- Modeling α-Synuclein Propagation with Preformed Fibril Injections
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Hyun Kyung Chung, Hoang-Anh Ho, Dayana Pérez-Acuña, Seung-Jae Lee
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J Mov Disord. 2020;13(1):77-79. Published online October 14, 2019
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DOI: https://doi.org/10.14802/jmd.19046.e
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Corrects: J Mov Disord 2019;12(3):139
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- Modeling α-Synuclein Propagation with Preformed Fibril Injections
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Hyun Kyung Chung, Hoang-Anh Ho, Dayana Pérez-Acuña, Seung-Jae Lee
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J Mov Disord. 2019;12(3):139-151. Published online September 30, 2019
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DOI: https://doi.org/10.14802/jmd.19046
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Correction in: J Mov Disord 2020;13(1):77
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Abstract
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- The aggregation of α-synuclein (α-syn) has been implicated in the pathogenesis of many neurodegenerative disorders, including Parkinson’s disease (PD), dementia with Lewy bodies (DLB), and multiple system atrophy (MSA). Postmortem analyses of α-syn pathology, especially that of PD, have suggested that aggregates progressively spread from a few discrete locations to wider brain regions. The neuron-to-neuron propagation of α-syn has been suggested to be the underlying mechanism by which aggregates spread throughout the brain. Many cellular and animal models has been created to study cell-to-cell propagation. Recently, it has been shown that a single injection of preformed fibrils (PFFs) made of recombinant α-syn proteins into various tissues and organs of many different animal species results in widespread α-syn pathology in the central nervous system (CNS). These PFF models have been extensively used to study the mechanism by which aggregates spread throughout the brain. Here, we review what we have learned from PFF models, describe the nature of PFFs and the neuropathological features, neurophysiological characteristics, and behavioral outcomes of the models.
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- Mechanism of Anti-α-Synuclein Immunotherapy
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Jun Sung Lee, Seung-Jae Lee
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J Mov Disord. 2016;9(1):14-19. Published online January 25, 2016
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DOI: https://doi.org/10.14802/jmd.15059
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- Immunization therapy targeting α-synuclein has emerged as a promising approach for Parkinson’s disease and perhaps for other synucleinopathies. Several antibodies have shown therapeutic effects in mouse models of synucleinopathies and have alleviated the pathological and behavioral phenotypes of these mice. The mechanisms through which the immunization therapy works were initially puzzling, especially given that α-synuclein is a typical cytosolic protein. Recent studies, however, suggested that extracellular α-synuclein is an important pathogenic entity, and hence, a target for immunotherapy. Here, we review the literature describing immunization therapy for synucleinopathies in mouse models and provide current thoughts on the potential mechanisms underlying the therapeutic effects of α-synuclein immunotherapy.
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