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Age, Gene/Environment Susceptibility-Reykjavik Study: multidisciplinary applied phenomics.

https://arctichealth.org/en/permalink/ahliterature78517
Source
Am J Epidemiol. 2007 May 1;165(9):1076-87
Publication Type
Article
Date
May-1-2007
Author
Harris Tamara B
Launer Lenore J
Eiriksdottir Gudny
Kjartansson Olafur
Jonsson Palmi V
Sigurdsson Gunnar
Thorgeirsson Gudmundur
Aspelund Thor
Garcia Melissa E
Cotch Mary Frances
Hoffman Howard J
Gudnason Vilmundur
Author Affiliation
Laboratory of Epidemiology, Demography, and Biometry, Intramural Research Program, National Institute on Aging, Bethesda, MD 20892-9205, USA. Harris99@mail.nih.gov
Source
Am J Epidemiol. 2007 May 1;165(9):1076-87
Date
May-1-2007
Language
English
Publication Type
Article
Keywords
Age Factors
Aged
Aged, 80 and over
Aging - genetics - pathology
Body Composition
Cardiovascular Diseases - epidemiology - genetics
Chronic Disease
Dementia - epidemiology - genetics
Disease Susceptibility
Environment
Female
Genotype
Geriatrics
Health Status Indicators
Humans
Iceland - epidemiology
Male
Osteoporosis - epidemiology - genetics
Phenotype
Questionnaires
Risk Assessment - methods
Risk factors
Variation (Genetics)
Abstract
In anticipation of the sequencing of the human genome and description of the human proteome, the Age, Gene/Environment Susceptibility-Reykjavik Study (AGES-Reykjavik) was initiated in 2002. AGES-Reykjavik was designed to examine risk factors, including genetic susceptibility and gene/environment interaction, in relation to disease and disability in old age. The study is multidisciplinary, providing detailed phenotypes related to the cardiovascular, neurocognitive (including sensory), and musculoskeletal systems, and to body composition and metabolic regulation. Relevant quantitative traits, subclinical indicators of disease, and medical diagnoses are identified by using biomarkers, imaging, and other physiologic indicators. The AGES-Reykjavik sample is drawn from an established population-based cohort, the Reykjavik Study. This cohort of men and women born between 1907 and 1935 has been followed in Iceland since 1967 by the Icelandic Heart Association. The AGES-Reykjavik cohort, with cardiovascular risk factor assessments earlier in life and detailed late-life phenotypes of quantitative traits, will create a comprehensive study of aging nested in a relatively genetically homogeneous older population. This approach should facilitate identification of genetic factors that contribute to healthy aging as well as the chronic conditions common in old age.
PubMed ID
17351290 View in PubMed
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Cerebral infarcts and cognitive performance: importance of location and number of infarcts.

https://arctichealth.org/en/permalink/ahliterature90519
Source
Stroke. 2009 Mar;40(3):677-82
Publication Type
Article
Date
Mar-2009
Author
Saczynski Jane S
Sigurdsson Sigurdur
Jonsdottir Maria K
Eiriksdottir Gudny
Jonsson Palmi V
Garcia Melissa E
Kjartansson Olafur
Lopez Oscar
van Buchem Mark A
Gudnason Vilmunder
Launer Lenore J
Author Affiliation
Division of Geriatric Medicine, Meyers Primary Care Institute, University of Massachusetts Medical School, Worcester, MA 01605, USA. jane.saczynski@umassmed.edu
Source
Stroke. 2009 Mar;40(3):677-82
Date
Mar-2009
Language
English
Publication Type
Article
Keywords
Aged
Cardiovascular Diseases - epidemiology
Cerebral Infarction - genetics - pathology - psychology
Cognition Disorders - genetics - pathology - psychology
Dementia - diagnosis - psychology
Female
Humans
Iceland - epidemiology
Magnetic Resonance Imaging
Male
Neuropsychological Tests
Risk factors
Abstract
BACKGROUND AND PURPOSE: Cerebral infarcts increase the risk for cognitive impairment. The relevance of location and number of infarcts with respect to cognitive function is less clear. METHODS: We studied the cross-sectional association between number and location of infarcts and cognitive performance in 4030 nondemented participants of the Age Gene/Environment Susceptibility-Reykjavik Study. Composite scores for memory, processing speed, and executive function were created from a neuropsychological battery. Subcortical, cortical, and cerebellar infarcts were identified on brain MRI. We performed linear regression analyses adjusted for demographic and vascular risk factors, depression, white matter lesions, and atrophy. RESULTS: Compared to participants with no infarcts, those with infarcts in multiple locations (n=287, 7%) had slower processing speed (beta=-0.19; P1 location is associated with poor performance in memory, processing speed, and executive function, independent of cardiovascular comorbidities, white matter lesions, and brain atrophy, suggesting that both the number and the distribution of infarcts jointly contribute to cognitive impairment.
Notes
Comment In: Stroke. 2009 Mar;40(3):667-919131649
Erratum In: Stroke. 2009 Apr;40(4):287
PubMed ID
19131654 View in PubMed
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Cognitive impairment: an increasingly important complication of type 2 diabetes: the age, gene/environment susceptibility--Reykjavik study.

https://arctichealth.org/en/permalink/ahliterature91773
Source
Am J Epidemiol. 2008 Nov 15;168(10):1132-9
Publication Type
Article
Date
Nov-15-2008
Author
Saczynski Jane S
Jónsdóttir María K
Garcia Melissa E
Jonsson Palmi V
Peila Rita
Eiriksdottir Gudny
Olafsdottir Elin
Harris Tamara B
Gudnason Vilmundur
Launer Lenore J
Author Affiliation
Division of Geriatric Medicine, University of Massachusetts Medical School, Biotech Four, Suite 315, 377 Plantation Street, Worcester, MA 01605, USA. jane.saczynski@umassmed.edu
Source
Am J Epidemiol. 2008 Nov 15;168(10):1132-9
Date
Nov-15-2008
Language
English
Publication Type
Article
Keywords
Aged
Blood glucose
Cognition Disorders - diagnosis - epidemiology - etiology
Cohort Studies
Diabetes Mellitus, Type 2 - complications - diagnosis - epidemiology
Environment
Fasting - blood
Female
Genetic Predisposition to Disease
Glycemic Index
Hemoglobin A, Glycosylated
Humans
Iceland - epidemiology
Logistic Models
Male
Psychological Tests
Questionnaires
Abstract
Persons with type 2 diabetes are at increased risk of cognitive dysfunction. Less is known about which cognitive abilities are affected and how undiagnosed diabetes and impaired fasting glucose relate to cognitive performance. The authors explored this question using data from 1,917 nondemented men and women (average age = 76 years) in the population-based Age, Gene/Environment Susceptibility-Reykjavik Study (2002-2006). Glycemic status groups included diagnosed diabetes (self-reported diabetes or diabetic medication use; n = 163 (8.5%)), undiagnosed diabetes (fasting blood glucose >or=7.0 mmol/L without diagnosed diabetes; n = 55 (2.9%)), and impaired fasting glucose (fasting blood glucose 5.6-6.9 mmol/L; n = 744 (38.8%)). Composites of memory, processing speed (PS), and executive function were constructed from a neuropsychological battery. Linear regression was used to investigate cross-sectional differences in cognitive performance between glycemic groups, adjusted for demographic and health factors. Persons with diagnosed diabetes had slower PS than normoglycemics (beta = -0.12; P or=15 years was associated with significantly poorer PS and executive function. Undiagnosed diabetics had slower PS (beta = -0.22; P
PubMed ID
18836152 View in PubMed
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