Research Topics
Genomes and Genes
Species | Lars BertramSummaryAffiliation: Harvard University Country: USA Publications
Research Grants
| Collaborators
|
Detail Information
Publications
A QTL genome scan of the metabolic syndrome and its component traitsMatthew B McQueen
Department of Epidemiology, Harvard School of Public Health, Boston, Massachusetts, USA
BMC Genet 4:S96. 2003..We used genotype and phenotype data from the Framingham Heart Study to perform a full-genome scan for quantitative trait loci underlying the metabolic syndrome...- The genetic epidemiology of neurodegenerative diseaseLars Bertram
Genetics and Aging Research Unit, MassGeneral Institute for Neurodegenerative Diseases, Department of Neurology, Massachusetts General Hospital, Harvard Medical School, Charlestown, Massachusetts 02129, USA
J Clin Invest 115:1449-57. 2005.... - Genetic research in schizophrenia: new tools and future perspectivesLars Bertram
Genetics and Aging Research Unit, MGH East MassGeneral Institute for Neurodegenerative Disease, Department of Neurology, Massachusetts General Hospital, Charlestown, MA 02129, USA
Schizophr Bull 34:806-12. 2008..20 [range 1.06-1.45]) but nominally significant risk effects. This review discusses some of the strengths and limitations of the SzGene database, which could become a useful bioinformatics tool within the schizophrenia research community... - Systematic meta-analyses of Alzheimer disease genetic association studies: the AlzGene databaseLars Bertram
Genetics and Aging Research Unit, MassGeneral Institute for Neurodegenerative Disease MIND, Department of Neurology, Massachusetts General Hospital, Charlestown, Massachusetts 02129, USA
Nat Genet 39:17-23. 2007..67 for protective alleles). Our database provides a powerful tool for deciphering the genetics of Alzheimer disease, and it serves as a potential model for tracking the most viable gene candidates in other genetically complex diseases... - Thirty years of Alzheimer's disease genetics: the implications of systematic meta-analysesLars Bertram
Genetics and Aging Research Unit, MassGeneral Institute for Neurodegenerative Diseases, Department of Neurology, Massachusetts General Hospital, 114 16th Street, Charlestown, Massachusetts 02129, USA
Nat Rev Neurosci 9:768-78. 2008..This Review discusses the putative pathogenetic roles and common biochemical pathways of some of the most genetically and biologically compelling of these potential AD risk factors... - The LDLR locus in Alzheimer's disease: a family-based study and meta-analysis of case-control dataLars Bertram
Genetics and Aging Research Unit, MassGeneral Institute for Neurodegenerative Diseases, Department of Neurology, Massachusetts General Hospital, Harvard Medical School, Charlestown, MA 02129, USA
Neurobiol Aging 28:18.e1-4. 2007..Based on our data, it seems unlikely that these genetic variants in LDLR make a significant contribution to AD risk in the general population... - GAB2 as an Alzheimer disease susceptibility gene: follow-up of genomewide association resultsBrit Maren M Schjeide
Genetics and Aging Research Unit, MassGeneral Institute for Neurodegenerative Disease, Department of Neurology, Massachusetts General Hospital, Harvard Medical School, 114 16th St, Charlestown, MA 02129, USA
Arch Neurol 66:250-4. 2009..To our knowledge, these findings have not been independently replicated... - Assessment of Alzheimer's disease case-control associations using family-based methodsBrit Maren M Schjeide
MassGeneral Institute for Neurodegenerative Disease MIND, Department of Neurology, Massachusetts General Hospital, Charlestown, MA 02129, USA
Neurogenetics 10:19-25. 2009..Further fine-mapping and functional analyses are warranted to elucidate the potential biochemical mechanisms and epidemiological relevance of these genes... - Genome-wide association analysis reveals putative Alzheimer's disease susceptibility loci in addition to APOELars Bertram
Genetics and Aging Research Unit, Mass General Institute for Neurodegenerative Disease MIND, Department of Neurology, Massachusetts General Hospital, Charlestown, MA 02129, USA
Am J Hum Genet 83:623-32. 2008.... - Decreased catalytic activity of the insulin-degrading enzyme in chromosome 10-linked Alzheimer disease familiesMinji Kim
