Because proper astrocytic NF-κB-mediated responses must be tightly regulated and limited, the accumulation and perpetuation of inflammatory signals then drive unintended neurotoxic outcomes, such as mitochondrial impairment, neuronal senescence, and neurodegenerative-like phenotypes (i.e., PD, ALS)83. Here, NFKB1 is linked to amyotrophic lateral sclerosis.