Olfactory impairment is one of the earliest non-motor manifestations of Parkinsons disease,which is accompanied by abnormal α-synuclein (α-syn) deposition in olfactory neurons.However,the mechanistic basis of this association is not well understood.To address this issue,we examined olfactory function in transgenic mice overexpressing human α-syn in the olfactory bulb (OB) and olfactory epithelium (OE).