Abstract Body

MCI in Parkinson's disease (PD) has been a heterogeneous clinical entity caused by various brain pathologies. According to cross-sectional studies, it is present in approximately 25% of all PD patients; attention/executive function deficits seem to be most prevalent. Early cognitive deficits predominantly affect attention and executive functions and result particularly from dopamine depletion in the basal ganglia. The cholinergic system has been implicated in cognitive dysfunction and in PD dementia in particular; serotonergic, glutamatergic, and noradrenergic systems could also be involved. Recent studies have pointed out the impact of metabolic syndrome and its treatment potential in decreasing the risk of cognitive decline in PD. Recommendations for symptomatic treatment with acetylcholinesterase inhibitors and memantine in PD-dementia have been published. Several drugs (e.g. rivastigmine, rasagiline, atomotoxetine) have been tested also in MCI-PD populations in small randomized placebo-controlled studies, however, without any conclusive positive results. Future studies should use specific biomarkers to help to identify distinct PD subgroups that might benefit from potential novel therapies. Non-pharmacological interventions may be beneficial in distinct patient subgroups, including exercise, cognitive training, non-invasive brain stimulation methods, and other techniques to enhance angiogenesis, synaptic plasticity, and neurogenesis. Neuroprotective or disease-modifying drugs for treatment of mild cognitive impairment in PD or even for preclinical stages are awaited.