Fernando Valdivieso

Summary

Country: Spain

Publications

  1. ncbi request reprint The uncertain anatomy of Alzheimer's disease
    John Hardy
    Laboratory of Neurogenetics, National Institute on Aging, National Institutes of Health, Room 6C103, Building 10, MSC1589, Bethesda, MD 20892, USA
    Neurobiol Aging 25:719-20; discussion 743-6. 2004
  2. pmc Genetic variation in the tau protein phosphatase-2A pathway is not associated with Alzheimer's disease risk
    José L Vázquez-Higuera
    Neurology Service and CIBERNED, Marqués de Valdecilla University Hospital University of Cantabria and IFIMAV, Santander, Spain
    BMC Res Notes 4:327. 2011
  3. pmc Caspase-1 genetic variation is not associated with Alzheimer's disease risk
    José Luis Vázquez-Higuera
    Neurology Service and CIBERNED, Marques de Valdecilla University Hospital, Santander, Spain
    BMC Med Genet 11:32. 2010
  4. pmc DYRK1A genetic variants are not linked to Alzheimer's disease in a Spanish case-control cohort
    José Luis Vázquez-Higuera
    Neurology Service and CIBERNED, Marques de Valdecilla University Hospital, University of Cantabria, Santander, Spain
    BMC Med Genet 10:129. 2009
  5. ncbi request reprint Presenilin 1 mutation in an african american family presenting with atypical Alzheimer dementia
    Gregory A Rippon
    Department of Neurology, Mayo Clinic, Rochester, MN, USA
    Arch Neurol 60:884-8. 2003
  6. ncbi request reprint The amyloid hypothesis of Alzheimer's disease: progress and problems on the road to therapeutics
    John Hardy
    Laboratories of Neurogenetics, National Institute on Aging, Bethesda, MD 20892, USA
    Science 297:353-6. 2002
  7. ncbi request reprint Amyloid at the blood vessel wall
    John Hardy
    Nat Med 12:756-7. 2006
  8. ncbi request reprint Problems and solutions in the genetic analysis of late-onset Alzheimer's disease
    John Hardy
    Laboratory of Neurogenetics, National Institute on Aging, National Institutes of Health, Bethesda, MD 20892 3707, USA
    Neurodegener Dis 1:213-7. 2004
  9. ncbi request reprint Cholesterol 25-hydroxylase on chromosome 10q is a susceptibility gene for sporadic Alzheimer's disease
    Andreas Papassotiropoulos
    Division of Psychiatry Research, University of Zurich, Zurich, Switzerland
    Neurodegener Dis 2:233-41. 2005
  10. ncbi request reprint Alzheimer's disease: the amyloid cascade hypothesis: an update and reappraisal
    John Hardy
    Laboratory of Neurogenetics, National Institute on Aging, Porter Neuroscience Building, 35, Convent Drive, Bethesda, MD20892, USA
    J Alzheimers Dis 9:151-3. 2006

Collaborators

Detail Information

Publications65

  1. ncbi request reprint The uncertain anatomy of Alzheimer's disease
    John Hardy
    Laboratory of Neurogenetics, National Institute on Aging, National Institutes of Health, Room 6C103, Building 10, MSC1589, Bethesda, MD 20892, USA
    Neurobiol Aging 25:719-20; discussion 743-6. 2004
  2. pmc Genetic variation in the tau protein phosphatase-2A pathway is not associated with Alzheimer's disease risk
    José L Vázquez-Higuera
    Neurology Service and CIBERNED, Marqués de Valdecilla University Hospital University of Cantabria and IFIMAV, Santander, Spain
    BMC Res Notes 4:327. 2011
    ..abstract:..
  3. pmc Caspase-1 genetic variation is not associated with Alzheimer's disease risk
    José Luis Vázquez-Higuera
    Neurology Service and CIBERNED, Marques de Valdecilla University Hospital, Santander, Spain
    BMC Med Genet 11:32. 2010
    ..CASP1 genetic variation (G+7/in6A, rs501192) has been associated with susceptibility to myocardial infarction and cardiovascular death risk. We examined the contribution of this gene to the susceptibility for AD...