Genetics and Aging Research Unit, MassGeneral Institute for Neurodegenerative Disease, Massachusetts General Hospital, Charlestown, Massachusetts 02129, and Department of Molecular and Cellular Biochemistry, University of Kentucky, Lexington 40536, USA
J Biol Chem 282:7825-32. 2007.... - Effects of ubiquilin 1 on the unfolded protein responseAlice Lu
Genetics and Aging Research Unit, MassGeneral Institute for Neurodegenerative Disease, Massachusetts General Hospital, Charlestown, MA, 02129 4404, USA
J Mol Neurosci 38:19-30. 2009..These findings suggest that overexpression UBQLN1 transcript variants TV1-3, but not TV4, exert a protective effect during the UPR by attenuating CHOP induction and potentially increasing cell viability... - Association of GSK3B with Alzheimer disease and frontotemporal dementiaBarbara A J Schaffer
Department of Neurology, David Geffen School of Medicine, University of California, Los Angeles, 2506 Gonda, 695 Charles E Young Dr S, Los Angeles, CA 90095 1761, USA
Arch Neurol 65:1368-74. 2008..As a known tau kinase, GSK3B is a promising candidate gene in the remaining cases of FTD and in AD, for which tau mutations have not been found... - Systematic meta-analyses and field synopsis of genetic association studies in schizophrenia: the SzGene databaseNicole C Allen
Genetics and Aging Research Unit, MassGeneral Institute for Neurodegenerative Disease, Department of Neurology, Massachusetts General Hospital, Charlestown, Massachusetts 02129, USA
Nat Genet 40:827-34. 2008..As such, it could serve as a model for field synopses of genetic associations in other common and genetically complex disorders... - Ubiquilin 1 modulates amyloid precursor protein trafficking and Abeta secretionMikko Hiltunen
Genetics and Aging Research Unit, MassGeneral Institute for Neurodegenerative Disease, Massachusetts General Hospital, Charlestown, MA 02129, USA
J Biol Chem 281:32240-53. 2006..These findings suggest that changes in UBQLN1 steady-state levels affect APP trafficking and processing, thereby influencing the generation of Abeta... - The current status of Alzheimer's disease genetics: what do we tell the patients?Lars Bertram
Genetics and Aging Research Unit, Department of Neurology, Massachusetts General Hospital, 114 16th Street, Charlestown, MA 02129, USA
Pharmacol Res 50:385-96. 2004..This review focuses on the analytic tools used to identify genes in complex diseases, and then provides a summary of recent linkage and association findings indicating the existence of novel late-onset AD genes on several chromosomes... - Family-based association between Alzheimer's disease and variants in UBQLN1Lars Bertram
Genetics and Aging Research Unit, MassGeneral Institute for Neurodegenerative Disease, Department of Neurology, Massachusetts General Hospital, Charlestown 02129, USA
N Engl J Med 352:884-94. 2005..The gene encoding ubiquilin 1 (UBQLN1) is one of several candidate genes for Alzheimer's disease located near a well-established linkage peak on chromosome 9q22... - Evidence of altered posteromedial cortical FMRI activity in subjects at risk for Alzheimer diseaseMaija Pihlajamaki
Department of Neurology, Brigham and Women s Hospital, Harvard Medical School, MA, USA
Alzheimer Dis Assoc Disord 24:28-36. 2010..Altered fMRI activity of the posteromedial areas of the brain default network may be an early indicator of risk for AD... - Alzheimer's disease: one disorder, too many genes?Lars Bertram
Genetics and Aging Research Unit, Department of Neurology and Mass General Institute for Neurodegenerative Diseases, Massachusetts General Hospital, Harvard Medical School, Charlestown, MA, USA
Hum Mol Genet 13:R135-41. 2004..This should serve to greatly decrease the likelihood of false positive and false negative findings reported in future years... - Results of a high-resolution genome screen of 437 Alzheimer's disease familiesDeborah Blacker
Massachusetts General Hospital, Charlestown, MA, USA
Hum Mol Genet 12:23-32. 2003..Although some of these will surely prove to be false positives, these linkage signals should provide a valuable framework for future studies aimed at identifying additional susceptibility genes for late-onset AD... - Twenty years of the Alzheimer's disease amyloid hypothesis: a genetic perspectiveRudolph E Tanzi
