Furthermore, histological studies have shown reduced parvalbumin interneuron numbers in post-mortem motor cortices of ALS patients [101] and animal models of ALS [102,103], and a decreased number of neuropeptide Y-positive interneurons at symptom onset coupled with progressive reduction of calretinin-positive interneurons from symptom onset up to the end stage in the motor cortex of an ALS mouse model [104]. Here, PVALB is linked to amyotrophic lateral sclerosis.