  4. pmc DYRK1A genetic variants are not linked to Alzheimer's disease in a Spanish case-control cohort
    José Luis Vázquez-Higuera
    Neurology Service and CIBERNED, Marques de Valdecilla University Hospital, University of Cantabria, Santander, Spain
    BMC Med Genet 10:129. 2009
    ....
  5. ncbi request reprint Presenilin 1 mutation in an african american family presenting with atypical Alzheimer dementia
    Gregory A Rippon
    Department of Neurology, Mayo Clinic, Rochester, MN, USA
    Arch Neurol 60:884-8. 2003
    ..Mutations in 3 genes (presenilin 1 and 2 and amyloid precursor protein) are associated with presenile AD. Presenilin 1 gene mutations have not been described in African Americans...
  6. ncbi request reprint The amyloid hypothesis of Alzheimer's disease: progress and problems on the road to therapeutics
    John Hardy
    Laboratories of Neurogenetics, National Institute on Aging, Bethesda, MD 20892, USA
    Science 297:353-6. 2002
    ..The rest of the disease process, including formation of neurofibrillary tangles containing tau protein, is proposed to result from an imbalance between Abeta production and Abeta clearance...
  7. ncbi request reprint Amyloid at the blood vessel wall
    John Hardy
    Nat Med 12:756-7. 2006
  8. ncbi request reprint Problems and solutions in the genetic analysis of late-onset Alzheimer's disease
    John Hardy
    Laboratory of Neurogenetics, National Institute on Aging, National Institutes of Health, Bethesda, MD 20892 3707, USA
    Neurodegener Dis 1:213-7. 2004
    ..In this article, we discuss the complexity of the problem and the pitfalls in the analytical methods that have been used and how we are approaching this problem...
  9. ncbi request reprint Cholesterol 25-hydroxylase on chromosome 10q is a susceptibility gene for sporadic Alzheimer's disease
    Andreas Papassotiropoulos
    Division of Psychiatry Research, University of Zurich, Zurich, Switzerland
    Neurodegener Dis 2:233-41. 2005
    ....
  10. ncbi request reprint Alzheimer's disease: the amyloid cascade hypothesis: an update and reappraisal
    John Hardy
    Laboratory of Neurogenetics, National Institute on Aging, Porter Neuroscience Building, 35, Convent Drive, Bethesda, MD20892, USA
    J Alzheimers Dis 9:151-3. 2006
    ..Here I recap the scientific and personal background of the delineation of the amyloid cascade hypothesis for Alzheimer's disease that I wrote with Gerry Higgins and the events leading to the writing of that influential review...
  11. pmc Association of HFE common mutations with Parkinson's disease, Alzheimer's disease and mild cognitive impairment in a Portuguese cohort
    Rita J Guerreiro
    Laboratory of Neurogenetics, National Institute on Aging, National Institutes of Health, Bethesda, USA
    BMC Neurol 6:24. 2006
    ..Several reports have tested the association of HFE variants with neurodegenerative diseases, such as AD and PD with conflicting results...
  12. ncbi request reprint The genetics of neurodegenerative diseases
    John Hardy
    Laboratory of Neurogenetics, National Institute on Aging, Bethesda, Maryland 20892, USA
    J Neurochem 97:1690-9. 2006
    ..This mechanistic understanding is now leading to therapeutic strategies based on this new understanding. As yet, however, no mechanistic therapies are in use in the clinic...
  13. ncbi request reprint Frontal temporal dementia: dissecting the aetiology and pathogenesis
    John Hardy
    Laboratory of Neurogenetics, National Institute on Aging, National Institute of Mental Health, Porter Neuroscience Building, 35 Convent Drive, Bethesda, MD, USA
    Brain 129:830-1. 2006
  14. ncbi request reprint Tangle diseases and the tau haplotypes
    John Hardy
    Laboratory of Neurogenetics, National Institutes on Aging and of Neurological Diseases and Stroke, National Institutes of Health, Bethesda, MD 20852, USA
    Alzheimer Dis Assoc Disord 20:60-2. 2006
    ..We discuss the reason for this disequilibrium, its evolutionary history, and the role of genetic variability at MAPT in the etiology of tauopathies...
