LRRK2: a common pathway for parkinsonism, pathogenesis and prevention?
暂无分享,去创建一个
[1] M. Farrer,et al. LRRK2 mutations are a common cause of Parkinson's disease in Spain , 2006, European journal of neurology.
[2] Irene Litvan,et al. Lrrk2 and Lewy body disease , 2006, Annals of neurology.
[3] T. Meitinger,et al. The Parkinson disease causing LRRK2 mutation I2020T is associated with increased kinase activity. , 2006, Human molecular genetics.
[4] T. Nägele,et al. Type and frequency of mutations in the LRRK2 gene in familial and sporadic Parkinson's disease*. , 2005, Brain : a journal of neurology.
[5] A. Brice,et al. Proteomic analysis of parkin knockout mice: alterations in energy metabolism, protein handling and synaptic function , 2005, Journal of neurochemistry.
[6] A. Singleton,et al. Mutations in the gene LRRK2 encoding dardarin (PARK8) cause familial Parkinson's disease: clinical, pathological, olfactory and functional imaging and genetic data. , 2005, Brain : a journal of neurology.
[7] C. Ross,et al. Parkinson's disease-associated mutations in leucine-rich repeat kinase 2 augment kinase activity. , 2005, Proceedings of the National Academy of Sciences of the United States of America.
[8] D. Selkoe,et al. Dopamine covalently modifies and functionally inactivates parkin , 2005, Nature Medicine.
[9] M. Farrer,et al. Lrrk2 pathogenic substitutions in Parkinson's disease , 2005, Neurogenetics.
[10] M. Farrer,et al. LRRK2 mutations in Parkinson disease , 2005, Neurology.
[11] K. Lim,et al. Familial-associated mutations differentially disrupt the solubility, localization, binding and ubiquitination properties of parkin. , 2005, Human molecular genetics.
[12] R. Hilker,et al. Lewy body Parkinson's disease in a large pedigree with 77 Parkin mutation carriers , 2005, Annals of neurology.
[13] Hongjun Song,et al. Accumulation of the Authentic Parkin Substrate Aminoacyl-tRNA Synthetase Cofactor, p38/JTV-1, Leads to Catecholaminergic Cell Death , 2005, The Journal of Neuroscience.
[14] Andrew J Lees,et al. Atypical unclassifiable parkinsonism on Guadeloupe: An environmental toxic hypothesis , 2005, Movement disorders : official journal of the Movement Disorder Society.
[15] A. Dürr,et al. LRRK2 haplotype analyses in European and North African families with Parkinson disease: a common founder for the G2019S mutation dating from the 13th century. , 2005, American journal of human genetics.
[16] M. Spillantini,et al. Alpha‐synuclein dysfunction in Lewy body diseases , 2005, Movement disorders : official journal of the Movement Disorder Society.
[17] B. Hyman,et al. Tau Suppression in a Neurodegenerative Mouse Model Improves Memory Function , 2005, Science.
[18] M. Farrer,et al. LRRK2 R1441G in Spanish patients with Parkinson's disease , 2005, Neuroscience Letters.
[19] Makoto Hashimoto,et al. Effects of α-Synuclein Immunization in a Mouse Model of Parkinson’s Disease , 2005, Neuron.
[20] Mark R Cookson,et al. The biochemistry of Parkinson's disease. , 2005, Annual review of biochemistry.
[21] Pasko Rakic,et al. Mixed lineage kinase–c‐jun N‐terminal kinase signaling pathway: A new therapeutic target in Parkinson's disease , 2005, Movement disorders : official journal of the Movement Disorder Society.
[22] Kazuko Hasegawa,et al. An LRRK2 mutation as a cause for the parkinsonism in the original PARK8 family , 2005, Annals of neurology.
[23] M. Feany,et al. α-Synuclein phosphorylation controls neurotoxicity and inclusion formation in a Drosophila model of Parkinson disease , 2005, Nature Neuroscience.
[24] Timothy Lynch,et al. Identification of a novel LRRK2 mutation linked to autosomal dominant parkinsonism: evidence of a common founder across European populations. , 2005, American journal of human genetics.
[25] Tom Robinson,et al. Vascular parkinsonism--an important cause of parkinsonism in older people. , 2005, Age and ageing.
[26] J. Tschopp,et al. The RIP kinases: crucial integrators of cellular stress. , 2005, Trends in biochemical sciences.
