Log in / Register
Home arrow Health arrow Cognitive impairment and dementia in Parkinson disease


Dementia is more frequently observed in autosomal dominant forms of PD (particularly in cases caused by SNCA mutation) than in the recessive forms. The genetic basis of dementia occurring in apparently sporadic PD is less well understood, with variability in APOE and GBA being the most consistent genetic risk factors. The primary goal of disease genetics is to shed light onto the molecular aetiology of disease with an eye toward defining potential points for therapeutic intervention. Clearly there has been substantial progress in the genetics of PD (and implicitly PD-D); however, there is still a long way to go. The tools are now at hand to achieve a more complete understanding of the genetic basis of common complex diseases, including PD-D. Not only will a more complete genetic understanding of these diseases inform us about aetiology, but it is also likely to add more clarity to the idea that this disease is aetiologically similar to DLB and AD. There will certainly be challenges to a successful dissection of the genetic basis of PD-D, perhaps the most immediate of which is that of achieving sufficient sample size to detect and confirm a genuine genetic association; however, for the first time the route to success is relatively clear.


  • 1. Kitada T, Asakawa S, Hattori N, et al. Mutations in the parkin gene cause autosomal recessive juvenile parkinsonism. Nature 1998; 392: 605-8.
  • 2. Valente EM, Abou-Sleiman PM, Caputo V, et al. Hereditary early-onset Parkinson’s disease caused by mutations in PINK1. Science 2004; 304: 1158-60.
  • 3. Bonifati V, Rizzu P, van Baren MJ, et al. Mutations in the DJ-1 gene associated with autosomal recessive early-onset parkinsonism. Science 2003; 299: 256-9.
  • 4. Zimprich A, Benet-Pages A, Struhal W, et al. A mutation in VPS35, encoding a subunit of the ret- romer complex, causes late-onset Parkinson disease. Am J Hum Genet 2011; 89: 168-75.
  • 5. Vilarino-Guell C, Wider C, Ross OA, et al., VPS35 mutations in Parkinson disease. Am J Hum Genet 2011; 89: 162-7.
  • 6. Deng H, Gao K, Jankovic J. The VPS35 gene and Parkinson’s disease. Mov Disord 2013; 28: 569-75.
  • 7. Sharma M, Ioannidis JP, Aasly JO, et al. A multi-centre clinico-genetic analysis of the VPS35 gene in Parkinson disease indicates reduced penetrance for disease-associated variants. J Med Genet 2012; 49: 721-6.
  • 8. Polymeropoulos MH, Higgins JJ, Golbe LI, et al. Mapping of a gene for Parkinson’s disease to chromosome 4q21-q23. Science 1996; 274: 1197-9.
  • 9. Polymeropoulos MH, Lavedan C, Leroy E, et al., Mutation in the alpha-synuclein gene identified in families with Parkinson’s disease. Science 1997; 276: 2045-7.
  • 10. Spillantini MG, Schmidt ML, Lee VM, et al. Alpha-synuclein in Lewy bodies. Nature 1997; 388: 839-40.
  • 11. Kruger R, Kuhn W, Muller T, et al. Ala30Pro mutation in the gene encoding alpha-synuclein in Parkinson’s disease. Nat Genet 1998; 18: 106-8.
  • 12. Zarranz JJ, Alegre J, Gomez-Esteban JC, et al. The new mutation, E46K, of alpha-synuclein causes Parkinson and Lewy body dementia. Ann Neurol 2004; 55: 164-73.
  • 13. Proukakis C, Dudzik CG, Brier T, et al. A novel alpha-synuclein missense mutation in Parkinson disease. Neurology 2013; 80: 1062-4.
  • 14. Kiely AP, Asi YT, Kara E, et al. Alpha-synucleinopathy associated with G51D SNCA mutation: a link between Parkinson’s disease and multiple system atrophy? Acta Neuropathol 2013; 125: 753-69.
  • 15. Singleton AB, Farrer M, Johnson J, et al. Alpha-synuclein locus triplication causes Parkinson’s disease. Science 2003; 302: 841.
  • 16. Chartier-Harlin MC, Kachergus J, Roumier C, et al. Alpha-synuclein locus duplication as a cause of familial Parkinson’s disease. Lancet 2004; 364: 1167-9.
