Haikal Caroline, Winston Graham M, Kaplitt Michael G
Weill Cornell Medicine, Department of Neurological Surgery, New York, NY, United States.
Aligning Science Across Parkinson's Collaborative Research Network, Chevy Chase, MD, United States.
Front Aging Neurosci. 2024 Jul 22;16:1369733. doi: 10.3389/fnagi.2024.1369733. eCollection 2024.
Cognitive impairments are a common feature of synucleinopathies such as Parkinson's Disease Dementia and Dementia with Lewy Bodies. These pathologies are characterized by accumulation of Lewy bodies and Lewy neurites as well as neuronal cell death. Alpha-synuclein is the main proteinaceous component of Lewy bodies and Lewy neurites. To model these pathologies , toxins that selectively target certain neuronal populations or different means of inducing alpha-synuclein aggregation can be used. Alpha-synuclein accumulation can be induced by genetic manipulation, viral vector overexpression or the use of preformed fibrils of alpha-synuclein. In this review, we summarize the cognitive impairments associated with different models of synucleinopathies and relevance to observations in human diseases.
认知障碍是帕金森病痴呆症和路易体痴呆症等突触核蛋白病的常见特征。这些病症的特点是路易小体和路易神经突的积累以及神经元细胞死亡。α-突触核蛋白是路易小体和路易神经突的主要蛋白质成分。为了模拟这些病症，可以使用选择性靶向某些神经元群体的毒素或诱导α-突触核蛋白聚集的不同方法。α-突触核蛋白的积累可以通过基因操作、病毒载体过表达或使用α-突触核蛋白的预形成纤维来诱导。在这篇综述中，我们总结了与不同突触核蛋白病模型相关的认知障碍以及与人类疾病观察结果的相关性。
