ArticleNPJ Parkinson's disease2025
The homozygous LRRK2.p.N1437D point mutation mouse is a novel model of parkinsonism.
Lin-Hua Gan, Yi-Min Sun, Xin-Yue Zhou, Zhi-Yuan Qi, Feng-Tao Liu, Yi-Lin Tang, Wen-Bo Yu, Bao-Guo Xiao, Jian Wang, Jian-Jun Wu
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In one paragraphArticle in NPJ Parkinson's disease, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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Lin-Hua Gan *Department of Neurology and National Research Center for Aging and Medicine & National Center for Neurological Disorders, State Key Laboratory of Medical Neurobiology, Huashan Hospital, Fudan University, Shanghai, China.
Yi-Min Sun *Department of Neurology and National Research Center for Aging and Medicine & National Center for Neurological Disorders, State Key Laboratory of Medical Neurobiology, Huashan Hospital, Fudan University, Shanghai, China.
Xin-Yue ZhouDepartment of Neurology and National Research Center for Aging and Medicine & National Center for Neurological Disorders, State Key Laboratory of Medical Neurobiology, Huashan Hospital, Fudan University, Shanghai, China.
Zhi-Yuan QiDepartment of Neurology and National Research Center for Aging and Medicine & National Center for Neurological Disorders, State Key Laboratory of Medical Neurobiology, Huashan Hospital, Fudan University, Shanghai, China.
Feng-Tao LiuDepartment of Neurology and National Research Center for Aging and Medicine & National Center for Neurological Disorders, State Key Laboratory of Medical Neurobiology, Huashan Hospital, Fudan University, Shanghai, China.ORCID http://orcid.org/0000-0001-7688-1631 Yi-Lin TangDepartment of Neurology and National Research Center for Aging and Medicine & National Center for Neurological Disorders, State Key Laboratory of Medical Neurobiology, Huashan Hospital, Fudan University, Shanghai, China.ORCID http://orcid.org/0000-0003-2819-6554 Wen-Bo YuDepartment of Neurology and National Research Center for Aging and Medicine & National Center for Neurological Disorders, State Key Laboratory of Medical Neurobiology, Huashan Hospital, Fudan University, Shanghai, China.
Bao-Guo XiaoDepartment of Neurology and National Research Center for Aging and Medicine & National Center for Neurological Disorders, State Key Laboratory of Medical Neurobiology, Huashan Hospital, Fudan University, Shanghai, China.
Jian WangDepartment of Neurology and National Research Center for Aging and Medicine & National Center for Neurological Disorders, State Key Laboratory of Medical Neurobiology, Huashan Hospital, Fudan University, Shanghai, China. wangjian_hs@fudan.edu.cn.ORCID http://orcid.org/0000-0002-2748-395X Jian-Jun WuDepartment of Neurology and National Research Center for Aging and Medicine & National Center for Neurological Disorders, State Key Laboratory of Medical Neurobiology, Huashan Hospital, Fudan University, Shanghai, China. wujianjun@fudan.edu.cn.ORCID http://orcid.org/0000-0001-6438-6334 Funding
China Postdoctoral Science Foundation 2022M710742National Natural Science Foundation of China (National Science Foundation of China) 82171421National Natural Science Foundation of China (National Science Foundation of China) 82201406National Natural Science Foundation of China (National Science Foundation of China) 82271511National Natural Science Foundation of China (National Science Foundation of China) 82371261National Natural Science Foundation of China (National Science Foundation of China) 82371432National Natural Science Foundation of China (National Science Foundation of China) 92249302
6 · The paper itselfAbstract
The leucine-rich repeat kinase 2 (LRRK2) gene is one of the most common genetic causes of autosomal dominant Parkinson's disease (PD) and a common genetic risk factor for sporadic PD. However, aged mice with common LRRK2 point mutations fail to exhibit age-related PD-associated behavioral and pathological impairments. We generated a novel mouse model harboring the LRRK2.p.N1437D point mutation (c.4309 A > G; NM_98578). Here, the homozygous N1437D mutation, but not the heterozygous mutation, led to an increase in the autophosphorylation, substrate phosphorylation, and GTP-binding capacity of LRRK2. Heterozygous N1437D mice also showed unaffected behavior and pathology while the homozygous mice exhibited PD-associated behavioral change at 25-26 months, dopamine system damage, lipofuscin accumulation, and lipid peroxidation in substantia nigra dopaminergic neurons at 26-27 months. The new N1437D point mutation mouse does not require LRRK2 overexpression and may better mimic the pathological characteristics of LRRK2 mutation in the ROC-COR region.
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PMID40155632
PMCPMC11953335
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