  • 17. Farrer M, Kachergus J, Forno L, et al. Comparison of kindreds with parkinsonism and alpha- synuclein genomic multiplications. Ann Neurol 2004; 55: 174-9.
  • 18. Gwinn-Hardy K, Mehta ND, Farrer M, et al. Distinctive neuropathology revealed by alpha-synuclein antibodies in hereditary parkinsonism and dementia linked to chromosome 4p. Acta Neuropathol 2000; 99: 663-72.
  • 19. Kruger R, Kuhn W, Leenders KL, et al. Familial parkinsonism with synuclein pathology: clinical and PET studies of A30P mutation carriers. Neurology 2001; 56: 1355-62.
  • 20. Appel-Cresswell S, Vilarino-Guell C, Encarnacion M, et al. Alpha-synuclein p.H50Q, a novel pathogenic mutation for Parkinson’s disease. Mov Disord 2013; 28: 811-13.
  • 21. Tokutake T, Ishikawa A, Yoshimura N, et al. Clinical and neuroimaging features of patient with early-onset Parkinson’s disease with dementia carrying SNCA p.G51D mutation. Parkinsonism Relat Disord 2014; 20: 262-4.
  • 22. Lesage S, Anheim M, Letournel F, et al. G51D alpha-synuclein mutation causes a novel parkinsonian- pyramidal syndrome. Ann Neurol 2013; 73: 459-71.
  • 23. Markopoulou K, Wszolek ZK, Pfeiffer RF. A Greek-American kindred with autosomal dominant, levodopa-responsive parkinsonism and anticipation. Ann Neurol 1995; 38: 373-8.
  • 24. Markopoulou K, Wszolek ZK, Pfeiffer RF, et al. Reduced expression of the G209A alpha-synuclein allele in familial Parkinsonism. Ann Neurol 1999; 46: 374-81.
  • 25. Spira PJ, Sharpe DM, Halliday G, et al. Clinical and pathological features of a Parkinsonian syndrome in a family with an Ala53Thr alpha-synuclein mutation. Ann Neurol 2001; 49: 313-19.
  • 26. Bostantjopoulou S, Katsarou Z, Papadimitriou A, et al. Clinical features of parkinsonian patients with the alpha-synuclein (G209A) mutation. Mov Disord 2001; 16: 1007-13.
  • 27. Papapetropoulos S, Paschalis C, Athanassiadou A, et al. Clinical phenotype in patients with alpha- synuclein Parkinson’s disease living in Greece in comparison with patients with sporadic Parkinson’s disease. J Neurol Neurosurg Psychiatry 2001; 70: 662-5.
  • 28. Ahn TB, Kim SY, Kim JY, et al., Alpha-synuclein gene duplication is present in sporadic Parkinson disease. Neurology 2008; 70: 43-9.
  • 29. Ibanez P, Bonnet AM, Debarges B, et al. Causal relation between alpha-synuclein gene duplication and familial Parkinson’s disease. Lancet 2004; 364: 1169-71.
  • 30. Nishioka K, Hayashi S, Farrer MJ, et al. Clinical heterogeneity of alpha-synuclein gene duplication in Parkinson’s disease. Ann Neurol 2006; 59: 298-309.
  • 31. Fuchs J, Nilsson C, Kachergus J, et al. Phenotypic variation in a large Swedish pedigree due to SNCA duplication and triplication. Neurology 2007; 68: 916-22.
  • 32. Ikeuchi T, Kakita A, Shiga A, et al. Patients homozygous and heterozygous for SNCA duplication in a family with parkinsonism and dementia. Arch Neurol 2008; 65: 514-19.
  • 33. Obi T, Nishioka K, Ross OA, et al. Clinicopathologic study of a SNCA gene duplication patient with Parkinson disease and dementia. Neurology 2008; 70: 238-41.
  • 34. Ross OA, Braithwaite AT, Skipper LM, et al. Genomic investigation of alpha-synuclein multiplication and parkinsonism. Ann Neurol 2008; 63: 743-50.
  • 35. Uchiyama T, Ikeuchi T, Ouchi Y, et al. Prominent psychiatric symptoms and glucose hypometabo- lism in a family with a SNCA duplication. Neurology 2008; 71: 1289-91.
  • 36. Nishioka K, Ross OA, Ishii K, et al. Expanding the clinical phenotype of SNCA duplication carriers. Mov Disord 2009; 24: 1811-19.
