Animal model of the motor neuron disease amyotrophic lateral sclerosis (ALS), has implicated apoptotis in the neuronal degeneration evident in this disease. Mice showing ALS-like symptoms, as well as several human families with ALS, have a missense mutation in the gene coding for DOD-1. A defective enzyme enhances neuronal cell death by activating interleukin converting enzyme (ICE), an initia of apoptosis. The role of caspase-1 and caspase-3 in the apoptotic process is apparent and the use of the caspase inhibitor zVAD-fink demonstrated some promise in slowing neural death by apoptosis and prolonging life in mice with ALS-like symptoms. We discuss the possible mechanisms of caspase enzymes cascade activation and their central role in apoptosis and possibly in neural death.
|Pages (from-to)||1100-1104, 1115|
|State||Published - Nov 2001|