  15. ncbi request reprint Has the amyloid cascade hypothesis for Alzheimer's disease been proved?
    John Hardy
    Laboratory of Neurogenetics, National Institute on Aging, National Institutes of Health, Building 35, Room 1A1015, 35 Convent Drive, Room 1A1015 MSC 3707, Bethesda, MD 20892 3707, USA
    Curr Alzheimer Res 3:71-3. 2006
    ..In this article, I summarize the major pieces of evidence adduced to support the amyloid cascade hypothesis and point out their limitations...
  16. ncbi request reprint A presenilin-1 mutation (T245P) in transmembrane domain 6 causes early onset Alzheimer's disease
    Terri Edwards-Lee
    Los Angeles Biomedical Research Institute, Harbor UCLA Medical Center, 1124 West Carson Street, Torrance, CA 90502, USA
    Neurosci Lett 398:251-2. 2006
    ..The position of the mutation is in the transmembrane domain that harbors the aspartic acid residue which is believed to be part of the active site of gamma-secretase...
  17. ncbi request reprint Characterization of two APP gene promoter polymorphisms that appear to influence risk of late-onset Alzheimer's disease
    Debomoy K Lahiri
    Department of Psychiatry, Institute of Psychiatric Research, Indiana University School of Medicine, 791 N Union Drive, Indianapolis, IN 46202, USA
    Neurobiol Aging 26:1329-41. 2005
    ..Characterization of the activity of a regulatory polymorphism of the APP gene points towards understanding mechanisms that likely underlie the majority of AD cases and may contribute to promoter-based drug design...
  18. ncbi request reprint Genetic variability at the LXR gene (NR1H2) may contribute to the risk of Alzheimer's disease
    Omanma Adighibe
    Laboratory of Neurogenetics, National Institute on Aging, National Institutes of Health, Porter Neuroscience Building, 35 Convent Drive, Bethesda, MD 20892 3707, USA
    Neurobiol Aging 27:1431-4. 2006
    ..As part of this analysis, we have assessed the NR1H2 gene on chromosome 19 and report here a modest association with the locus in sibpairs with late onset disease...
  19. ncbi request reprint A hundred years of Alzheimer's disease research
    John Hardy
    Laboratory of Neurogenetics, National Institute on Aging, Porter Neuroscience Building, Bethesda, Maryland 20892, USA
    Neuron 52:3-13. 2006
    ..The progress toward effective mechanistic therapy is reviewed...
  20. pmc Characteristics of frontotemporal dementia patients with a Progranulin mutation
    Edward D Huey
    Cognitive Neuroscience Section, National Institute of Neurological Disorders and Stroke, National Institutes of Health, Bethesda, MD 20892 1440, USA
    Ann Neurol 60:374-80. 2006
    ..The range of mutations of PGRN that can result in the FTD phenotype and the clinical presentation of patients with PGRN mutations have yet to be determined...
  21. ncbi request reprint The MAPT H1c risk haplotype is associated with increased expression of tau and especially of 4 repeat containing transcripts
    Amanda J Myers
    Laboratory of Neurogenetics, National Institute on Aging, National Institutes of Health, 35 Convent Drive, Bethesda, MD 20892 3707, USA
    Neurobiol Dis 25:561-70. 2007
    ..We discuss these findings both in terms of the problems facing the dissection of the etiologies of complex traits and the pathogenesis of the tauopathies...
  22. doi request reprint Neurofibrillary tau pathology modulated by genetic variation of alpha-synuclein
    Terhi Peuralinna
    Molecular Neurology Programme, Biomedicum, University of Helsinki, Helsinki, Finland
    Ann Neurol 64:348-52. 2008
    ..These results suggest for the first time that variation of alpha-synuclein modulates neurofibrillary tau pathology and support the recent observations of an interaction of alpha-synuclein and tau in neurodegeneration...
  23. pmc Parietal lobe deficits in frontotemporal lobar degeneration caused by a mutation in the progranulin gene
    Jonathan D Rohrer
    Dementia Research Centre, Institute of Neurology, University College London, London, England
    Arch Neurol 65:506-13. 2008
    ..To describe the clinical, neuropsychologic, and radiologic features of a family with a C31LfsX35 mutation in the progranulin gene CCDS11483.1)...
