Abstract

Developing neurons are programmed to die by an apoptotic pathway unless they are rescued by extrinsic growth factors that generate an anti-apoptotic response. By contrast, adult neurons need to survive for the lifetime of the organism, and their premature death can cause irreversible functional deficits. The default apoptotic pathway is shut down when development is complete, and consequently growth factors are no longer required to prevent death. To protect against accidental apoptotic cell death, anti-apoptotic mechanisms are activated in mature neurons in response to stress. Loss or reduced activity of these intrinsic anti-apoptotic 'brakes' might contribute to or accelerate neurodegeneration, whereas their activation might rescue neurons from injury or genetic abnormalities.

Author affiliations

1. Day Neuromuscular Research Lab, Department of Neurology, Massachusetts General Hospital and Harvard Medical School, Boston, Massachusetts 02129, USA.
2. Neural Plasticity Research Group, Department of Anaesthesia and Critical Care, Massachusetts General Hospital and Harvard Medical School, Boston, Massachusetts 02129, USA.

Correspondence to: Clifford J. Woolf² Email: cwoolf@partners.org

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