Increasing knowledge of neuron death mediators has led to gene therapy tech
niques for neuroprotection. Overexpression of numerous genes enhances survi
val after necrotic or neurodegenerative damage. Nonetheless, although encou
raging, little is accomplished if a neuron is spared from death, but not fr
om dysfunction. This article reviews neuroprotection experiments that inclu
de some measure of function, and synthesizes basic principles relating to i
ts maintenance. Variations in gene delivery systems, including virus-type a
nd latency between damage onset and vector delivery, probably impact the th
erapeutic outcome. Additionally, functional sparing might depend on factors
related to insult severity, neuron type involved or the step in the death
cascade that is targeted.