  24. ncbi request reprint Sorl1 as an Alzheimer's disease predisposition gene?
    Jennifer A Webster
    Neurogenomics Division, Translational Genomics Research Institute, Phoenix, Ariz, USA
    Neurodegener Dis 5:60-4. 2008
    ..Here we present the results of our large case-control whole-genome scan at over 500,000 polymorphisms which presents weak evidence for association and potentially narrows the association interval...
  25. ncbi request reprint Genome-wide linkage analysis of 723 affected relative pairs with late-onset Alzheimer's disease
    Marian L Hamshere
    Biostatistics and Bioinformatics Unit, School of Medicine, Cardiff University, Heath Park, Cardiff CF14 4XN, UK
    Hum Mol Genet 16:2703-12. 2007
    ..Where samples overlapped, the genotyping consistency was high, estimated to average at 97.3%. Our large-scale linkage analysis consolidates clear evidence for a susceptibility locus for LOAD on 10q21.2...
  26. ncbi request reprint A presenilin 1 mutation (L420R) in a family with early onset Alzheimer disease, seizures and cotton wool plaques, but not spastic paraparesis
    Antony E Shrimpton
    Department of Pathology, SUNY Upstate Medical University, 750 E Adams St, Syracuse, NY 13210, USA
    Neuropathology 27:228-32. 2007
    ..p.L420R (g.1508T > G) is the mutation responsible for EOAD, seizures and CWP without SP in this family...
  27. pmc GAB2 alleles modify Alzheimer's risk in APOE epsilon4 carriers
    Eric M Reiman
    Neurogenomics Division, Translational Genomics Research Institute, Phoenix, AZ, 85004, USA
    Neuron 54:713-20. 2007
    ..Our findings suggest that GAB2 modifies LOAD risk in APOE epsilon4 carriers and influences Alzheimer's neuropathology...
  28. ncbi request reprint A high-density whole-genome association study reveals that APOE is the major susceptibility gene for sporadic late-onset Alzheimer's disease
    Keith D Coon
    Neurogenomics Division, Translational Genomics Research Institute, Phoenix, Ariz 85004, USA
    J Clin Psychiatry 68:613-8. 2007
    ....
  29. ncbi request reprint Testing for linkage and association across the dihydrolipoyl dehydrogenase gene region with Alzheimer's disease in three sample populations
    Abraham M Brown
    Burke Medical Research Institute, 785 Mamaroneck Avenue, White Plains, NY 10605, USA
    Neurochem Res 32:857-69. 2007
    ..Finally, minimum sample size calculations using parameters from the DLD locus suggest that sample sizes on the order of 1,000 total cases and controls are needed to detect association for a wide range of genetic model parameters...
  30. pmc Putting presenilins centre stage. Introduction to the Talking Point on the role of presenilin mutations in Alzheimer disease
    John Hardy
    Laboratory of Neurogenetics, National Institute on Aging, Porter Neuroscience Building, National Institutes of Health Main Campus, Bethesda, Maryland 20892, USA
    EMBO Rep 8:134-5. 2007
  31. ncbi request reprint Insulin-degrading enzyme haplotypes affect insulin levels but not dementia risk
    Lauren Marlowe
    Laboratorie of Neurogenetics, Intramural Research Program, National Institute on Aging, Bethesda, MD 20892, USA
    Neurodegener Dis 3:320-6. 2006
    ..Insulin-degrading enzyme (IDE) polymorphism is hypothesized to regulate insulin levels as well as processes involved in neuronal compromise found in dementia...
  32. ncbi request reprint Does Abeta 42 have a function related to blood homeostasis?
    John Hardy
    Laboratory of Neurogenetics, National Institute on Aging, Porter Neuroscience Building, NIH Main Campus, Bethesda, MD 20892, USA
    Neurochem Res 32:833-5. 2007
    ..In this review, I discuss the possibility that Abeta42 has a physiologic function in blood vessel homeostasis and the consequences that this might have for theories concerning the pathogenesis of Alzheimer's disease and for treatment...
