Loss of leucine-rich repeat kinase 2 causes impairment of protein degradation pathways, accumulation of α-synuclein, and apoptotic cell death in aged mice

نویسندگان

  • Youren Tong
  • Hiroo Yamaguchi
  • Emilie Giaime
  • Scott Boyle
  • Raphael Kopan
  • Raymond J. Kelleher
  • Jie Shen
چکیده

Center for Neurologic Diseases, Department of Neurology, Brigham and Women’s Hospital, Program in Neuroscience, Harvard Medical School, Boston, MA 02115; Department of Developmental Biology, Washington University School of Medicine, St. Louis, MO 63110; and Center for Human Genetic Research, Department of Neurology, Massachusetts General Hospital, Program in Neuroscience, Harvard Medical School, Boston, MA 02115

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منابع مشابه

Loss of leucine-rich repeat kinase 2 causes impairment of protein degradation pathways, accumulation of alpha-synuclein, and apoptotic cell death in aged mice.

Mutations in leucine-rich repeat kinase 2 (LRRK2) are the most common genetic cause of Parkinson's disease. LRRK2 is a large protein containing a small GTPase domain and a kinase domain, but its physiological role is unknown. To identify the normal function of LRRK2 in vivo, we generated two independent lines of germ-line deletion mice. The dopaminergic system of LRRK2(-/-) mice appears normal,...

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Leucine-Rich Repeat Kinase 2 Regulates the Progression of Neuropathology Induced by Parkinson's-Disease-Related Mutant α-synuclein

Mutations in alpha-synuclein and Leucine-rich repeat kinase 2 (LRRK2) are linked to autosomal dominant forms of Parkinson's disease (PD). However, little is known about any potential pathophysiological interplay between these two PD-related genes. Here we show in transgenic mice that although overexpression of LRRK2 alone did not cause neurodegeneration, the presence of excess LRRK2 greatly acc...

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Mutations in the leucine-rich repeat kinase 2 (LRRK2) gene are the most common genetic cause of Parkinson's disease. Here, we investigated whether the G2019S LRRK2 mutation causes morphological and/or functional changes at nigro-striatal dopamine neurons. Density of striatal dopaminergic terminals, nigral cell counts, tyrosine hydroxylase protein levels as well as exocytotic dopamine release me...

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تاریخ انتشار 2010