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No alterations in α-synuclein gene dosage observed in sporadic Parkinson's disease

2006; Wiley; Volume: 21; Issue: 5 Linguagem: Inglês

10.1002/mds.20863

1531-8257

Caroline H. Williams‐Gray, An Goris, Thomas Foltynie, Joanne Brown, Melanie Maranian, Amie Walton, D. A. S. Compston, Stephen Sawcer, Roger A. Barker,

Nuclear Receptors and Signaling

Movement DisordersVolume 21, Issue 5 p. 731-732 Letter to the Editor No alterations in α-synuclein gene dosage observed in sporadic Parkinson's disease Caroline H. Williams-Gray MRCP, Caroline H. Williams-Gray MRCP [email protected] Cambridge Centre for Brain Repair, Department of Clinical Neurosciences, University of Cambridge, Cambridge, United KingdomSearch for more papers by this authorAn Goris PhD, An Goris PhD Neurology Unit, Department of Clinical Neurosciences, University of Cambridge, Cambridge, United Kingdom Laboratory for Clinical and, Experimental Neurology, Katholieke Universiteit Leuven, Leuven, BelgiumSearch for more papers by this authorThomas Foltynie PhD, MRCP, Thomas Foltynie PhD, MRCP Cambridge Centre for Brain Repair, Department of Clinical Neurosciences, University of Cambridge, Cambridge, United KingdomSearch for more papers by this authorJoanne Brown BA(Hons), Joanne Brown BA(Hons) Cambridge Centre for Brain Repair, Department of Clinical Neurosciences, University of Cambridge, Cambridge, United KingdomSearch for more papers by this authorMelanie Maranian, Melanie Maranian Neurology Unit, Department of Clinical Neurosciences, University of Cambridge, Cambridge, United KingdomSearch for more papers by this authorAmie Walton BSc(Hons), Amie Walton BSc(Hons) Neurology Unit, Department of Clinical Neurosciences, University of Cambridge, Cambridge, United KingdomSearch for more papers by this authorD. Alastair Compston PhD, FRCP, D. Alastair Compston PhD, FRCP Neurology Unit, Department of Clinical Neurosciences, University of Cambridge, Cambridge, United KingdomSearch for more papers by this authorStephen J. Sawcer PhD, MRCP, Stephen J. Sawcer PhD, MRCP Neurology Unit, Department of Clinical Neurosciences, University of Cambridge, Cambridge, United KingdomSearch for more papers by this authorRoger A. Barker PhD, MRCP, Roger A. Barker PhD, MRCP Cambridge Centre for Brain Repair, Department of Clinical Neurosciences, University of Cambridge, Cambridge, United KingdomSearch for more papers by this author Caroline H. Williams-Gray MRCP, Caroline H. Williams-Gray MRCP [email protected] Cambridge Centre for Brain Repair, Department of Clinical Neurosciences, University of Cambridge, Cambridge, United KingdomSearch for more papers by this authorAn Goris PhD, An Goris PhD Neurology Unit, Department of Clinical Neurosciences, University of Cambridge, Cambridge, United Kingdom Laboratory for Clinical and, Experimental Neurology, Katholieke Universiteit Leuven, Leuven, BelgiumSearch for more papers by this authorThomas Foltynie PhD, MRCP, Thomas Foltynie PhD, MRCP Cambridge Centre for Brain Repair, Department of Clinical Neurosciences, University of Cambridge, Cambridge, United KingdomSearch for more papers by this authorJoanne Brown BA(Hons), Joanne Brown BA(Hons) Cambridge Centre for Brain Repair, Department of Clinical Neurosciences, University of Cambridge, Cambridge, United KingdomSearch for more papers by this authorMelanie Maranian, Melanie Maranian Neurology Unit, Department of Clinical Neurosciences, University of Cambridge, Cambridge, United KingdomSearch for more papers by this authorAmie Walton BSc(Hons), Amie Walton BSc(Hons) Neurology Unit, Department of Clinical Neurosciences, University of Cambridge, Cambridge, United KingdomSearch for more papers by this authorD. Alastair Compston PhD, FRCP, D. Alastair Compston PhD, FRCP Neurology Unit, Department of Clinical Neurosciences, University of Cambridge, Cambridge, United KingdomSearch for more papers by this authorStephen J. Sawcer PhD, MRCP, Stephen J. Sawcer PhD, MRCP Neurology Unit, Department of Clinical Neurosciences, University of Cambridge, Cambridge, United KingdomSearch for more papers by this authorRoger A. Barker PhD, MRCP, Roger A. Barker PhD, MRCP Cambridge Centre for Brain Repair, Department of Clinical Neurosciences, University of Cambridge, Cambridge, United KingdomSearch for more papers by this author First published: 21 March 2006 https://doi.org/10.1002/mds.20863Citations: 4Read the full textAboutPDF ToolsRequest permissionExport citationAdd to favoritesTrack citation ShareShare Give accessShare full text accessShare full-text accessPlease review our Terms and Conditions of Use and check box below to share full-text version of article.I have read and accept the Wiley Online Library Terms and Conditions of UseShareable LinkUse the link below to share a full-text version of this article with your friends and colleagues. Learn more.Copy URL Share a linkShare onEmailFacebookTwitterLinkedInRedditWechat No abstract is available for this article. References 1 Berg D, Niwar M, Maass S, et al. Alpha-synuclein and Parkinson's disease: implications from the screening of more than 1,900 patients. Mov Disord 2005; 20: 1191–1194. 2 Chartier-Harlin MC, Kachergus J, Roumier C, et al. Alpha-synuclein locus duplication as a cause of familial Parkinson's disease. Lancet 2004; 364: 1167–1169. 3 Ibanez P, Bonnet AM, Debarges B, et al. Causal relation between alpha-synuclein gene duplication and familial Parkinson's disease. Lancet 2004; 364: 1169–1171. 4 Singleton AB, Farrer M, Johnson J, et al. Alpha-synuclein locus triplication causes Parkinson's disease. Science 2003; 302: 841. 5 Farrer M, Kachergus J, Forno L, et al. Comparison of kindreds with parkinsonism and alpha-synuclein genomic multiplications. Ann Neurol 2004; 55: 174–179. 6 Livak KJ, Schmittgen TD. Analysis of relative gene expression data using real-time quantitative PCR and the 2(-delta delta C(T)) method. Methods 2001; 25: 402–408. 7 Johnson J, Hague SM, Hanson M, et al. SNCA multiplication is not a common cause of Parkinson disease or dementia with Lewy bodies. Neurology 2004; 63: 554–556. 8 Hope AD, Myhre R, Kachergus J, et al. Alpha-synuclein missense and multiplication mutations in autosomal dominant Parkinson's disease. Neurosci Lett 2004; 367: 97–100. 9 Gispert S, Trenkwalder C, Mota-Vieira L, Kostic V, Auburger G. Failure to find alpha-synuclein gene dosage changes in 190 patients with familial Parkinson disease. Arch Neurol 2005; 62: 96–98. 10 Lockhart PJ, Kachergus J, Lincoln S, et al. Multiplication of the alpha-synuclein gene is not a common disease mechanism in Lewy body disease. J Mol Neurosci 2004; 24: 337–342. 11 Mellick GD, Maraganore DM, Silburn PA. Australian data and meta-analysis lend support for alpha-synuclein (NACP-Rep1) as a risk factor for Parkinson's disease. Neurosci Lett 2005; 375: 112–116. Citing Literature Volume21, Issue5May 2006Pages 731-732 ReferencesRelatedInformation