Neuronal death occurs naturally during brain development and is a comm
on response to an external insult. Cell death, whose mechanisms are cu
rrently being elucidated, appears in three forms: necrosis, apoptosis
and programmed cell death, Recently, attention has focused on a family
of cysteine proteases whose prototype is interleukin-1 beta convertin
g enzyme (ICE), ICE, essential for IL-1 beta production and, thus, cri
tical to necrotic mechanisms, also plays a role in apoptosis mediated
through the stimulation of the lymphocyte fas antigen, The absence of
ICE expression in neurons makes ICE an unlikely direct participant in
neuronal death, However, the existence of ICE family members in neuron
s combined with the pharmacological inhibition of both apoptosis in vi
tro and programmed cell death during development make ICE homologs can
didates for mediating these two forms of cell death, Since several neu
rodegenerative diseases as well as at least one neurological disorder
may have an apoptotic component, antagonists of this protease family m
ay be neuroprotective.