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ADHD as a risk factor for incident unprovoked seizures and epilepsy in children.

https://arctichealth.org/en/permalink/ahliterature30239
Source
Arch Gen Psychiatry. 2004 Jul;61(7):731-6
Publication Type
Article
Date
Jul-2004
Author
Dale C Hesdorffer
Petur Ludvigsson
Elias Olafsson
Gunnar Gudmundsson
Olafur Kjartansson
W Allen Hauser
Author Affiliation
Gertrude H. Sergievsky Center, College of Physicians & Surgeons, and Department of Epidemiology, Mailman School of Public Health, Columbia University, New York, NY 10032, USA.
Source
Arch Gen Psychiatry. 2004 Jul;61(7):731-6
Date
Jul-2004
Language
English
Publication Type
Article
Keywords
Attention Deficit Disorder with Hyperactivity - diagnosis - epidemiology
Case-Control Studies
Child
Child, Preschool
Comorbidity
Comparative Study
Electroencephalography
Epilepsy - diagnosis - epidemiology
Female
Humans
Iceland - epidemiology
Magnetic Resonance Imaging
Male
Population Surveillance
Prevalence
Psychiatric Status Rating Scales
Research Support, U.S. Gov't, P.H.S.
Risk factors
Seizures - diagnosis - epidemiology
Tomography, X-Ray Computed
Abstract
BACKGROUND: Attention-deficit/hyperactivity disorder (ADHD) occurs more frequently than expected in prevalent cohorts with epilepsy. The association has been attributed to the epilepsy or its treatment, although it is impossible to determine in previous studies which condition occurs first. OBJECTIVES: To conduct a population-based case-control study of all newly diagnosed unprovoked seizures among Icelandic children younger than 16 years to address the question of time order. DESIGN: Children with seizures were matched to the next 2 same-sex births from the population registry. The Diagnostic Interview Schedule for Children was used to make a DSM-IV diagnosis of ADHD in a standardized fashion among cases and controls aged 3 to 16 years. RESULTS: A history of ADHD was 2.5-fold more common among children with newly diagnosed seizures than among control subjects (95% confidence interval [CI], 1.1-5.5). The association was restricted to ADHD predominantly inattentive type (odds ratio [OR], 3.7; 95% CI, 1.1-12.8), not ADHD predominantly hyperactive-impulsive type (OR, 1.8; 95% CI, 0.6-5.7) or ADHD combined type (OR, 2.5; 95% CI, 0.3-18.3). Seizure type, etiology, sex, or seizure frequency at diagnosis (1 or >1) did not affect findings. CONCLUSION: Attention-deficit/hyperactivity disorder occurs more often than expected before unprovoked seizures, suggesting a common antecedent for both conditions.
PubMed ID
15237085 View in PubMed
Less detail

The AGES-Reykjavik study atlases: Non-linear multi-spectral template and atlases for studies of the ageing brain.

https://arctichealth.org/en/permalink/ahliterature282555
Source
Med Image Anal. 2017 May 06;39:133-144
Publication Type
Article
Date
May-06-2017
Author
Lars Forsberg
Sigurdur Sigurdsson
Jesper Fredriksson
Asdis Egilsdottir
Bryndis Oskarsdottir
Olafur Kjartansson
Mark A van Buchem
Lenore J Launer
Vilmundur Gudnason
Alex Zijdenbos
Source
Med Image Anal. 2017 May 06;39:133-144
Date
May-06-2017
Language
English
Publication Type
Article
Abstract
Quantitative analyses of brain structures from Magnetic Resonance (MR) image data are often performed using automatic segmentation algorithms. Many of these algorithms rely on templates and atlases in a common coordinate space. Most freely available brain atlases are generated from relatively young individuals and not always derived from well-defined cohort studies. In this paper, we introduce a publicly available multi-spectral template with corresponding tissue probability atlases and regional atlases, optimised to use in studies of ageing cohorts (mean age 75 ± 5 years). Furthermore, we provide validation data from a regional segmentation pipeline to assure the integrity of the dataset.
