Consistently, heterozygous deletion of VPS35 in AD mice results in a significant increase in Aβ level in the mouse hippocampus, accompanied with AD-like phenotypes including cognitive memory deficits, defective long-term potentiation (LTP) and impaired postsynaptic glutamatergic neurotransmission in early adult age [125]. This evidence concerns the gene VPS35 and Alzheimer disease.