In the AD animal model, APP/PS1 mice and TgCRND8 mice at the preplaque stage showed motor deficits, but not a motor learning deficit (i.e., deficit in performance improvement for each trial as shown in the current study), and a decline in LTD in cerebellar parallel fiber-Purkinje cell synapses, suggesting impairment in the cell biological basis of short-term motor learning [72, 75]. This evidence concerns the gene PSEN1 and Alzheimer disease.