Cognitive impairment in Parkinson’s disease (PD) has unique characteristics. It mainly impairs executive functions (i.e., planning, organizing, thinking, judging, and problem solving) and visuospatial deficits, and eventually enters a dementia state in advanced stages. Many papers borrow the DSM-IV AD diagnostic criteria as a reference for the diagnosis of Parkinson’s disease dementia (PDD), which is actually inappropriate because PDD cognitive impairment has its own unique characteristics. 1. Impairment of executive function. Executive function impairment is the most prominent cognitive impairment in Parkinson’s disease. Many studies at home and abroad have confirmed that PD patients have impaired sequencing, temporal order and working memory, and execution of planned operations. Patients and family members often complain that patients have difficulty completing routine tasks, especially when the tasks require multiple steps and are in a certain order, indicating impaired executive function. Executive function can be understood by asking how the process of preparing a meal, organizing a household, or the procedure for a simple task. It is important to note, however, that a careful distinction should be made as to whether these difficulties are due to motor impairment, which can be identified by simple activities that require less motor skill. Our previous series of studies on working memory impairment in PD found that early Parkinson’s disease patients had impaired spatial working memory while object working memory was relatively preserved. By the middle stage, object working memory was also impaired. Further studies found that early PD spatial working memory impairment was mainly relative spatial (i.e., distance) working memory, while absolute spatial (location) working memory was not significantly different compared to healthy controls. The verbal working memory examination revealed that PD patients had significantly lower scores on the phonological verbal working memory examination compared to the control group, while the semantic verbal working memory examination had lower scores compared to the control group, but there was no significant difference. 2, Visuospatial impairment is also a common and prominent symptom of cognitive impairment in Parkinson’s disease. Some scholars used three different sizes of English letters and performed a letter recognition task on them, and found that the PD patient group had significantly poorer recognition of large letters than the control group, suggesting that Parkinson’s disease may affect the patients’ ability to perceive a large spatial composition, which may be an abnormal perceptual attention bias caused by dopamine deficiency. Patients often complain of blurred vision and difficulty reading, but routine ophthalmologic examination often reveals no abnormal findings. 3. Difficulty in learning and free recall of new information, while recognition is well maintained. Patients complain of poor memory but are given cues to help recall and can even go so far as to name details. Recent prospective memory studies of PD patients have found that event-based prospective memory is impaired in PD patients but not time-based prospective memory. Although PD patients have hoarseness, slow speech rate, reduced speech volume and phonological impairment, and some difficulty in language comprehension can be found during language examination, this may reflect slow motor and thinking in PD rather than impairment of language neural mechanisms in the brain. In conclusion, cognitive impairment in PD shows features of subcortical dementia, whereas cognitive impairment in AD shows features of cortical cognitive impairment, I. Mechanisms of cognitive impairment in PD It is self-evident that the basis of cognitive impairment in PD is degeneration of nigrostriatal cells, but it does not explain the more extensive cognitive impairment in patients. The pathological presence of cortical and subcortical Lewy vesicles may also be associated with cognitive impairment. the significant loss of cholinergic cells in the basal nucleus of Meynert in PD is the basis for the current application of cholinesterase inhibitor therapy in PDD. However, the prominent executive dysfunction in PD cognitive impairment is difficult to explain with these. Disruption of the frontal-striatal loop is currently thought to be involved. The decrease in DA in the striatum results in depletion of DA in the prefrontal lobe, which has been confirmed by several studies. For example, the loop originating from the dorsolateral prefrontal to the caudate nucleus and pallidum is associated with executive functions such as planning, organization, problem solving, and memory extraction, and the dorsolateral prefrontal loop is impaired early in PD. Therefore, even non-demented PD patients can show symptoms of cognitive impairment. The PET study revealed that the uptake of 18F-fluorodopa in the nucleus accumbens, caudate nucleus and frontal cortex was reduced in PD patients; and the caudate nucleus inflow constants were negatively correlated with anti-interference attention tests, especially interference time, and the frontal inflow constants were positively correlated with digit expansion, verbal fluency, and vocabulary immediate recall tests, fully demonstrating the role of the prefrontal cortex-basal ganglia dopamine projection system in frontal cognitive function The role of The diagnosis of cognitive impairment in Parkinson’s disease is possible in the early stages of Parkinson’s disease, but it does not meet the criteria for dementia. The concept of mild cognitive impairment (MCI) has not yet been introduced into PD cognitive impairment. However, there is a need to establish PD-MCI diagnostic criteria to facilitate early detection and treatment, but this depends on a concerted effort.PD dementia is characterized by significant executive dysfunction and visual perceptual impairment. Some studies have attempted to differentiate PD from Alzheimer’s disease in terms of cognitive fluctuations, visual and auditory hallucinations, depression and sleep disturbances, but there is a lack of accepted diagnostic criteria for PD dementia. the diagnosis of PDD is more difficult, mainly because the symptoms of memory impairment in PD patients are not prominent, and cognitive impairment is often milder not recognized by patients or even family members, or is thought to be the cause of motor impairment. This criterion emphasizes two core symptoms of PDD: (1) the diagnostic criteria of PD should be met first, and (2) there is an insidious cognitive decline and progression after the disease, with more than one area of cognitive impairment, the severity of which should impair the ability to perform daily life. The domains of cognitive impairment are mainly attention, executive, visuospatial, memory and language. In contrast to the AD diagnostic criteria, the PDD criteria do not emphasize memory impairment. One study showed that about 67% of patients with PDD complained of memory problems, compared to 100% in AD. The characteristics of memory impairment are also different between the two. There may also be behavioral abnormalities such as apathy, mood, hallucinations and delusions. Atypical Parkinson’s disease should also be excluded. Dementia with Lewy body (DLB) and PDD are often difficult to distinguish. It is controversial whether they are separate diseases or different points in a disease process. Although there are no uniform diagnostic criteria for PD-MCI, Emre et al.’s diagnostic criteria for PDD can be used as a reference when cognitive and behavioral impairments do not impair the patient’s ability to perform daily life and work. PD-MCI can be diagnosed when cognitive and behavioral deficits do not impair the patient’s ability to perform daily life and work. PD cognitive deficits have their own psychological characteristics, memory deficits are often not significant, and executive and visuospatial deficits are characteristic. The diagnosis of PD cognitive impairment is not particularly difficult when the impairment is severe enough to meet the criteria for dementia, but it is difficult to make a diagnosis at the PD-MCI stage, especially because there is no uniform diagnostic criteria for PD-MCI, which is a problem that needs to be addressed. This is a problem that needs to be addressed.