of National Interest (PRIN)
- Alzheimer's Association [NIRG-11-204588]
- Telethon Foundation
- Italian Ministry of Health
- Italian Ministry of Research, through Ricerca Finalizzata
- Ricerca Corrente
- Fondo per gli Investimenti della Ricerca di Base (FIRB)
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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.
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