Since VU01 administration does not affect wildtype behavior, we addressed the effects of VU01 in preventing synaptic dysfunction (electrophysiology) and the underlying memory deficits (behavior) driven by progressive accumulation of oligomers of Aβ (oAβ) and tau (otau) in 6-month old 3xTg-AD mice using saline-injected age-matched 3xTg-AD siblings where PLD1 levels are elevated18 as appropriate controls. This evidence concerns the gene PLD1 and Alzheimer disease.