Genomes and Genes
Debby W Tsuang
Affiliation: University of Washington
- Familial occurrence of dementia with Lewy bodiesDebby W Tsuang
Department of Psychiatry and Behavioral Sciences, University of Washington, Seattle, WA 98108, USA
Am J Geriatr Psychiatry 12:179-88. 2004....
- Tau phosphorylation pathway genes and cerebrospinal fluid tau levels in Alzheimer's diseaseLynn M Bekris
Geriatric Research, Education, and Clinical Center GRECC, VA Puget Sound Health Care System, Seattle, Washington 98108, USA
Am J Med Genet B Neuropsychiatr Genet 159:874-83. 2012..These results suggest that rs7768046 and rs913275 both influence CSF tau levels in an AD-associated manner...
- Inheritance model introduces differential bias in CNV calls between parents and offspringSulgi Kim
Division of Medical Genetics, Department of Medicine, University of Washington, Seattle, Washington 98195 7720, USA
Genet Epidemiol 36:488-98. 2012..Our results advise need for caution in use of the Joint-model calls in CNV association studies with family-based datasets...
- The UCHL1 S18Y polymorphism and Parkinson's disease in a Japanese populationKatherine W Snapinn
Department of Epidemiology, University of Washington School of Public Health, Seattle, Washington, USA
Parkinsonism Relat Disord 17:473-5. 2011..47-1.20; YY vs. SS, OR, 0.64; 95% CI, 0.36-1.14; trend test, P=0.12). These results indicate that, if involved in PD, the S18Y variant is not a major determinant of risk and its effect might be restricted to early-onset disease...
- Genetics of Alzheimer diseaseLynn M Bekris
Department of Medicine, University of Washington School of Medicine, Seattle, WA 98108, USA
J Geriatr Psychiatry Neurol 23:213-27. 2010..Identification of these genes has led to a number of animal models that have been useful to study the pathogenesis underlying AD. In this article, we provide an overview of the clinical and genetic features of AD...
- Lewy body pathology in late-onset familial Alzheimer's disease: a clinicopathological case seriesDebby W Tsuang
Mental Illness Research, Education, and Clinical Centers, Veteran Affairs Puget Sound Health Care System, Seattle, WA 98108, USA
J Alzheimers Dis 9:235-42. 2006..Lewy body pathology (LBP) is a common finding in Alzheimer's disease (AD), but the pathophysiology for this coexistent pathology remains unclear...
- ADAM10 expression and promoter haplotype in Alzheimer's diseaseLynn M Bekris
Geriatric Research, Education, and Clinical Center GRECC, VA Puget Sound Health Care System, Seattle, WA, USA
Neurobiol Aging 33:2229.e1-2229.e9. 2012..Taken together, these findings suggest that ADAM10 expression is modulated according to a promoter haplotype that is influenced in a brain region- and cell type-specific manner...
- Familial dementia with Lewy bodies with an atypical clinical presentationLauren T Bonner
Department of Veterans Affairs Northwest Network Mental Illness Research, Education, and Clinical Center, University of Washington, Seattle 98108, USA
J Geriatr Psychiatry Neurol 16:59-64. 2003..Family history revealed 7 relatives with a history of dementia including 4 with possible or probable DLB. This case is unique because of the FTLD-like presentation, positive family history of dementia, and autopsy confirmation of DLB...
- Cognitive impairment in older adults without dementia: clinical and pathologic outcomes in a community-based sampleLucy Y Wang
Mental Illness Research, Education, and Clinical Center, VA Puget Sound Health Care System, Seattle, Washington, USA
J Geriatr Psychiatry Neurol 22:256-65. 2009..4 +/- 2.1 vs 3.1 +/- 2.7, P = .02). These observations are consistent with the view that nondemented patients with underlying AD may be more likely to present with memory than nonmemory cognitive impairment...