  33. ncbi request reprint The persistence of memory
    Mark R Cookson
    Laboratory of Neurogenetics, National Institute on Aging, Bethesda, MD, USA
    N Engl J Med 355:2697-8. 2006
  34. ncbi request reprint Green tea epigallocatechin-3-gallate (EGCG) modulates amyloid precursor protein cleavage and reduces cerebral amyloidosis in Alzheimer transgenic mice
    Kavon Rezai-Zadeh
    Silver Child Development Center, Department of Psychiatry and Behavioral Medicine, University of South Florida, Tampa, Florida 33613, USA
    J Neurosci 25:8807-14. 2005
    ..These data raise the possibility that EGCG dietary supplementation may provide effective prophylaxis for AD...
  35. pmc Dense-core plaques in Tg2576 and PSAPP mouse models of Alzheimer's disease are centered on vessel walls
    Samir Kumar-Singh
    Department of Molecular Genetics VIB8, Neurodegenerative Brain Diseases Research Group, Molecular Neuropathology Project, University of Antwerp, Universiteitsplein 1, B 2610 Antwerp, Belgium
    Am J Pathol 167:527-43. 2005
    ....
  36. pmc Functional brain abnormalities in young adults at genetic risk for late-onset Alzheimer's dementia
    Eric M Reiman
    Positron Emission Tomography Center, Banner Good Samaritan Medical Center, Phoenix, AZ 85006, USA
    Proc Natl Acad Sci U S A 101:284-9. 2004
    ..Carriers of a common Alzheimer's susceptibility gene have functional brain abnormalities in young adulthood, several decades before the possible onset of dementia...
  37. ncbi request reprint Variation in the urokinase-plasminogen activator gene does not explain the chromosome 10 linkage signal for late onset AD
    Amanda J Myers
    Department of Psychiatry, Washington University School of Medicine, St Louis, Missouri, USA
    Am J Med Genet B Neuropsychiatr Genet 124:29-37. 2004
    ..Eight polymorphisms spanning the entire gene were examined using case control (CC) and family-based association methods. No association was observed by any method making it unlikely that variation in PLAU explains our linkage data...
  38. ncbi request reprint Alzheimer's disease: genetic evidence points to a single pathogenesis
    John Hardy
    Ann Neurol 54:143-4. 2003
  39. ncbi request reprint The relationship between amyloid and tau
    John Hardy
    Laboratory of Neurogenetics, NIA NIH, Building 10, 6C103, Bethesda, MD 20892, USA
    J Mol Neurosci 20:203-6. 2003
    ....
  40. ncbi request reprint Testing times for the "amyloid cascade hypothesis"
    John Hardy
    Laboratory of Neurogenetics, NIA NIH, Building 10, 6C103, Bethesda, MD 20892, USA
    Neurobiol Aging 23:1073-4. 2002
  41. ncbi request reprint An association study of a functional catalase gene polymorphism, -262C-->T, and patients with Alzheimer's disease
    Antonis Goulas
    Department of Pharmacology, School of Medicine, Aristotle University, Thessaloniki 54124, Greece
    Neurosci Lett 330:210-3. 2002
    ..No significant difference has emerged from the comparison of either genotype or allele frequencies (P>0.5). We conclude that the catalase gene -262C-->T polymorphism does not confer a protective effect with respect to AD...
  42. ncbi request reprint The tau locus is not significantly associated with pathologically confirmed sporadic Parkinson's disease
    Rohan de Silva
    Reta Lila Weston Institute of Neurological Studies, Royal Free and University College Medical School, London, UK
    Neurosci Lett 330:201-3. 2002
    ....
  43. ncbi request reprint Psychotic genes or forgetful ones?
    Simon Lovestone
    Neurology 59:11-2. 2002
  44. ncbi request reprint Toxic proteins in neurodegenerative disease
    J Paul Taylor
    Neurogenetics Branch, National Institute of Neurological Disorders and Stroke, Laboratory of Neurogenetics, National Institute on Aging, National Institutes of Health, Bethesda, MD 20892, USA
    Science 296:1991-5. 2002
    ..Increased understanding of the cellular mechanisms for disposal of abnormal proteins and of the effects of toxic protein accumulation on neuronal survival may allow the development of rational, effective treatment for these disorders...