  • 37. Sironi F, Trotta L, Antonini A, et al. Alpha-synuclein multiplication analysis in Italian familial Parkinson disease. Parkinsonism Relat Disord 2010; 16: 228-31.
  • 38. Shin CW, Kim HJ, Park SS, et al. Two Parkinson’s disease patients with alpha-synuclein gene duplication and rapid cognitive decline. Mov Disord 2010; 25: 957-9.
  • 39. Itokawa K, Sekine T, Funayama M, et al., A case of alpha-synuclein gene duplication presenting with head-shaking movements. Mov Disord 2013; 28: 384-7.
  • 40. Muenter MD, Forno LS, Hornykiewicz O, et al., Hereditary form of parkinsonism-dementia. Ann Neurol 1998; 43: 768-81.
  • 41. Sekine T, Kagaya H, Funayama M, et al. Clinical course of the first Asian family with Parkinsonism related to SNCA triplication. Mov Disord 2010; 25: 2871-5.
  • 42. Gwinn K, Devine MJ, Jin LW, et al. Clinical features, with video documentation, of the original familial Lewy body parkinsonism caused by alpha-synuclein triplication (Iowa kindred). Mov Disord 2011; 26: 2134-6.
  • 43. Kojovic M, Sheerin UM, Rubio-Agusti I, et al. Young-onset parkinsonism due to homozygous duplication of alpha-synuclein in a consanguineous family. Mov Disord 2012; 27: 1827-9.
  • 44. Kasten M, Klein C. The many faces of alpha-synuclein mutations. Mov Disord 2013; 28: 697-701.
  • 45. Cookson MR, Dauer W, Dawson T, et al. The roles of kinases in familial Parkinson’s disease. J Neuro- sci 2007; 27: 11865-8.
  • 46. Paisan-Ruiz C, Jain S, Evans EW, et al. Cloning of the gene containing mutations that cause PARK8- linked Parkinson’s disease. Neuron 2004; 44: 595-600.
  • 47. Zimprich A, Biskup S, Leitner P, et al. Mutations in LRRK2 cause autosomal-dominant parkinsonism with pleomorphic pathology. Neuron 2004; 44: 601-7.
  • 48. Farrer M, Stone J, Mata IF, et al. LRRK2 mutations in Parkinson disease. Neurology 2005; 65: 738-40.
  • 49. Bras JM, Guerreiro RJ, Ribeiro MH, et al. G2019S dardarin substitution is a common cause of Parkinson’s disease in a Portuguese cohort. Mov Disord 2005; 20: 1653-5.
  • 50. Mata IF, Taylor JP, Kachergus J, et al. LRRK2 R1441G in Spanish patients with Parkinson’s disease. Neurosci Lett 2005; 382: 309-11.
  • 51. Wszolek ZK, Vieregge P, Uitti RJ, et al. German-Canadian family (family A) with parkinsonism, amyotrophy, and dementia—Longitudinal observations. Parkinsonism Relat Disord 1997; 3: 125-39.
  • 52. Covy JP, Yuan W, Waxman EA, et al. Clinical and pathological characteristics of patients with leucine-rich repeat kinase-2 mutations. Mov Disord 2009; 24: 32-9.
  • 53. Meeus B, Verstraeten A, Crosiers D, et al. DLB and PDD: a role for mutations in dementia and Parkinson disease genes? Neurobiol Aging 2012; 33: 629.e5-629.e18.
  • 54. Healy DG, Falchi M, O’Sullivan SS, et al. Phenotype, genotype, and worldwide genetic penetrance of LRRK2-associated Parkinson’s disease: a case-control study. Lancet Neurol 2008; 7: 583-90.
  • 55. Di Fonzo A, Rohe CF, Ferreira J, et al., A frequent LRRK2 gene mutation associated with autosomal dominant Parkinson’s disease. Lancet 2005; 365: 412-15.
  • 56. Aasly JO, Toft M, Fernandez-Mata I, et al. Clinical features of LRRK2-associated Parkinson’s disease in central Norway. Ann Neurol 2005; 57: 762-5.
  • 57. Lesage S, Ibanez P, Lohmann E, et al. G2019S LRRK2 mutation in French and North African families with Parkinson’s disease. Ann Neurol 2005; 58: 784-7.
  • 58. Goldwurm S, Zini M, Di Fonzo A, et al. LRRK2 G2019S mutation and Parkinson’s disease: a clinical, neuropsychological and neuropsychiatric study in a large Italian sample. Parkinsonism Relat Disord 2006; 12: 410-19.
