Department of Neuroscience, Division of Pharmacology, Reproductive and Dentistry Sciences, School of Medicine, Federico II University of Naples, Via Pansini 5, 80131 Naples, Italy.
Department of Translational Medicine, Federico II University of Naples, 80138 Napoli, Italy.
Int J Mol Sci. 2024 Oct 25;25(21):11490. doi: 10.3390/ijms252111490.
Among the non-motor symptoms associated with Parkinson's disease (PD), cognitive impairment is one of the most common and disabling. It can occur either early or late during the disease, and it is heterogeneous in terms of its clinical manifestations, such as Subjective Cognitive Dysfunction (SCD), Mild Cognitive Impairment (MCI), and Parkinson's Disease Dementia (PDD). The aim of the present review is to delve deeper into the molecular mechanisms underlying cognitive decline in PD. This is extremely important to delineate the guidelines for the differential diagnosis and prognosis of the dysfunction, to identify the molecular and neuronal mechanisms involved, and to plan therapeutic strategies that can halt cognitive impairment progression. Specifically, the present review will discuss the pathogenetic mechanisms involved in the progression of cognitive impairment in PD, with attention to mitochondria and their contribution to synaptic dysfunction and neuronal deterioration in the brain regions responsible for non-motor manifestations of the disease.
在与帕金森病（PD）相关的非运动症状中，认知障碍是最常见和最具致残性的症状之一。它可以在疾病的早期或晚期发生，并且在临床表现方面具有异质性，如主观认知障碍（SCD）、轻度认知障碍（MCI）和帕金森病痴呆（PDD）。本综述的目的是深入探讨 PD 认知下降的分子机制。这对于划定认知障碍功能障碍的鉴别诊断和预后的指导方针、确定涉及的分子和神经元机制以及规划可以阻止认知障碍进展的治疗策略非常重要。具体来说，本综述将讨论 PD 认知障碍进展中涉及的发病机制，重点关注线粒体及其对大脑中负责疾病非运动表现的区域中突触功能障碍和神经元恶化的贡献。
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