  45. ncbi request reprint Apolipoprotein E4 and tau allele frequencies among Choctaw Indians
    J Neil Henderson
    Department of Health Promotion Sciences, University of Oklahoma, Oklahoma City 73190, USA
    Neurosci Lett 324:77-9. 2002
    ....
  46. ncbi request reprint The tau H1 haplotype is associated with Parkinson's disease in the Norwegian population
    Matt Farrer
    Laboratory of Familial Movement Disorders, Mayo Clinic, Jacksonville, FL, USA
    Neurosci Lett 322:83-6. 2002
    ..52; 95% confidence interval: 2.64-11.10; P=2.17x10(-6)). Findings provide evidence that tau participates in the PD pathogenic process and demonstrate the value of isolated populations in mapping complex traits...
  47. ncbi request reprint ApoE epsilon3-haplotype modulates Alzheimer beta-amyloid deposition in the brain
    Liisa Myllykangas
    Department of Pathology, University of Helsinki and Helsinki University Central Hospital, Helsinki, Finland
    Am J Med Genet 114:288-91. 2002
    ..These results indicate that there is significant allelic variation in the ApoE gene region, which modulates brain amyloid deposition and AD risk, independent of the ApoE protein polymorphism...
  48. ncbi request reprint Full genome screen for Alzheimer disease: stage II analysis
    Amanda Myers
    Department of Psychiatry, Washington University School of Medicine, St Louis, Missouri 63110, USA
    Am J Med Genet 114:235-44. 2002
    ..Of the seven markers we tested in family-based and case control samples, the only nominally positive association we found was with the 167 bp allele of marker D10S1217 (chi-square=7.11, P=0.045, df=1)...
  49. ncbi request reprint Toward Alzheimer therapies based on genetic knowledge
    John Hardy
    Laboratory of Neurogenetics, National Institute on Aging, National Institutes of Health, Bethesda, Maryland 20892, USA
    Annu Rev Med 55:15-25. 2004
    ....
  50. ncbi request reprint CHIP and Hsp70 regulate tau ubiquitination, degradation and aggregation
    Leonard Petrucelli
    Mayo Clinic, Jacksonville, FL 32224, USA
    Hum Mol Genet 13:703-14. 2004
    ..Hsp70/CHIP may therefore play an important role in the pathogenesis of tauopathies and also represents a potential therapeutic target...
  51. ncbi request reprint An association study of the cholesteryl ester transfer protein TaqI B polymorphism with late onset Alzheimer's disease
    Liana Fidani
    Department of General Biology, School of Medicine, Aristotle University, Thessaloniki 54124, Greece
    Neurosci Lett 357:152-4. 2004
    ..CETP TaqI B did not interact significantly with either APOE epsilon4 or LPLS447X, in this study...
  52. ncbi request reprint Chromosome 21 BACE2 haplotype associates with Alzheimer's disease: a two-stage study
    Liisa Myllykangas
    Department of Pathology, Helsinki University Central Hospital, Helsinki, Finland
    J Neurol Sci 236:17-24. 2005
    ..08). BACE2 haplotype association with AD in two independent datasets provides further evidence for an AD susceptibility locus on chromosome 21q within or close to BACE2...
  53. pmc Correlations between apolipoprotein E epsilon4 gene dose and brain-imaging measurements of regional hypometabolism
    Eric M Reiman
    Positron Emission Tomography Center, Banner Good Samaritan Medical Center, Phoenix, AZ 85006, USA
    Proc Natl Acad Sci U S A 102:8299-302. 2005
    ..This study raises the possibility of using PET as a quantitative presymptomatic endophenotype to help evaluate the individual and aggregate effects of putative genetic and nongenetic modifiers of AD risk...
  54. ncbi request reprint Association studies between risk for late-onset Alzheimer's disease and variants in insulin degrading enzyme
    Petra Nowotny
    Department of Psychiatry, Washington University School of Medicine, St Louis, MO 63110, USA
    Am J Med Genet B Neuropsychiatr Genet 136:62-8. 2005
    ..Although our results are not universally negative, we were unable to replicate the results of previous studies and conclude that common variants or haplotypes of these variants in IDE are not major risk factors for LOAD...
