FUS and amyotrophic lateral sclerosis: Further studies revealed that the endogenously expressed mutant FUS can upregulate the expression of both NEAT1_1 and NEAT1_2 and promote excessive formation of structurally and functionally compromised paraspeckles, which, together with the observed accumulation of nonparaspeckle NEAT1_1, may contribute to disease severity in patients with ALS-FUS [145, 146].