RANBP2 and amyotrophic lateral sclerosis: CA3 overexpression resulted in a marked increase in the steady state level of RANBP2, a component of the nuclear pore complex [32], and may be the mechanism responsible for the observed down-regulation of pathways related to the following neurodegenerative diseases: Parkinson’s, Huntington’s, Alzheimer’s, ALS and prion diseases.