  55. ncbi request reprint The architecture of the tau haplotype block in different ethnicities
    Hon Chung Fung
    Laboratory of Neurogenetics, National Institute on Aging, National Institutes of Health, 35 Convent Drive, Building 35, Room 1A1008, MSC 3707, Bethesda, MD 20892, USA
    Neurosci Lett 377:81-4. 2005
    ..We discuss this observation in terms of the establishment of the haplotype structure and the possible impact of the tau haplotype on neurodegeneration in humans...
  56. ncbi request reprint Genome screen for loci influencing age at onset and rate of decline in late onset Alzheimer's disease
    Peter Holmans
    Biostatistics and Bioinformatics Unit, Wales College of Medicine, Heath Park, Cardiff, United Kingdom
    Am J Med Genet B Neuropsychiatr Genet 135:24-32. 2005
    ..08) and chromosome 9 (max LOD = 3.34). The previously reported genome-wide linkage of AD to chromosome 10 was not influenced by any of the covariates studied...
  57. ncbi request reprint Genetic association of the APP binding protein 2 gene (APBB2) with late onset Alzheimer disease
    Yonghong Li
    Celera Diagnostics, Alameda, California 94502, USA
    Hum Mutat 25:270-7. 2005
    ..43 [95% CI: 1.61-3.67]; OR(het)=2.15 [95% CI: 1.46-3.17]; P=0.00006) in the combined sample set. Our data raise the possibility that genetic variations in APBB2 may affect LOAD susceptibility...
  58. ncbi request reprint The tau H2 haplotype is almost exclusively Caucasian in origin
    Whitney Evans
    Laboratory of Neurogenetics, National Institute on Aging, National Institutes of Health, Bethesda, MD 20892, USA
    Neurosci Lett 369:183-5. 2004
    ..We discuss this observation in terms of the origin of the H2 haplotype and the epidemiology of the tauopathies...
  59. ncbi request reprint Profile: John Hardy
    Bruce Diamond
    Nat Med 10:1009. 2004
  60. ncbi request reprint Association of the dihydrolipoamide dehydrogenase gene with Alzheimer's disease in an Ashkenazi Jewish population
    Abraham M Brown
    Dementia Research Service, Burke Medical Research Institute, 785 Mamaroneck Ave, White Plains, New York 10605, USA
    Am J Med Genet B Neuropsychiatr Genet 131:60-6. 2004
    ..0009, n = 83) and the Ashkenazi Jewish subseries (P = 0.017, n = 49). The DLD genotype appears to operate independently of APOE in conferring AD risk...
  61. ncbi request reprint Is amyloid plaque imaging the key to monitoring brain pathology of Alzheimer's disease in vivo?
    John Hardy
    Laboratory of Neurogenetics, National Institute on Aging, National Institutes of Health, Building 35, 35 Convent Drive, Room 1A1015 MSC 3707, Bethesda, MD 20892 3707, USA
    Eur J Nucl Med Mol Imaging 31:1539-40. 2004
  62. ncbi request reprint How many pathways are there to nigral death?
    John Hardy
    Ann Neurol 56:316-8. 2004
  63. ncbi request reprint Association of ABCA1 with late-onset Alzheimer's disease is not observed in a case-control study
    Yonghong Li
    Celera Diagnostics, Alameda, CA, USA
    Neurosci Lett 366:268-71. 2004
    ..Further, we did not observe significant and replicated association of other ABCA1 SNPs we examined with the disease, thus these ABCA1 variants do not appear to influence the risk of LOAD in this study...
  64. ncbi request reprint The structure of the tau haplotype in controls and in progressive supranuclear palsy
    Alan M Pittman
    Reta Lila Weston Institute of Neurological Studies, University College London, UK
    Hum Mol Genet 13:1267-74. 2004
    ..We show that the entire, fully extended H1 haplotype is associated with PSP, which implicates several other genes in addition to MAPT, as candidate pathogenic loci...
  65. ncbi request reprint Identifying genetic factors in Parkinson disease
    Matt Farrer
    JAMA 287:715-6. 2002