[27] C. Ross,et al. Parkin Mediates Nonclassical, Proteasomal-Independent Ubiquitination of Synphilin-1: Implications for Lewy Body Formation , 2005, The Journal of Neuroscience.
[28] Nicholas W Wood,et al. A common LRRK2 mutation in idiopathic Parkinson's disease , 2005, The Lancet.
[29] Tatiana Foroud,et al. Genetic screening for a single common LRRK2 mutation in familial Parkinson's disease , 2005, The Lancet.
[30] Vincenzo Bonifati,et al. A frequent LRRK2 gene mutation associated with autosomal dominant Parkinson's disease , 2005, The Lancet.
[31] Andrew Lees,et al. Cloning of the Gene Containing Mutations that Cause PARK8-Linked Parkinson's Disease , 2004, Neuron.
[32] Thomas Meitinger,et al. Mutations in LRRK2 Cause Autosomal-Dominant Parkinsonism with Pleomorphic Pathology , 2004, Neuron.
[33] M. Chesselet,et al. Alpha-synuclein and transgenic mouse models , 2004, Neurobiology of Disease.
[34] Giuseppe Battaglia,et al. Double-knockout mice for alpha- and beta-synucleins: effect on synaptic functions. , 2004, Proceedings of the National Academy of Sciences of the United States of America.
[35] M. Farrer,et al. α‐Synuclein promoter confers susceptibility to Parkinson's disease , 2004 .
[36] M. Farrer,et al. Linkage disequilibrium and association of MAPT H1 in Parkinson disease. , 2004, American journal of human genetics.
[37] Philippe Amouyel,et al. α-synuclein locus duplication as a cause of familial Parkinson's disease , 2004, The Lancet.
[38] J. Schulz. Neuronal pathology in Parkinson’s disease , 2004, Cell and Tissue Research.
[39] Peter T. Lansbury,et al. Impaired Degradation of Mutant α-Synuclein by Chaperone-Mediated Autophagy , 2004, Science.
[40] D. Labarthe,et al. Incidence of Amyotrophic Lateral Sclerosis and of the Parkinsonism-Dementia Complex of Guam, 1950–1989 , 2004, Neuroepidemiology.
[41] C. Haass,et al. How does parkin ligate ubiquitin to Parkinson's disease? , 2004, EMBO reports.
[42] W. Kamphorst,et al. Phenotypic Variation in Frontotemporal Dementia and Parkinsonism Linked to Chromosome 17 , 2004, Dementia and Geriatric Cognitive Disorders.
[43] David W. Miller,et al. α-Synuclein in blood and brain from familial Parkinson disease with SNCA locus triplication , 2004, Neurology.
[44] R. Nussbaum,et al. Hereditary Early-Onset Parkinson's Disease Caused by Mutations in PINK1 , 2004, Science.
[45] G. Mardon,et al. Drosophila parkin mutants have decreased mass and cell size and increased sensitivity to oxygen radical stress , 2004, Development.
[46] Joachim Klose,et al. Mitochondrial Dysfunction and Oxidative Damage in parkin-deficient Mice* , 2004, Journal of Biological Chemistry.
[47] P. Lockhart,et al. Parkin genetics: one model for Parkinson's disease. , 2004, Human molecular genetics.
[48] John Hardy,et al. CHIP and Hsp70 regulate tau ubiquitination, degradation and aggregation , 2004 .
[49] D. Goldstein,et al. UCHL1 is a Parkinson's disease susceptibility gene. , 2004 .
[50] Steven P. Gygi,et al. CHIP-Hsc70 Complex Ubiquitinates Phosphorylated Tau and Enhances Cell Survival* , 2004, Journal of Biological Chemistry.
[51] J. Hoenicka,et al. The new mutation, E46K, of α‐synuclein causes parkinson and Lewy body dementia , 2004, Annals of neurology.
[52] Matthew J. Farrer,et al. Comparison of kindreds with parkinsonism and α‐synuclein genomic multiplications , 2004 .
[53] Eugene M. Johnson,et al. Mixed-lineage kinases: a target for the prevention of neurodegeneration. , 2004, Annual review of pharmacology and toxicology.
[54] Janel O. Johnson,et al. α-Synuclein Locus Triplication Causes Parkinson's Disease , 2003, Science.
[55] Jeffrey H. Kordower,et al. The role of α-synuclein in Parkinson's disease: insights from animal models , 2003, Nature Reviews Neuroscience.
[56] R. Nussbaum,et al. Functional analysis of intra-allelic variation at NACP-Rep1 in the α-synuclein gene , 2003, Human Genetics.