PubMed ID
28501699 View in PubMed
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The AGES-Reykjavik study atlases: Non-linear multi-spectral template and atlases for studies of the ageing brain.

https://arctichealth.org/en/permalink/ahliterature292006
Source
Med Image Anal. 2017 Jul; 39:133-144
Publication Type
Journal Article
Date
Jul-2017
Author
Lars Forsberg
Sigurdur Sigurdsson
Jesper Fredriksson
Asdis Egilsdottir
Bryndis Oskarsdottir
Olafur Kjartansson
Mark A van Buchem
Lenore J Launer
Vilmundur Gudnason
Alex Zijdenbos
Author Affiliation
The Icelandic Heart Association, Kopavogur, Iceland; Department of Neuroscience, Karolinska Institutet, Stockholm, Sweden. Electronic address: larsef@me.com.
Source
Med Image Anal. 2017 Jul; 39:133-144
Date
Jul-2017
Language
English
Publication Type
Journal Article
Keywords
Aged
Aging
Algorithms
Anatomy, Artistic
Atlases as Topic
Brain - diagnostic imaging
Female
Humans
Image Processing, Computer-Assisted - methods
Magnetic Resonance Imaging - methods
Male
Abstract
Quantitative analyses of brain structures from Magnetic Resonance (MR) image data are often performed using automatic segmentation algorithms. Many of these algorithms rely on templates and atlases in a common coordinate space. Most freely available brain atlases are generated from relatively young individuals and not always derived from well-defined cohort studies. In this paper, we introduce a publicly available multi-spectral template with corresponding tissue probability atlases and regional atlases, optimised to use in studies of ageing cohorts (mean age 75 ± 5 years). Furthermore, we provide validation data from a regional segmentation pipeline to assure the integrity of the dataset.
Notes
Cites: Neuroimage. 2010 Feb 1;49(3):2352-65 PMID 19857578
Cites: Neuroimage. 2004;23 Suppl 1:S208-19 PMID 15501092
Cites: Stroke. 2008 Apr;39(4):1134-41 PMID 18323507
Cites: J Cereb Blood Flow Metab. 1990 Jul;10 (4):443-57 PMID 2347878
Cites: Neuron. 2002 Jan 31;33(3):341-55 PMID 11832223
Cites: Neuroimage. 2008 Feb 1;39(3):1064-80 PMID 18037310
Cites: Neuroimage. 1997 Oct;6(3):209-17 PMID 9344825
Cites: NMR Biomed. 2015 Apr;28(4):468-85 PMID 25802212
Cites: Neuroimage. 2006 Oct 15;33(1):115-26 PMID 16860573
Cites: Neuroimage. 2011 Jan 1;54(1):313-27 PMID 20656036
Cites: Neuroimage. 2009 Jul 1;46(3):726-38 PMID 19245840
Cites: Neuroimage. 2001 Jul;14(1 Pt 1):21-36 PMID 11525331
Cites: J Comput Assist Tomogr. 1994 Mar-Apr;18(2):192-205 PMID 8126267
Cites: IEEE Trans Med Imaging. 2007 Apr;26(4):479-86 PMID 17427735
Cites: Image Vis Comput. 2001 Jan 1;19(1-2):3-24 PMID 19890483
Cites: Neuroimage. 2005 Jul 15;26(4):1009-18 PMID 15908234
Cites: Comput Methods Programs Biomed. 2011 Dec;104(3):e158-77 PMID 21871688
Cites: IEEE Trans Med Imaging. 2002 Oct;21(10):1280-91 PMID 12585710
Cites: Ann N Y Acad Sci. 2002 Nov;977:141-8 PMID 12480744
Cites: Neuroimage. 1995 Jun;2(2):89-101 PMID 9343592
Cites: Neuroimage. 2007 Apr 1;35(2):686-97 PMID 17320415
Cites: Neuroimage. 2002 Jan;15(1):273-89 PMID 11771995
Cites: Hum Brain Mapp. 2002 Nov;17(3):143-55 PMID 12391568
Cites: IEEE Trans Med Imaging. 2009 Aug;28(8):1266-77 PMID 19228554
Cites: Inf Process Med Imaging. 2001;2082:488-501 PMID 21218175