  • 59. Belarbi S, Hecham N, Lesage S, et al. LRRK2 G2019S mutation in Parkinson’s disease: a neuropsychological and neuropsychiatric study in a large Algerian cohort. Parkinsonism Relat Disord 2010; 16: 676-9.
  • 60. Ben Sassi S, Nabli F, Hentati E, et al. Cognitive dysfunction in Tunisian LRRK2 associated Parkinson’s disease. Parkinsonism Relat Disord 2012; 18: 243-6.
  • 61. Scott WK, Grubber JM, Conneally PM, et al. Fine mapping of the chromosome 12 late-onset Alzheimer disease locus: potential genetic and phenotypic heterogeneity. Am J Hum Genet 2000; 66: 922-32.
  • 62. Takao M, Ghetti B, Hayakawa I, et al. A novel mutation (G217D) in the Presenilin 1 gene (PSEN1) in a Japanese family: presenile dementia and parkinsonism are associated with cotton wool plaques in the cortex and striatum. Acta Neuropathol 2002; 104: 155-70.
  • 63. Piscopo P, Marcon G, Piras MR, et al. A novel PSEN2 mutation associated with a peculiar phenotype. Neurology 2008; 70: 1549-54.
  • 64. Ozawa T, Takano H, Onodera O, et al. No mutation in the entire coding region of the alpha-synuclein gene in pathologically confirmed cases of multiple system atrophy. Neurosci Lett 1999; 270: 110-12.
  • 65. Lincoln SJ, Ross OA, Milkovic NM, et al. Quantitative PCR-based screening of alpha-synuclein multiplication in multiple system atrophy. Parkinsonism Relat Disord 2007; 13: 340-2.
  • 66. Scholz SW, Houlden H, Schulte C, et al. SNCA variants are associated with increased risk for multiple system atrophy. Ann Neurol 2009; 65: 610-14.
  • 67. Al-Chalabi A, Durr A, Wood NW, et al. Genetic variants of the alpha-synuclein gene SNCA are associated with multiple system atrophy. PLoS ONE 2009; 4: e7114.
  • 68. Yun JY, Lee WW, Lee JY, et al. SNCA variants and multiple system atrophy. Ann Neurol 2010; 67: 554-5.
  • 69. Robert M, Mathuranath, PS. Tau and tauopathies. Neurol India 2007; 55: 11-16.
  • 70. Hirokawa N. Microtubule organization and dynamics dependent on microtubule-associated proteins. Curr Opin Cell Biol 1994; 6: 74-81.
  • 71. Goedert M, Spillantini MG, Potier MC, et al. Cloning and sequencing of the cDNA encoding an isoform of microtubule-associated protein tau containing four tandem repeats: differential expression of tau protein mRNAs in human brain. EMBO J 1989; 8: 393-9.
  • 72. Gustke N, Trinczek B, Biernat J, et al. Domains of tau protein and interactions with microtubules. Biochemistry 1994; 33: 9511-22.
  • 73. Rademakers R, Hutton M. The genetics of frontotemporal lobar degeneration. Curr Neurol Neurosci Rep 2007; 7: 434-42.
  • 74. Mirra SS, Murrell JR, Gearing M, et al. Tau pathology in a family with dementia and a P301L mutation in tau. J Neuropathol Exp Neurol 1999; 58: 335-45.
  • 75. Nasreddine ZS, Loginov M, Clark LN, et al. From genotype to phenotype: a clinical pathological, and biochemical investigation of frontotemporal dementia and parkinsonism (FTDP-17) caused by the P301L tau mutation. Ann Neurol 1999; 45: 704-15.
  • 76. Mahley RW, Rail SC Jr. Apolipoprotein E: far more than a lipid transport protein. Annu Rev Genomics Hum Genet 2000; 1: 507-37.
  • 77. Saunders AM, Strittmatter WJ, Schmechel D, et al., Association of apolipoprotein E allele epsilon 4 with late-onset familial and sporadic Alzheimer’s disease. Neurology 1993; 43: 1467-72.
  • 78. van Duijn CM, de Knijff P, Cruts M, et al. Apolipoprotein E4 allele in a population-based study of early-onset Alzheimer’s disease. Nat Genet 1994; 7: 74-8.
