Eye movements in genetic parkinsonisms affecting the α-synuclein, PARK9, and manganese network
暂无分享,去创建一个
[1] M. Aschner,et al. Untangling the Manganese-α-Synuclein Web , 2016, Front. Neurosci..
[2] B. Gaymard,et al. Eye Movements in Ephedrone-Induced Parkinsonism , 2014, PloS one.
[3] B. Oostra,et al. Mutations in SLC30A10 cause parkinsonism and dystonia with hypermanganesemia, polycythemia, and chronic liver disease. , 2012, American journal of human genetics.
[4] Masaya Segawa,et al. Initiation and inhibitory control of saccades with the progression of Parkinson's disease – Changes in three major drives converging on the superior colliculus , 2011, Neuropsychologia.
[5] A. Sprenger,et al. Eye movement disorders in ATP13A2 mutation carriers (PARK9) , 2010, Movement disorders : official journal of the Movement Disorder Society.
[6] S. Pappatà,et al. Novel ATP13A2 (PARK9) homozygous mutation in a family with marked phenotype variability , 2010, neurogenetics.
[7] S. Lindquist,et al. α-Synuclein is part of a diverse and highly conserved interaction network that includes PARK9 and manganese toxicity , 2009, Nature Genetics.
[8] Jan Gründemann,et al. Hereditary parkinsonism with dementia is caused by mutations in ATP13A2, encoding a lysosomal type 5 P-type ATPase , 2006, Nature Genetics.
[9] A. Lees,et al. Kufor Rakeb Disease: Autosomal recessive, levodopa‐responsive parkinsonism with pyramidal degeneration, supranuclear gaze palsy, and dementia , 2005, Movement disorders : official journal of the Movement Disorder Society.
[10] Douglas C. Miller,et al. A large kindred with autosomal dominant Parkinson's disease , 1990, Annals of neurology.