- SNCA variant associated with Parkinson disease and plasma alpha-synuclein levelIgnacio F Mata
Geriatric Research Education and Clinical Center, Veterans Affairs Puget Sound Health Care System, Mailstop S 182, 1660 S Columbian Way, Seattle, WA 98108, USA
Arch Neurol 67:1350-6. 2010..A functional repeat polymorphism in the SNCA promoter (REP1) conveys susceptibility for Parkinson disease (PD). There is also increasing evidence that single-nucleotide polymorphisms (SNPs) elsewhere in the gene are associated with PD risk...
- Comprehensive analysis of APOE and selected proximate markers for late-onset Alzheimer's disease: patterns of linkage disequilibrium and disease/marker associationChang En Yu
Geriatric Research, Education, and Clinical Center, Veterans Affairs Puget Sound Health Care System, Seattle, WA 98108, USA
Genomics 89:655-65. 2007..These observations diminish the possibility that loci in the TOMM40 gene may have a major effect on the risk for LOAD in Caucasians...
- Support for the N-methyl-D-aspartate receptor hypofunction hypothesis of schizophrenia from exome sequencing in multiplex familiesAndrew E Timms
Department of Pathology, University of Washington School of Medicine, Seattle, USA
JAMA Psychiatry 70:582-90. 2013..Investigation of genetic forms of schizophrenia will lead to a better understanding of the underlying molecular pathways, which will then enable targeted approaches for disease prevention and treatment...
- Proteomic identification of novel proteins in cortical lewy bodiesJames B Leverenz
Department of Neurology, School of Medicine, University of Washington, Seattle, WA 98104, USA
Brain Pathol 17:139-45. 2007..Further investigation of these novel candidates is also necessary to ensure that the potential proteins in cortical LBs are not identified incorrectly because of incomplete current human protein database...
- Antisaccade performance in schizophrenia patients, their first-degree biological relatives, and community comparison subjects: data from the COGS studyAllen D Radant
Department of Psychiatry and Behavioral Sciences, University of Washington and Department of Veteran Affairs, VISN 20, Mental Illness Research, Education, and Clinical Center, Seattle, Washington 98108, USA
Psychophysiology 47:846-56. 2010..Given the significant heritability of antisaccade performance, the effects of a genetic polymorphism is one possible explanation of our results...
- Genetics of dementiaDebby W Tsuang
Departments of Psychiatry and Behavioral Sciences and Epidemiology, University of Washington, Seattle, WA, USA
Med Clin North Am 86:591-614. 2002..Future clinical and molecular genetics findings hold many clinical implications. It is likely that new diagnostic and therapeutic strategies for dementing disorders are just on the horizon...
- Successful multi-site measurement of antisaccade performance deficits in schizophreniaAllen D Radant
Department of Psychiatry and Behavioral Sciences, University of Washington, Seattle, Washington, United States
Schizophr Res 89:320-9. 2007..These results confirm previous findings of antisaccade deficits in schizophrenia subjects and support the use of the antisaccade task as a potential schizophrenia endophenotype in multi-site genetic studies...
- Evidence for involvement of GNB1L in autismYing Zhang Chen
Department of Medicine Medical Genetics, University of Washington, Seattle, Washington 98195 7720, USA
Am J Med Genet B Neuropsychiatr Genet 159:61-71. 2012..Prior studies provided evidence that GNB1L may have a role in schizophrenia. Our findings support involvement of GNB1L in ASDs as well...
- Empiric refinement of the pathologic assessment of Lewy-related pathology in the dementia patientJames B Leverenz
Department of Veterans Affairs Northwest Network Mental Illness and Parkinson s Disease Research, University of Washington, Seattle, WA 98108, USA
Brain Pathol 18:220-4. 2008..In addition, this modification allows for more limited sampling of brain regions for classification of LRP. We propose that these modified criteria for the categorization of LRP be utilized in patients with a history of dementia...
