Parkinson's disease (PD) is a progressive neurodegenerative disorder, characterized by resting tremor, rigidity, and bradykinesia. Additionally, a wide spectrum of early non-motor symptoms has been described, among which cognitive impairment is one of the most relevant.Several studies show that interventions focused on cognitive stimulation can play an important role in preventing or delaying the onset of dementia in patients with neurodegenerative diseases. In this perspective, we aimed at investigating the synaptic mechanisms mediating the effects of cognitive enrichment in two mouse models of PD: PTEN-induced kinase1 knockout (PINK1-/-) mice, as a model of monogenic parkinsonism, and mice overexpressing human wild-type α-synuclein (ASYN, line 61, kindly provided by Dr. R. Rissman, UC San Diego), as a model of sporadic PD. We performed slice electrophysiology recordings from the striatum and the hippocampus of both mouse models. In standard environmental conditions (NE), we observed the lack of long-term synaptic depression (LTD) in the striatum of both animal models. We therefore compared the effects of an unimodal cognitive enrichment (CE) and a multimodal enrichment (EE, including both cognitive and motor stimulation) on the impairment of long-term synaptic plasticity in the striatum in PINK1-/- and ASYN mice. We found that the CE was not sufficient to restore LTD, whereas the EE was able to completely rescue the expression of long-term synaptic plasticity in the striatum of PD mice. These observations provide a likely mechanism for the efficacy of multimodal stimulation as a non-pharmacological add-on intervention to slow the progression of cognitive deficits in PD.