IntroductionParkinson’s disease (PD) – human neurodegenerative disorder with dopamine deficit as major pathology. Primary symptom of PD is movement dysfunction but different other symptoms may be found in patients. Specific emphasis is directed at cognitive decline and harbingers of dementia. There are 5 main ways to correct functional activity of dopamine synapse: levodopa [1], dopamine agonists [1], amantadine [2], monoamine oxidase inhibitors [3], anticholinergic drugs [4]. We aimed to assess the possible side effects of these medications on cognitive functions in PD patients without dementia. Cognitive potential P300 is associated with information processing, memory, attention, and it’s objective electroencephalography-based (EEG) approach for our goal.Methods92 PD humans (age 46-74, men and women, Hoehn-Yahr stage 2-3) and 26 healthy volunteers participated in present study. The study was approved in advance by the Ethical Committee of the Institute of Gerontology (Ukraine) and was in accordance with the Declaration of Helsinki. Cognitive dysfunctions in patients were evaluated on UPDRS-1 scale (The Unified Parkinson’s Disease Rating Scale, part 1): 0-1 points for lower level and 2-4 points for higher level. All patients got their usual treatment; there were not additional prescriptions in connection with present study. Dosage of drugs per day: levodopa 150-375 mg – low dose, 400-887.5 – high; dopamine agonists 1.5-3 mg; amantadine 100-200 mg; monoamine oxidase inhibitors 6-7 mg; anticholinergic drugs 0,5-2 mg. Patients were divided into groups based on one of five types of medication, levodopa dosage and level of cognitive impairment (higher or lower). P300 was recorded in oddball paradigm task with auditory stimuli using NeuroCom Pro EEG system (XAI-Medica, Ukraine). We applied sLORETA (standardized low resolution brain electromagnetic tomography) [5] to identify the sources of P300 activity. Statistical analysis was performed by test for independent samples (P < 0.05, bootstrapping with 5000 samples).ResultsWe have found increased activity of P300 sources in right middle frontal gyrus in patients with higher level of cognitive impairment (n=42). Similar differences in this area also were revealed in PD patients who didn’t take dopamine agonist (n=52). Highest levodopa dosage leads to decreasing of P300 source’s activity in same frontal region (n=23). In addition, PD subjects with greater doses of levodopa (more 400 mg/day) demonstrated enhanced P300 generators in right parietal area (n=23). There were no significant differences in all other cases.ConclusionsHigh levodopa dosage and absence of dopamine agonists in treatment regimen were associated with deviations in cognitive processes. These changes in P300 generators may serve as possible harbingers of future dementia in PD patients