Genetics and Aging Research Unit, MassGeneral Institute for Neurodegenerative Diseases, Department of Neurology, Massachussetts General Hospital, Harvard Medical School, Charlestown, Massachussetts 02129, USA
Cell 120:545-55. 2005..Here we assess the amyloid hypothesis based on both known and putative Alzheimer's disease genes... - Family-based association test for time-to-onset data with time-dependent differences between the hazard functionsHongyu Jiang
Department of Biostatistics, Harvard School of Public Health, 655 Huntington Avenue, Boston, MA 02115, USA
Genet Epidemiol 30:124-32. 2006..In addition to power increases of 100% over the original FBAT-Logrank test, we also gain insight into the age at which a genotype exerts the greatest influence on disease risk... - Genetic association of Alzheimer's disease with multiple polymorphisms in alpha-2-macroglobulinAleister J Saunders
Genetics and Aging Research Unit, Department of Neurology, Massachusetts General Hospital, Harvard Medical School, Charlestown, MA 02129, USA
Hum Mol Genet 12:2765-76. 2003..However, the negative case - control studies suggest that any underlying pathogenic polymorphisms have a modest effect, and may operate primarily among individuals with a family history of AD... - Partial loss-of-function mutations in insulin-degrading enzyme that induce diabetes also impair degradation of amyloid beta-proteinWesley Farris
Department of Neurology, Center for Neurologic Diseases, Brigham and Women's Hospital, Boston, Massachusetts 02115, USA
Am J Pathol 164:1425-34. 2004..Our findings have relevance for the emerging genetic evidence suggesting that IDE may be a late-onset AD-risk gene, and for the epidemiological relationships among hyperinsulinemia, DM2, and AD... - Longitudinal changes in white matter disease and cognition in the first year of the Alzheimer disease neuroimaging initiativeOwen Carmichael
Department of Neurology, School of Medicine, University of California, Davis, CA, USA
Arch Neurol 67:1370-8. 2010.... - Single-nucleotide polymorphism rs498055 on chromosome 10q24 is not associated with Alzheimer disease in two independent family samplesLars Bertram
Am J Hum Genet 79:180-3; author reply 183-4. 2006 - Follow-up mapping supports the evidence for linkage in the candidate region at 9q22 in the NIMH Alzheimer's disease Genetics Initiative cohortRodney T Perry
Department of Epidemiology and International Health, University of Alabama at Birmingham, Birmingham, Alabama 35294 0022, USA
Am J Med Genet B Neuropsychiatr Genet 144:220-7. 2007..In an effort to pinpoint this putative AD susceptibility gene, we have begun to analyze SNPs in other candidate genes in and around this narrowed region to test for additional associations to AD... - Alzheimer's disease: The latest suspectRudolph E Tanzi
Nature 454:706-8. 2008 - Is alpha-T catenin (VR22) an Alzheimer's disease risk gene?Lars Bertram
J Med Genet 44:e63. 2007..As the underlying effects are probably small, and are only seen in families with multiple affected members, the population-wide significance of this finding remains to be determined... - Genome-wide linkage analysis of 723 affected relative pairs with late-onset Alzheimer's diseaseMarian 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... - Exploring candidate gene associations with neuropsychological performanceMatthew B McQueen
Institute for Behavioral Genetics, University of Colorado at Boulder, Boulder, Colorado 80309 0447, USA
Am J Med Genet B Neuropsychiatr Genet 144:987-91. 2007.... - Evaluation of the potential excess of statistically significant findings in published genetic association studies: application to Alzheimer's diseaseFotini K Kavvoura
Department of Hygiene and Epidemiology, University of Ioannina School of Medicine, Ioannina, Greece
Am J Epidemiol 168:855-65. 2008..The excess was seen for all levels of statistical significance and also for studies with borderline P values (P = 0.05-0.10). The excess of significant findings may represent significance-chasing biases in a setting of massive testing...
Research Grants
- SEARCH FOR NOVEL EARLY-ONSET ALZHEIMER'S GENESLars Bertram; Fiscal Year: 2007..While we have devised a strategy that integrates the best available methods to identify complex disease genes, we will routinely adjust our strategy to account for methodologic advances in this rapidly evolving field. ..