In order to gain some mechanistic insights on how the exposure to LF-MF might interfere with pathogenesis in ALS and AD, we analyzed the levels of toxic protein species (mutant SOD1, APP, Aβ species), the appearance of protein aggregates which is reminiscent for an affected protein homeostasis (in mutant SOD1 spinal cords) and glial activation in affected tissues of APP23 and mutant SOD1 mice. The gene discussed is SOD1; the disease is amyotrophic lateral sclerosis.