To this end, the identification of mislocalized proteins caused by the AMPK-mediated impairment of nuclear–cytoplasmic shuttling, the molecular understanding of stalled translation complexes by disease-causing proteins in SGs, and the discovery of genetic modulations/pharmacological tools to preserve sufficient protein synthesis in an energy crisis will provide critical features of the association between energy dysfunction and neurodegeneration, and may pave the way to identify new drugs for neurodegenerative disease. This evidence concerns the gene PRKAA2 and neurodegenerative disease.