Cites: Philos Trans R Soc Lond B Biol Sci. 2001 Aug 29;356(1412):1293-322 PMID 11545704
Cites: Clin Chem. 1974 Dec;20(12):1535-42 PMID 4430131
Cites: Biometrics. 1996 Dec;52(4):1195-203 PMID 8962450
Cites: Neuroimage. 2012 Feb 15;59(4):3862-3870 PMID 22119006
Cites: Hum Brain Mapp. 1994;1(3):173-84 PMID 24578038
Cites: Clin Neuroradiol. 2016 Dec;26(4):423-430 PMID 25791203
PubMed ID
28501699 View in PubMed
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Arterial stiffness, pressure and flow pulsatility and brain structure and function: the Age, Gene/Environment Susceptibility--Reykjavik study.

https://arctichealth.org/en/permalink/ahliterature129735
Source
Brain. 2011 Nov;134(Pt 11):3398-407
Publication Type
Article
Date
Nov-2011
Author
Gary F Mitchell
Mark A van Buchem
Sigurdur Sigurdsson
John D Gotal
Maria K Jonsdottir
Ólafur Kjartansson
Melissa Garcia
Thor Aspelund
Tamara B Harris
Vilmundur Gudnason
Lenore J Launer
Author Affiliation
Cardiovascular Engineering, Inc., Norwood, MA 02062, USA. garyfmitchell@mindspring.com
Source
Brain. 2011 Nov;134(Pt 11):3398-407
Date
Nov-2011
Language
English
Publication Type
Article
Keywords
Age Factors
Aged
Aged, 80 and over
Aorta - physiopathology
Blood Flow Velocity - physiology
Blood Pressure - physiology
Brain - blood supply - pathology - physiopathology
Cardiovascular Diseases - pathology - physiopathology
Carotid Arteries - physiopathology
Female
Gene-Environment Interaction
Humans
Iceland
Male
Prospective Studies
Pulsatile Flow - physiology
Risk factors
Vascular Stiffness - physiology
Abstract
Aortic stiffness increases with age and vascular risk factor exposure and is associated with increased risk for structural and functional abnormalities in the brain. High ambient flow and low impedance are thought to sensitize the cerebral microcirculation to harmful effects of excessive pressure and flow pulsatility. However, haemodynamic mechanisms contributing to structural brain lesions and cognitive impairment in the presence of high aortic stiffness remain unclear. We hypothesized that disproportionate stiffening of the proximal aorta as compared with the carotid arteries reduces wave reflection at this important interface and thereby facilitates transmission of excessive pulsatile energy into the cerebral microcirculation, leading to microvascular damage and impaired function. To assess this hypothesis, we evaluated carotid pressure and flow, carotid-femoral pulse wave velocity, brain magnetic resonance images and cognitive scores in participants in the community-based Age, Gene/Environment Susceptibility--Reykjavik study who had no history of stroke, transient ischaemic attack or dementia (n = 668, 378 females, 69-93 years of age). Aortic characteristic impedance was assessed in a random subset (n = 422) and the reflection coefficient at the aorta-carotid interface was computed. Carotid flow pulsatility index was negatively related to the aorta-carotid reflection coefficient (R = -0.66, P
Notes
Cites: J Appl Physiol (1985). 2008 Nov;105(5):1652-6018772322
Cites: J Gerontol A Biol Sci Med Sci. 2008 Aug;63(8):848-5418772473
Cites: Hypertension. 2008 Dec;52(6):1120-618852384