- Salivary cortisol and memory function in human agingGe Li
Department of Psychiatry and Behavioral Sciences, University of Washington, Seattle, WA 98195, USA
Neurobiol Aging 27:1705-14. 2006..Previous studies have suggested that elevated glucocorticoid concentrations alter hippocampal neuronal morphology, inhibit neurogenesis, and impair cognition...
- Propranolol for disruptive behaviors in nursing home residents with probable or possible Alzheimer disease: a placebo-controlled studyElaine R Peskind
Department of Veterans Affairs Northwest Network VISN 20 Mental Illness Research, Education and Clinical Center, Seattle, WA, USA
Alzheimer Dis Assoc Disord 19:23-8. 2005..We evaluated the efficacy of the beta-adrenergic antagonist propranolol for treatment-resistant disruptive behaviors and overall behavioral status in nursing home residents with probable or possible AD...
- The effect of algorithms on copy number variant detectionDebby W Tsuang
Department of Psychiatry and Behavioral Sciences, University of Washington, Seattle, Washington, United States of America
PLoS ONE 5:e14456. 2010....
- LRRK2 mutations and risk variants in Japanese patients with Parkinson's diseaseCyrus P Zabetian
Department of Neurology, University of Washington School of Medicine, Seattle, Washington, USA
Mov Disord 24:1034-41. 2009..However, LRRK2 mutations appear to be rare among Japanese patients with PD...
- Familial dementia with lewy bodies: a clinical and neuropathological study of 2 familiesDebby W Tsuang
Department of Veterans Affairs Northwest Network Mental Illness Research, Education, and Clinical Center, VA Puget Sound Health Care System, 1660 S Columbian Way, Mailstop 116MIRECC, Seattle, WA 98108, USA
Arch Neurol 59:1622-30. 2002..Few families with DLB have been described with detailed clinical, pathological, and genetic assessments...
- The Consortium on the Genetics of Endophenotypes in Schizophrenia: model recruitment, assessment, and endophenotyping methods for a multisite collaborationMonica E Calkins
Neuropsychiatry Section, Department of Psychiatry, University of Pennsylvania, 10 Gates, 3400 Spruce St, Philadelphia, PA 19104, USA
Schizophr Bull 33:33-48. 2007..The purpose of this article is to provide a description of the COGS structure and methods, including participant recruitment and assessment...
- Initial heritability analyses of endophenotypic measures for schizophrenia: the consortium on the genetics of schizophreniaTiffany A Greenwood
Department of Psychiatry, University of California San Diego, La Jolla, USA
Arch Gen Psychiatry 64:1242-50. 2007..Exploration of the genetic architecture of specific endophenotypes may be a powerful strategy for understanding the genetic basis of schizophrenia...
- Analysis of the LRRK2 G2019S mutation in Alzheimer DiseaseCyrus P Zabetian
Arch Neurol 63:156-7. 2006
- Co-morbidity of TDP-43 proteinopathy in Lewy body related diseasesHanae Nakashima-Yasuda
Department of Pathology and Laboratory Medicine, Center for Neurodegenerative Disease Research, University of Pennsylvania School of Medicine, HUP Maloney 3rd Floor, Philadelphia, PA 19104 4283, USA
Acta Neuropathol 114:221-9. 2007..This study expands the concept of TDP-43 proteinopathies by implicating TDP-43 lesions in mechanisms of neurodegeneration in LB disorders...
- Linkage of chromosome 13q32 to schizophrenia in a large veterans affairs cooperative study sampleStephen V Faraone
Brockton West Roxbury Veterans Affairs Medical Center, Brockton, Massachusetts, USA
Am J Med Genet 114:598-604. 2002..57; P = 0.01) at 79.0 cM between markers D13S1241 (76.3 cM) and D13S159 (79.5 cM). Both ethnic groups showed a peak in this region. The peak is within 3 cM of the peak reported by Brzustowicz et al. [1999: Am J Hum Genet 65:1096-1103]...