BCL2 and amyotrophic lateral sclerosis: CGP 3466 has been reported to rescue dopaminergic neurons from death and to subsequently inhibit the development of motor symptoms in rodent models of PD by preventing mitochondria-mediated apoptosis.49 Additionally, Bcl-2 overexpression and the deletion of pro-apoptotic BAX and BAK have been shown to exert neuroprotection in ALS mice by blocking the apoptosis of lumbar spinal motor neurons and delaying the onset of symptoms.50