Cites: Stroke. 2009 Mar;40(3):677-8219131654
Cites: Hypertension. 2009 Apr;53(4):668-7319237680
Cites: Stroke. 2009 Apr;40(4):1229-3619246701
Cites: JAMA. 2009 Jun 24;301(24):2563-7019549973
Cites: Radiology. 2009 Dec;253(3):681-819864506
Cites: Circulation. 2010 Feb 2;121(4):505-1120083680
Cites: Eur Radiol. 2010 May;20(5):1132-819915847
Cites: Stroke. 2010 May;41(5):891-720360538
Cites: Circulation. 2010 Oct 5;122(14):1379-8620855656
Cites: Ann Neurol. 2000 Feb;47(2):145-5110665484
Cites: Hypertension. 2001 May;37(5):1236-4111358934
Cites: Arterioscler Thromb Vasc Biol. 2001 Dec;21(12):2046-5011742883
Cites: Hypertension. 2002 Jan;39(1):10-511799071
Cites: Circulation. 2002 Jun 25;105(25):2955-6112081987
Cites: IEEE Trans Med Imaging. 2002 Oct;21(10):1280-9112585710
Cites: Stroke. 2003 May;34(5):1203-612677025
Cites: Hypertension. 2004 Jun;43(6):1239-4515123572
Cites: Hypertension. 2004 Aug;44(2):134-915249547
Cites: J Psychiatr Res. 1975 Nov;12(3):189-981202204
Cites: Circulation. 1980 Jul;62(1):105-167379273
Cites: Med Biol Eng Comput. 1981 Sep;19(5):565-87334864
Cites: J Am Coll Cardiol. 1992 Oct;20(4):952-631527307
Cites: Stroke. 1997 Mar;28(3):652-99056627
Cites: Psychol Aging. 1998 Mar;13(1):8-209533186
Cites: J Gerontol B Psychol Sci Soc Sci. 1999 May;54(3):P155-6010363036
Cites: Circulation. 2005 Jun 28;111(25):3384-9015967850
Cites: Hypertension. 2005 Sep;46(3):454-6216103272
Cites: Stroke. 2005 Oct;36(10):2193-716151027
Cites: Circulation. 2005 Dec 13;112(24):3722-816330686
Cites: Circulation. 2006 Feb 7;113(5):657-6316461838
Cites: Circulation. 2006 Feb 7;113(5):664-7016461839
Cites: Stroke. 2007 Mar;38(3):888-9217272780
Cites: J Hypertens. 2007 May;25(5):1035-4017414668
Cites: Am J Epidemiol. 2007 May 1;165(9):1076-8717351290
Cites: Circulation. 2007 May 22;115(20):2628-3617485578
Cites: Hypertension. 2008 Jan;51(1):99-10418025297
Cites: Hypertension. 2008 Apr;51(4):1123-818259005
Cites: Am J Hypertens. 2008 Dec;21(12):1304-918802428
PubMed ID
22075523 View in PubMed
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Birth size and brain function 75 years later.

https://arctichealth.org/en/permalink/ahliterature260782
Source
Pediatrics. 2014 Oct;134(4):761-70
Publication Type
Article
Date
Oct-2014
Author
Majon Muller
Sigurdur Sigurdsson
Olafur Kjartansson
Palmi V Jonsson
Melissa Garcia
Mikaela B von Bonsdorff
Ingibjorg Gunnarsdottir
Inga Thorsdottir
Tamara B Harris
Mark van Buchem
Vilmundur Gudnason
Lenore J Launer
Source
Pediatrics. 2014 Oct;134(4):761-70
Date
Oct-2014
Language
English
Publication Type
Article
Keywords
Adult
Aged
Aged, 80 and over
Aging - physiology
Birth Weight - physiology
Brain - physiology
Cognition - physiology
Cohort Studies
Female
Follow-Up Studies
Humans
Iceland - epidemiology
Male
Middle Aged
Population Surveillance - methods
Abstract
There are several lines of evidence pointing to fetal and other early origins of diseases of the aging brain, but there are no data directly addressing the hypotheses in an older population. We investigated the association of fetal size to late-age measures of brain structure and function in a large cohort of older men and women and explored the modifying effect of education on these associations.
