24), which elicits overexpression of mutant forms of amyloid precursor protein (APP), presenilin-1 (PS-1) and microtubule-associated protein tau proteins. In another transgenic AD model, the APP/PS1 mice, implementation of voluntary exercise regimens was found to result in repression of HOTAIR expression. The diminishment of the sponging effects of HOTAIR on miR-130a-3p was proposed to be associated with the voluntary exercise-induced recovery of memory functions in the Morris water maze test and attenuation of pro-inflammatory responses in these mice (Ref. 25). The gene discussed is HOTAIR; the disease is Alzheimer disease.