Parkinson disease (PD) is the second most common neurodegenerative disorder, affecting >1% of the population ≥65 years of age and with a prevalence set to double by 2030. In addition to the defining motor symptoms of PD, multiple non-motor symptoms occur; among them, cognitive impairment is common and can potentially occur at any disease stage. Cognitive decline is usually slow and insidious, but rapid in some cases. Recently, the focus has been on the early cognitive changes, where executive and visuospatial impairments are typical and can be accompanied by memory impairment, increasing the risk for early progression to dementia. Other risk factors for early progression to dementia include visual hallucinations, older age and biomarker changes such as cortical atrophy, as well as Alzheimer-type changes on functional imaging and in cerebrospinal fluid, and slowing and frequency variation on EEG. However, the mechanisms underlying cognitive decline in PD remain largely unclear. Cortical involvement of Lewy body and Alzheimer-type pathologies are key features, but multiple mechanisms are likely involved. Cholinesterase inhibition is the only high-level evidence-based treatment available, but other pharmacological and non-pharmacological strategies are being tested. Challenges include the identification of disease-modifying therapies as well as finding biomarkers to better predict cognitive decline and identify patients at high risk for early and rapid cognitive impairment.

帕金森病 (PD) 是第二大最常见的神经退行性疾病，影响超过 1% 的 65 岁以上人群，到 2030 年患病率将增加一倍。 除了 PD 的运动症状外，多种非运动症状发生; 其中，认知障碍很常见，并且可能发生在任何疾病阶段。认知衰退通常是缓慢而隐匿的，但在某些情况下会迅速。最近，重点一直放在早期认知变化上，其中执行和视觉空间障碍是典型的，并且可能伴有记忆障碍，增加了早期进展为痴呆症的风险。早期进展为痴呆症的其他风险因素包括视幻觉、老年和生物标志物变化，如皮质萎缩、以及功能成像和脑脊液的阿尔茨海默型变化，以及脑电图的减慢和频率变化。然而，PD 认知能力下降的潜在机制在很大程度上仍不清楚。路易体和阿尔茨海默型病理的皮质受累是关键特征，但可能涉及多种机制。胆碱酯酶抑制是唯一可用的高水平循证治疗，但其他药理学和非药理学策略正在测试中。挑战包括确定疾病修饰疗法以及寻找生物标志物以更好地预测认知能力下降并识别早期和快速认知障碍的高风险患者。路易体和阿尔茨海默型病理的皮质受累是关键特征，但可能涉及多种机制。胆碱酯酶抑制是唯一可用的高水平循证治疗，但其他药理学和非药理学策略正在测试中。挑战包括确定疾病修饰疗法以及寻找生物标志物以更好地预测认知能力下降并识别早期和快速认知障碍的高风险患者。路易体和阿尔茨海默型病理的皮质受累是关键特征，但可能涉及多种机制。胆碱酯酶抑制是唯一可用的高水平循证治疗，但其他药理学和非药理学策略正在测试中。挑战包括确定疾病修饰疗法以及寻找生物标志物以更好地预测认知能力下降并识别早期和快速认知障碍的高风险患者。