Within the AGES (Age Gene/Environment Susceptibility)-Reykjavik population-based cohort (born between 1907 and 1935), archived birth records were abstracted for 1254 men and women who ~75 years later underwent an examination that included brain MRI and extensive cognitive assessment.
Adjustment for intracranial volume, demographic and medical history characteristics, and lower Ponderal index at birth (per kg/m(3)), an indicator of third-trimester fetal wasting, was significantly associated with smaller volumes of total brain and white matter; ßs (95% confidence intervals) were -1.0 (-1.9 to -0.0) and -0.5 (-1.0 to -0.0) mL. Furthermore, lower Ponderal index was associated with slower processing speed and reduced executive functioning but only in those with low education (ß [95% confidence interval]: -0.136 [-0.235 to -0.036] and -0.077 [-0.153 to -0.001]).
This first study of its kind provides clinical measures suggesting that smaller birth size, as an indicator of a suboptimal intrauterine environment, is associated with late-life alterations in brain tissue volume and function. In addition, it shows that the effects of a suboptimal intrauterine environment on late-life cognitive function were present only in those with lower educational levels.
PubMed ID
25180277 View in PubMed
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Brain tissue volumes in the general population of the elderly: the AGES-Reykjavik study.

https://arctichealth.org/en/permalink/ahliterature129325
Source
Neuroimage. 2012 Feb 15;59(4):3862-70
Publication Type
Article
Date
Feb-15-2012
Author
Sigurdur Sigurdsson
Thor Aspelund
Lars Forsberg
Jesper Fredriksson
Olafur Kjartansson
Bryndis Oskarsdottir
Palmi V Jonsson
Gudny Eiriksdottir
Tamara B Harris
Alex Zijdenbos
Mark A van Buchem
Lenore J Launer
Vilmundur Gudnason
Author Affiliation
The Icelandic Heart Association, Kopavogur, Iceland. sigurdur@hjarta.is
Source
Neuroimage. 2012 Feb 15;59(4):3862-70
Date
Feb-15-2012
Language
English
Publication Type
Article
Keywords
Age Factors
Aged
Aged, 80 and over
Atrophy
Brain - pathology
Female
Humans
Magnetic Resonance Imaging
Male
Organ Size
Abstract
Imaging studies have reported conflicting findings on how brain structure differs with age and sex. This may be explained by discrepancies and limitations in study population and study design. We report a study on brain tissue volumes in one of the largest cohorts of individuals studied to date of subjects with high mean age (mean ± standard deviation (SD) 76 ± 6 years). These analyses are based on magnetic resonance imaging (MRI) scans acquired at baseline on 4303 non-demented elderly, and 367 who had a second MRI, on average 2.5 ± 0.2 years later. Tissue segmentation was performed with an automatic image analysis pipeline. Total brain parenchymal (TBP) volume decreased with increasing age while there was an increase in white matter hyperintensities (WMH) in both sexes. A reduction in both normal white matter (NWM)- and gray matter (GM) volume contributed to the brain shrinkage. After adjusting for intra-cranial volume, women had larger brain volumes compared to men (3.32%, p
PubMed ID
22119006 View in PubMed
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Coronary artery calcium, brain function and structure: the AGES-Reykjavik Study.