[57] P. Davies,et al. Hyperphosphorylation and aggregation of tau in mice expressing normal human tau isoforms , 2003, Journal of neurochemistry.
[58] H. Payami,et al. A linkage study of candidate loci in familial Parkinson's Disease , 2003, BMC neurology.
[59] Jeremy N. Skepper,et al. α-Synuclein Is Degraded by Both Autophagy and the Proteasome* , 2003, Journal of Biological Chemistry.
[60] S. Fahn. Description of Parkinson's Disease as a Clinical Syndrome , 2003, Annals of the New York Academy of Sciences.
[61] T. Iwatsubo,et al. Accumulation of Phosphorylated α‐Synuclein in Aging Human Brain , 2003 .
[62] J. C. Greene,et al. Mitochondrial pathology and apoptotic muscle degeneration in Drosophila parkin mutants , 2003, Proceedings of the National Academy of Sciences of the United States of America.
[63] Julián Benito-León,et al. Prevalence of PD and other types of parkinsonism in three elderly populations of central Spain , 2003, Movement disorders : official journal of the Movement Disorder Society.
[64] D. Twelves,et al. Systematic review of incidence studies of Parkinson's disease , 2003, Movement disorders : official journal of the Movement Disorder Society.
[65] Patrizia Rizzu,et al. Mutations in the DJ-1 Gene Associated with Autosomal Recessive Early-Onset Parkinsonism , 2002, Science.
[66] K. Østergaard,et al. Steele‐Richardson‐Olszewski syndrome in a patient with a single C212Y mutation in the parkin protein , 2002, Movement disorders : official journal of the Movement Disorder Society.
[67] P. Lansbury,et al. The UCH-L1 Gene Encodes Two Opposing Enzymatic Activities that Affect α-Synuclein Degradation and Parkinson's Disease Susceptibility , 2002, Cell.
[68] P. Lansbury,et al. Alpha-synuclein, especially the Parkinson's disease-associated mutants, forms pore-like annular and tubular protofibrils. , 2002, Journal of molecular biology.
[69] S. Tsuji,et al. A new locus for Parkinson's disease (PARK8) maps to chromosome 12p11.2–q13.1 , 2002, Annals of neurology.
[70] E. Masliah,et al. α-Synuclein is phosphorylated in synucleinopathy lesions , 2002, Nature Cell Biology.
[71] Seung-Jae Lee,et al. Membrane-bound α-Synuclein Has a High Aggregation Propensity and the Ability to Seed the Aggregation of the Cytosolic Form* , 2002, The Journal of Biological Chemistry.
[72] K. Wada,et al. Loss of Uch-L1 and Uch-L3 leads to neurodegeneration, posterior paralysis and dysphagia. , 2001, Human molecular genetics.
[73] Joshua M. Shulman,et al. Tauopathy in Drosophila: Neurodegeneration Without Neurofibrillary Tangles , 2001, Science.
[74] N. Quinn,et al. Clinical and pathologic abnormalities in a family with parkinsonism and parkin gene mutations , 2001, Neurology.
[75] Takayuki Harada,et al. Intragenic deletion in the gene encoding ubiquitin carboxy-terminal hydrolase in gad mice , 1999, Nature Genetics.
[76] J W Langston,et al. Parkinson disease in twins: an etiologic study. , 1999, JAMA.
[77] Georg Auburger,et al. The ubiquitin pathway in Parkinson's disease , 1998, Nature.
[78] Ronald C. Petersen,et al. Association of missense and 5′-splice-site mutations in tau with the inherited dementia FTDP-17 , 1998, Nature.
[79] S. Minoshima,et al. Mutations in the parkin gene cause autosomal recessive juvenile parkinsonism , 1998, Nature.
[80] Olaf Riess,et al. AlaSOPro mutation in the gene encoding α-synuclein in Parkinson's disease , 1998, Nature Genetics.
[81] Robert L. Nussbaum,et al. Mutation in the α-Synuclein Gene Identified in Families with Parkinson's Disease , 1997 .
[82] J. Hughes,et al. Accuracy of clinical diagnosis of idiopathic Parkinson's disease: a clinico-pathological study of 100 cases. , 1992, Journal of neurology, neurosurgery, and psychiatry.
[83] A. Hofman,et al. Prognosis with Parkinson's disease in europe: A collaborative study of population-based cohorts. Neurologic Diseases in the Elderly Research Group. , 2000, Neurology.