Alternatively, changes in the expression of the pri-miRNA processing enzymes, Drosha and Dgcr8, as have been described in the brains of Huntington’s Disease model mice and after NMDAR stimulation in vitro, could account for increased miRNA levels [10, 69], although such a mode of regulation would not explain why TAMs but not other miRNAs are increased by extrasynaptic NMDAR stimulation. Here, DGCR8 is linked to juvenile Huntington disease.