https://arctichealth.org/en/permalink/ahliterature97484
Source
Stroke. 2010 May;41(5):891-7
Publication Type
Article
Date
May-2010
Author
Jean-Sébastien Vidal
Sigurdur Sigurdsson
Maria K Jonsdottir
Gudny Eiriksdottir
Gudmundur Thorgeirsson
Olafur Kjartansson
Melissa E Garcia
Mark A van Buchem
Tamara B Harris
Vilmundur Gudnason
Lenore J Launer
Author Affiliation
National Institutes of Health, NIA/LEDB, 7201 Wisconsin Ave, Gateway Building, Suite 3C309, Bethesda, MD 20892-9205, USA.
Source
Stroke. 2010 May;41(5):891-7
Date
May-2010
Language
English
Publication Type
Article
Keywords
Aged
Aged, 80 and over
Aging - genetics - pathology - physiology
Brain - pathology - physiology
Calcinosis - epidemiology - genetics - pathology - physiopathology
Cognition Disorders - epidemiology - genetics - pathology
Cohort Studies
Coronary Artery Disease - epidemiology - genetics - pathology - physiopathology
Coronary Vessels - pathology - physiology
Cross-Sectional Studies
Environment
Female
Genetic Predisposition to Disease - epidemiology - genetics
Humans
Iceland - epidemiology
Magnetic Resonance Imaging
Male
Abstract
BACKGROUND AND PURPOSE: Several cardiovascular risk factors are associated with cognitive disorders in older persons. Little is known about the association of the burden of coronary atherosclerosis with brain structure and function. METHODS: This is a cross-sectional analysis of data from the Age, Gene, Environment Susceptibility (AGES)-Reykjavik Study cohort of men and women born 1907 to 1935. Coronary artery calcification (CAC), a marker of atherosclerotic burden, was measured with CT. Memory, speed of processing, and executive function composites were calculated from a cognitive test battery. Dementia was assessed in a multistep procedure and diagnosed according to international guidelines. Quantitative data on total intracranial and tissue volumes (total, gray matter volume, white matter volume, and white matter lesion volume), cerebral infarcts, and cerebral microbleeds were obtained with brain MRI. The association of CAC with dementia (n=165 cases) and cognitive function in nondemented subjects (n=4085), and separately with MRI outcomes, was examined in multivariate models adjusting for demographic and vascular risk factors. Analyses tested whether brain structure mediated the associations of CAC to cognitive function. RESULTS: Subjects with higher CAC were more likely to have dementia and lower cognitive scores, more likely to have lower white matter volume, gray matter volume, and total brain tissue, and to have more cerebral infarcts, cerebral microbleeds, and white matter lesions. The relations of cognitive performance and dementia to CAC were significantly attenuated when the models were adjusted for brain lesions and volumes. CONCLUSIONS: In a population-based sample, increasing atherosclerotic load assessed by CAC is associated with poorer cognitive performance and dementia, and these relations are mediated by evidence of brain pathology.
PubMed ID
20360538 View in PubMed
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Depression and suicide attempt as risk factors for incident unprovoked seizures.

https://arctichealth.org/en/permalink/ahliterature9104
Source
Ann Neurol. 2006 Jan;59(1):35-41
Publication Type
Article
Date
Jan-2006
Author
Dale C Hesdorffer
W Allen Hauser
Elias Olafsson
Petur Ludvigsson
Olafur Kjartansson
Author Affiliation
Gertrude H. Sergievsky Center, Columbia University, 630 West 168th Street, New York, NY 10032, USA. dch5@columbia.edu
Source
Ann Neurol. 2006 Jan;59(1):35-41
Date
Jan-2006
Language
English
Publication Type
Article
Keywords
Adolescent
Adult
Child
Depression - complications - physiopathology
Epilepsy - diagnosis - physiopathology
Female
Humans
Iceland
Male
Middle Aged
Research Support, N.I.H., Extramural
Risk factors
Seizures - etiology - physiopathology
Suicide, Attempted
Abstract
Major depression has been shown to increase the risk for development of epilepsy, but prior studies have not evaluated whether this is due to specific symptoms of depression. We conducted a population-based case-control study of all newly diagnosed unprovoked seizures among Icelandic children and adults aged 10 years and older to test the hypothesis that major depression is a risk factor for developing unprovoked seizure and epilepsy, and to address whether specific symptoms of depression account for this increased risk. Cases were matched to the next two same sex births from the population registry. Using standardized interviews, we ascertained symptoms of major depression to make a Diagnostic and Statistical Manual, Fourth Edition (DSM-IV) diagnosis. A history of major depression was 1.7-fold more common among cases than among controls (95% confidence interval, 1.1-2.7). A history of attempted suicide was 5.1-fold more common among cases than among controls (95% confidence interval, 2.2-11.5). Attempted suicide increased seizure risk even after adjusting for age, sex, cumulative alcohol intake, and major depression or number of symptoms of depression. Major depression and attempted suicide independently increase the risk for unprovoked seizure. These data suggest that depression and suicide attempt may be due to different underlying neurochemical pathways, each of which is important in the development of epilepsy.