  • 79. Parsian A, Racette B, Goldsmith LJ, et al. Parkinson’s disease and apolipoprotein E: possible association with dementia but not age at onset. Genomics 2002; 79: 458-61.
  • 80. Marder K, Maestre G, Cote L, et al. The apolipoprotein epsilon 4 allele in Parkinson’s disease with and without dementia. Neurology 1994; 44: 1330-1.
  • 81. Inzelberg R, Chapman J, Treves TA, et al. Apolipoprotein E4 in Parkinson disease and dementia: new data and meta-analysis of published studies. Alzheimer Dis Assoc Disord 1998; 12: 45-8.
  • 82. Pankratz N, Byder L, Halter C, et al. Presence of an APOE4 allele results in significantly earlier onset of Parkinson’s disease and a higher risk with dementia. Mov Disord 2006; 21: 45-9.
  • 83. Huang X, Chen P, Kaufer DI, et al. Apolipoprotein E and dementia in Parkinson disease: a metaanalysis. Arch Neurol 2006; 63: 189-93.
  • 84. Aharon-Peretz J, Rosenbaum H, Gershoni-Baruch R. Mutations in the glucocerebrosidase gene and Parkinson’s disease in Ashkenazi Jews. N Engl J Med 2004; 351: 1972-7.
  • 85. Sidransky E, Nalls MA, Aasly JO, et al. Multicenter analysis of glucocerebrosidase mutations in Parkinson’s disease. N Engl J Med 2009; 361: 1651-61.
  • 86. Nalls MA, Duran R, Lopez G, et al. A multicenter study of glucocerebrosidase mutations in dementia with Lewy bodies. J Am Med Assoc Neurol 2013; 70: 727-35.
  • 87. Goker-Alpan O, Giasson BI, Eblan MJ, et al. Glucocerebrosidase mutations are an important risk factor for Lewy body disorders. Neurology 2006; 67: 908-10.
  • 88. Clark LN, Kartsaklis LA, Wolf Gilbert R, et al. Association of glucocerebrosidase mutations with dementia with Lewy bodies. Arch Neurol 2009; 66: 578-83.
  • 89. Nishioka K, Ross OA, Vilarino-Guell C, et al. Glucocerebrosidase mutations in diffuse Lewy body disease. Parkinsonism Relat Disord 2011; 17: 55-7.
  • 90. Neumann J, Bras J, Deas E, et al. Glucocerebrosidase mutations in clinical and pathologically proven Parkinson’s disease. Brain 2009; 132: 1783-94.
  • 91. Seto-Salvia N, Pagonabarraga J, Houlden H, et al. Glucocerebrosidase mutations confer a greater risk of dementia during Parkinson’s disease course. Mov Disord 2012; 27: 393-9.
  • 92. Winder-Rhodes SE, Evans JR, Ban M, et al. Glucocerebrosidase mutations influence the natural history of Parkinson’s disease in a community-based incident cohort. Brain 2013; 136: 392-9.
  • 93. Zhang J, Song Y, Chen H, et al. The tau gene haplotype h1 confers a susceptibility to Parkinson’s disease. Eur Neurol 2005; 53: 15-21.
  • 94. Farrer M, Maraganore DM, Lockhart P, et al. Alpha-synuclein gene haplotypes are associated with Parkinson’s disease. Hum Mol Genet 2001; 10: 1847-51.
  • 95. Spadafora P, Annesi G, Pasqua AA, et al. NACP-REP1 polymorphism is not involved in Parkinson’s disease: a case-control study in a population sample from southern Italy. Neurosci Lett 2003; 351:
  • 75-8.
  • 96. International Parkinson’s Disease Genomics Consortium (IPDGC); Wellcome Trust Case Control Consortium 2 (WTCCC2). A two-stage meta-analysis identifies several new loci for Parkinson’s disease. PLoS Genet 2011; 7: e1002142.
  • 97. Nalls MA, Plagnol V, Hernandez DG, et al. Imputation of sequence variants for identification of genetic risks for Parkinson’s disease: a meta-analysis of genome-wide association studies. Lancet 2011; 377: 641-9.
  • 98. Zappia M, Annesi G, Nicoletti G, et al. Association of tau gene polymorphism with Parkinson’s disease. Neurol Sci 2003; 24: 223-4.
  • 99. Ezquerra M, Campdelacreu J, Gaig C, et al. Lack of association of APOE and tau polymorphisms with dementia in Parkinson’s disease. Neurosci Lett 2008; 448: 20-3.
