Cognitive impairment is a common finding in Parkinson’s disease（PD）, even in the early stages. The concept of mild cognitive impairment（MCI）in PD was recently formalized with diagnosis being reached after impairments in neuropsychological tasks become significant in at least one domain.
 The brain profile of cognitive deficits involves executive functions（e. g., planning, set shifting, set maintenance, problem solving）, attention and memory function. Memory deficits are characterized by impairments in delayed recall, temporal ordering and conditional associate learning. PD patients demonstrate relatively preserved recognition. Visuospatial dysfunctions have also been reported, while language is largely preserved. The existence of two distinct mild cognitive syndromes has also been suggested. One of these affects mainly the frontostriatal executive deficits that are modulated by dopaminergic medications and by a genetically determined level of prefrontal cortex dopamine release. The other affects the more‒posterior cortical abilities, such as visuospatial and memory functions, and is suggested to be associated with an increased risk for conversion to dementia. Cross‒sectional studies have commonly reported dementia in 20‒30％ of PD patients, although the 8‒year cumulative incidence of dementia may be as high as 78％. Factors associated with dementia in PD are age at onset, age at the time of examination, akinetic‒rigid form PD, depression, hallucination, rapid eye movement sleep behavioral disorder and severe olfactory deficits. Clinical features generally involve the same type of deficits as those found in MCI patients, which are more severe and more extensive. The phenomenology of the dementia syndrome is similar to that seen in dementia with Lewy bodies, and clinicopathological correlation studies have revealed varying results with regard to neurochemical deficits and the pathological substrate underlying cognitive impairment and dementia. Early cognitive impairment, particularly in the form of executive dysfunction, is indicative of mainly fronto‒striatal pathologic changes and might originate during nigrostriatal and subsequent mesocortical dopamine denervation. A potential parallel noradrenergic deficit and cholinergic deficit disturbance in patients without dementia might also contribute to MCI. Extensive pathological changes in Lewy bodies lead to widespread cortical and subcortical degeneration and profound cholinergic deficits, and might lead to the development of dementia. Several studies have revealed a significant correlation between dementia and Alzheimer‒type pathology.