PubMed ID
16217743 View in PubMed
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Diabetes, markers of brain pathology and cognitive function: the Age, Gene/Environment Susceptibility-Reykjavik Study.

https://arctichealth.org/en/permalink/ahliterature106113
Source
Ann Neurol. 2014 Jan;75(1):138-46
Publication Type
Article
Date
Jan-2014
Author
Chengxuan Qiu
Sigurdur Sigurdsson
Qian Zhang
Maria K Jonsdottir
Olafur Kjartansson
Gudny Eiriksdottir
Melissa E Garcia
Tamara B Harris
Mark A van Buchem
Vilmundur Gudnason
Lenore J Launer
Author Affiliation
Laboratory of Epidemiology and Population Sciences, National Institute on Aging, National Institutes of Health, Bethesda, MD; Aging Research Center, Department of Neurobiology, Care Sciences, and Society, Karolinska Institutet-Stockholm University, Stockholm, Sweden.
Source
Ann Neurol. 2014 Jan;75(1):138-46
Date
Jan-2014
Language
English
Publication Type
Article
Keywords
Aged
Aged, 80 and over
Aging - genetics - metabolism - pathology
Brain - pathology
Brain Diseases - epidemiology - genetics - pathology
Cognition - physiology
Cognition Disorders - epidemiology - genetics - pathology
Cohort Studies
Cross-Sectional Studies
Diabetes Mellitus - epidemiology - genetics - pathology
Disease Susceptibility - metabolism - pathology
Female
Humans
Iceland - epidemiology
Male
Abstract
We investigated whether, and the extent to which, vascular and degenerative lesions in the brain mediate the association of diabetes with poor cognitive performance.
This cross-sectional study included 4,206 participants (age?>?65 years; 57.8% women) of the Age, Gene/Environment Susceptibility-Reykjavik Study. Data were collected through interview, clinical examination, psychological testing, and laboratory tests. The composite scores on memory, information-processing speed, and executive function were derived from a cognitive test battery. Markers of cerebral macrovascular (cortical infarcts), microvascular (subcortical infarcts, cerebral microbleeds, and higher white matter lesion volume), and neurodegenerative (lower gray matter, normal white matter, and total brain tissue volumes) processes were assessed on magnetic resonance images. Mediation models were employed to test the mediating effect of brain lesions on the association of diabetes with cognitive performance controlling for potential confounders.
There were 462 (11.0%) persons with diabetes. Diabetes was significantly associated with lower scores on processing speed and executive function, but not with memory function. Diabetes was significantly associated with all markers of brain pathology. All of these markers were significantly associated with lower scores on memory, processing speed, and executive function. Formal mediation tests suggested that markers of cerebrovascular and degenerative pathology significantly mediated the associations of diabetes with processing speed and executive function.
Diabetes is associated with poor performance on cognitive tests of information-processing speed and executive function. The association is largely mediated by markers of both neurodegeneration and cerebrovascular disease. Older people with diabetes should be monitored for cognitive problems and brain lesions.