  • 100. Goris A, Williams-Gray CH, Clark GR et al. Tau and alpha-synuclein in susceptibility to, and dementia in, Parkinson’s disease. Ann Neurol 2007; 62: 145-53.
  • 101. De Marco EV, Tarantino P, Provenzano G, et al. Alpha-synuclein promoter haplotypes and dementia in Parkinson’s disease. Am J Med Genet B Neuropsychiatr Genet 2008; 147: 403-7.
  • 102. Camicioli R, Raiput A, Raiput M, et al. Apolipoprotein E epsilon4 and catechol-O-methyltransferase alleles in autopsy-proven Parkinson’s disease: relationship to dementia and hallucinations. Mov Disord 2005; 20: 989-94.
  • 103. Golab-Janowska M, Honczarenko K, Gawronska-Szklarz B, et al. CYP2D6 gene polymorphism as a probable risk factor for Alzheimer’s disease and Parkinson’s disease with dementia. Neurol Neurochir Pol 2007; 41: 113-21.
  • 104. Hubble JP, Kurth JH, Glatt SL, et al. Gene-toxin interaction as a putative risk factor for Parkinson’s disease with dementia. Neuroepidemiology 1998; 17: 96-104.
  • 105. Mattila KM, Rinne JO, Roytta M, et al. Dipeptidyl carboxypeptidase 1 (DCP1) and butyrylcholinest- erase (BCHE) gene interactions with the apolipoprotein E epsilon4 allele as risk factors in Alzheimer’s disease and in Parkinson’s disease with coexisting Alzheimer pathology. J Med Genet 2000; 37: 766-70.
  • 106. Isoe-Wada K, Maeda M, Yong J, et al. Positive association between an estrogen receptor gene polymorphism and Parkinson’s disease with dementia. Eur J Neurol 1999; 6: 431-5.
  • 107. Chung SJ, Jung Y, Hong M, et al. Alzheimer’s disease and Parkinson’s disease genome-wide association study top hits and risk of Parkinson’s disease in Korean population. Neurobiol Aging 2013; 34: 2695.e1-2695.e7.
  • 108. Kalinderi K, Bostantjopoulou S, Katsarou Z, et al., Lack of association of the PICALM rs3851179 polymorphism with Parkinson’s disease in the Greek population. Int J Neurosci 2012; 122: 502-605.
  • 109. Benitez BA, Cruchaga C. TREM2 and neurodegenerative disease. N Engl J Med 2013; 369: 1567-8.
  • 110. Rayaprolu S, Mullen B, Baker M, et al. TREM2 in neurodegeneration: evidence for association of the p.R47H variant with frontotemporal dementia and Parkinson’s disease. Mol Neurodegener 2013; 8: 19.
  • 111. Gao J, Huang X, Park Y, et al., An exploratory study on CLU, CR1 and PICALM and Parkinson disease. PLoS ONE 2011; 6: e24211.
  • 112. Maraganore DM, de Andrade M, Lesnick TG, et al. High-resolution whole-genome association study of Parkinson disease. Am J Hum Genet 2005; 77: 685-93.
  • 113. Chung SJ, Armasu SM, Biernacka JM, et al. Genomic determinants of motor and cognitive outcomes in Parkinson’s disease. Parkinsonism Relat Disord 2012; 18: 881-6.
  • 114. Moskvina V, Harold D, Russo G, et al. Analysis of genome-wide association studies of Alzheimer disease and of Parkinson disease to determine if these 2 diseases share a common genetic risk. J Am Med Assoc Neurol 2013; 70: 1268-76.
  • 115. Hindorff LA, Sethupathy P, Junkins HA, et al. Potential etiologic and functional implications of genome-wide association loci for human diseases and traits. Proc Natl Acad Sci USA 2009; 106: 9362-7.
  • 116. Welter D, MacArthur J, Morales J, et al. The NHGRI GWAS Catalog, a curated resource of SNP-trait associations. Nucleic Acids Res 2014; 42: D1001-D1006.
  • 117. Hardy J, Singleton A. Genomewide association studies and human disease. N Engl J Med 2009; 360: 1759-68.
Found a mistake? Please highlight the word and press Shift + Enter  
< Prev   CONTENTS   Next >
Business & Finance
Computer Science
Language & Literature
Political science