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Aplp1 interacts with Lag3 to facilitate transmission of pathologic α-synuclein

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机构： [1]Neuroregeneration and Stem Cell Programs, Institute for Cell Engineering, Johns Hopkins University School of Medicine, Baltimore, MD 21205, USA. [2]Department of Neurology, Johns Hopkins University School of Medicine, Baltimore, MD 21205, USA. [3]Adrienne Helis Malvin Medical Research Foundation, New Orleans, LA 70130-2685, USA. [4]Interdisciplinary Research Center on Biology and Chemistry, Shanghai Institute of Organic Chemistry, Chinese Academy of Sciences, 26 Qiuyue Road, Shanghai 201210, China. [5]University of the Chinese Academy of Sciences, 19 A Yuquan Road, Shijingshan District, Beijing 100049, China. [6]Institute for NanoBioTechnology, Johns Hopkins University, Baltimore, MD 21218, USA. [7]Department of Materials Science and Engineering, Whiting School of Engineering, Johns Hopkins University, Baltimore, MD 21218, USA. [8]Department of Bioengineering, Nagaoka University of Technology, 1603- 1 Kamitomiokamachi, Nagaoka, Niigata 940-2188, Japan. [9]Institute for Pharmacy and Molecular Biotechnology IPMB, Department of Functional Genomics, University of Heidelberg, Im Neuenheimer Feld 364, 69120 Heidelberg, Germany. [10]Hugo W. Moser Research Institute at Kennedy Krieger, 707 North Broadway, Baltimore, MD 21205, USA. [11]Department of Immunology, University of Pittsburgh School of Medicine, Pittsburgh, PA 15261, USA. [12]Tumor Microenvironment Center, UPMC Hillman Cancer Center, Pittsburgh, PA 15232, USA. [13]Department of Physiology, Johns Hopkins University School of Medicine, Baltimore, MD 21205, USA. [14]Solomon H. Snyder Department of Neuroscience, Johns Hopkins University School of Medicine, Baltimore, MD 21205, USA. [15]Department of Pharmacology and Molecular Sciences, Johns Hopkins University School of Medicine, Baltimore, MD 21205, USA. [16]Department of Neurology, Nanjing Brain Hospital, Nanjing, Jiangsu 210029, PR China. [17]Medical College, Yangzhou University, Yangzhou, Jiangsu 225001, PR China. [18]Department of Anesthesiology, West China Hospital, Sichuan University. The Research Units of West China (2018RU012)-Chinese Academy of Medical Sciences, West China Hospital, Sichuan University, Chengdu, Sichuan 610041, PR China. [19]Department of Brain and Cognitive Sciences, Massachusetts Institute of Technology, Cambridge, MA 02139, USA. [20]Department of Pharmacology, College of Medicine, Dong-A University, 32 Daesin Gongwwon-ro, Seo-gu, Busan 49201, Republic of Korea. [21]Department of Biological Science and Biotechnology, Chungbuk National University, Cheongju, Chungbuk 28644, Republic of Korea. [22]Department of Physiology, School of Basic Medical Sciences (Institute of Basic Medical Sciences), Shandong First Medical University & Shandong Academy of Medical Sciences, Jinan 250000, China. [23]Picower Institute for Learning and Memory, Cambridge, MA 02139, USA. [24]Harvard-MIT

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Pathologic α-synuclein (α-syn) spreads from cell-to-cell, in part, through binding to the lymphocyte-activation gene 3 (Lag3). Here we report that amyloid β precursor-like protein 1 (Aplp1) interacts with Lag3 that facilitates the binding, internalization, transmission, and toxicity of pathologic α-syn. Deletion of both Aplp1 and Lag3 eliminates the loss of dopaminergic neurons and the accompanying behavioral deficits induced by α-syn preformed fibrils (PFF). Anti-Lag3 prevents the internalization of α-syn PFF by disrupting the interaction of Aplp1 and Lag3, and blocks the neurodegeneration induced by α-syn PFF in vivo. The identification of Aplp1 and the interplay with Lag3 for α-syn PFF induced pathology deepens our insight about molecular mechanisms of cell-to-cell transmission of pathologic α-syn and provides additional targets for therapeutic strategies aimed at preventing neurodegeneration in Parkinson's disease and related α-synucleinopathies.© 2024. The Author(s).

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第一作者：

第一作者机构： [1]Neuroregeneration and Stem Cell Programs, Institute for Cell Engineering, Johns Hopkins University School of Medicine, Baltimore, MD 21205, USA. [2]Department of Neurology, Johns Hopkins University School of Medicine, Baltimore, MD 21205, USA. [3]Adrienne Helis Malvin Medical Research Foundation, New Orleans, LA 70130-2685, USA.

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通讯作者：

通讯机构： [1]Neuroregeneration and Stem Cell Programs, Institute for Cell Engineering, Johns Hopkins University School of Medicine, Baltimore, MD 21205, USA. [2]Department of Neurology, Johns Hopkins University School of Medicine, Baltimore, MD 21205, USA. [3]Adrienne Helis Malvin Medical Research Foundation, New Orleans, LA 70130-2685, USA. [13]Department of Physiology, Johns Hopkins University School of Medicine, Baltimore, MD 21205, USA. [14]Solomon H. Snyder Department of Neuroscience, Johns Hopkins University School of Medicine, Baltimore, MD 21205, USA. [15]Department of Pharmacology and Molecular Sciences, Johns Hopkins University School of Medicine, Baltimore, MD 21205, USA.

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