PubMed ID
24243491 View in PubMed
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Glycemic status and brain injury in older individuals: the age gene/environment susceptibility-Reykjavik study.

https://arctichealth.org/en/permalink/ahliterature150441
Source
Diabetes Care. 2009 Sep;32(9):1608-13
Publication Type
Article
Date
Sep-2009
Author
Jane S Saczynski
Sigurdur Siggurdsson
Palmi V Jonsson
Gudny Eiriksdottir
Elin Olafsdottir
Olafur Kjartansson
Tamara B Harris
Mark A van Buchem
Vilmundur Gudnason
Lenore J Launer
Author Affiliation
Division of Geriatric Medicine and Meyers Primary Care Institute, University of Massachusetts Medical School, Worcester, Massachusetts, USA. jane.saczynski@umassmed.edu
Source
Diabetes Care. 2009 Sep;32(9):1608-13
Date
Sep-2009
Language
English
Publication Type
Article
Keywords
Age Factors
Aged
Aged, 80 and over
Brain Injuries - epidemiology - pathology
Cerebral Infarction - epidemiology - pathology
Diabetes Mellitus, Type 2 - epidemiology - pathology
Disease Susceptibility
Female
Humans
Male
Sex Factors
Abstract
To examine the association of glycemic status to magnetic resonance imaging indicators of brain pathological changes.
This was a cross-sectional, population-based study of 4,415 men and women without dementia (mean age 76 years) participating in the Age Gene/Environment Susceptibility-Reykjavik Study. Glycemic status groups included the following: type 2 diabetes (self-report of diabetes, use of diabetes medications, or fasting blood glucose > or =7.0 mmol/l [11.1%]); impaired fasting glucose (IFG) (fasting blood glucose 5.6-6.9 mmol/l [36.2%]); and normoglycemic (52.7%). Outcomes were total brain volume, white and gray matter volume, white matter lesion (WML) volume, and presence of cerebral infarcts.
After adjustment for demographic and cardiovascular risk factors, participants with type 2 diabetes had significantly lower total brain volume (72.2 vs. 71.5%; P
Notes
Cites: N Engl J Med. 2004 Apr 1;350(14):1387-9715070788
Cites: J Neurol Neurosurg Psychiatry. 2003 Jan;74(1):70-612486269
Cites: Diabetes Care. 2004 Jul;27(7):1798-81115220270
Cites: J Psychiatr Res. 1975 Nov;12(3):189-981202204
Cites: Diabetes Metab Res Rev. 2006 Nov-Dec;22(6):423-3616506274
Cites: Neurology. 2006 Dec 12;67(11):1960-517159101
Cites: Am J Epidemiol. 2007 May 1;165(9):1076-8717351290
Cites: Diabetes Care. 2007 May;30(5):1193-917290035
Cites: Am J Cardiol. 2007 Jun 18;99(12A):112i-122i17599421
Cites: Stroke. 2008 May;39(5):1600-318369167
Cites: Diabetes Care. 2008 Sep;31(9):1761-618509209
Cites: Am J Epidemiol. 2008 Nov 15;168(10):1132-918836152
Cites: Diabetes Res Clin Pract. 2000 Dec;50(3):203-1211106835
Cites: Diabetes Metab. 2001 Sep;27(4 Pt 1):436-4711547217
Cites: IEEE Trans Med Imaging. 2002 Oct;21(10):1280-9112585710
Cites: Diabetes Care. 2004 Jan;27 Suppl 1:S5-S1014693921
Cites: Lancet Neurol. 2004 Mar;3(3):169-7814980532
Cites: Am J Epidemiol. 2001 Oct 1;154(7):635-4111581097
Cites: Nature. 2001 Dec 13;414(6865):782-711742409
Cites: Diabetes. 2002 Apr;51(4):1256-6211916953
Cites: Diabetes Care. 2004 May;27(5):1047-5315111519
PubMed ID
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