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The AGES-Reykjavik Study suggests that change in kidney measures is associated with subclinical brain pathology in older community-dwelling persons.

https://arctichealth.org/en/permalink/ahliterature292670
Source
Kidney Int. 2018 Jun 27; :
Publication Type
Journal Article
Date
Jun-27-2018
Author
Sanaz Sedaghat
Jie Ding
Gudny Eiriksdottir
Mark A van Buchem
Sigurdur Sigurdsson
M Arfan Ikram
Osorio Meirelles
Vilmundur Gudnason
Andrew S Levey
Lenore J Launer
Author Affiliation
Department of Epidemiology, Erasmus University Medical Center, Rotterdam, The Netherlands; Department of Preventive Medicine, Feinberg School of Medicine, Northwestern University, Chicago, Illinois, USA.
Source
Kidney Int. 2018 Jun 27; :
Date
Jun-27-2018
Language
English
Publication Type
Journal Article
Abstract
Decreased glomerular filtration rate (GFR) and albuminuria may be accompanied by brain pathology. Here we investigated whether changes in these kidney measures are linked to development of new MRI-detected infarcts and microbleeds, and progression of white matter hyperintensity volume. The study included 2671 participants from the population-based AGES-Reykjavik Study (mean age 75, 58.7% women). GFR was estimated from serum creatinine, and albuminuria was assessed by urinary albumin-to-creatinine ratio. Brain MRI was acquired at baseline (2002-2006) and 5 years later (2007-2011). New MRI-detected infarcts and microbleeds were counted on the follow-up scans. White matter hyperintensity progression was estimated as percent change in white matter hyperintensity volumes between the two exams. Participants with a large eGFR decline (over 3 ml/min per 1.73m2 per year) had more incident subcortical infarcts (odds ratio 1.53; 95% confidence interval 1.05, 2.22), and more marked progression of white matter hyperintensity volume (difference: 8%; 95% confidence interval: 4%, 12%), compared to participants without a large decline. Participants with incident albuminuria (over 30 mg/g) had 21% more white matter hyperintensity volume progression (95% confidence interval: 14%, 29%) and 1.86 higher odds of developing new deep microbleeds (95% confidence interval 1.16, 2.98), compared to participants without incident albuminuria. The findings were independent of cardiovascular risk factors. Changes in kidney measures were not associated with occurrence of cortical infarcts. Thus, larger changes in eGFR and albuminuria are associated with increased risk for developing manifestations of cerebral small vessel disease. Individuals with larger changes in these kidney measures should be considered as a high risk population for accelerated brain pathology.
PubMed ID
29960746 View in PubMed
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The AGES-Reykjavik Study suggests that change in kidney measures is associated with subclinical brain pathology in older community-dwelling persons.

https://arctichealth.org/en/permalink/ahliterature300494
Source
Kidney Int. 2018 09; 94(3):608-615
Publication Type
Journal Article
Research Support, N.I.H., Extramural
Research Support, N.I.H., Intramural
Research Support, Non-U.S. Gov't
Date
09-2018
Author
Sanaz Sedaghat
Jie Ding
Gudny Eiriksdottir
Mark A van Buchem
Sigurdur Sigurdsson
M Arfan Ikram
Osorio Meirelles
Vilmundur Gudnason
Andrew S Levey
Lenore J Launer
Author Affiliation
Department of Epidemiology, Erasmus University Medical Center, Rotterdam, The Netherlands; Department of Preventive Medicine, Feinberg School of Medicine, Northwestern University, Chicago, Illinois, USA.
Source
Kidney Int. 2018 09; 94(3):608-615
Date
09-2018
Language
English
Publication Type
Journal Article
Research Support, N.I.H., Extramural
Research Support, N.I.H., Intramural
Research Support, Non-U.S. Gov't
Keywords
Aged
Albuminuria - physiopathology - urine
Cerebral Small Vessel Diseases - diagnosis - epidemiology
Creatinine - urine
Disease Progression
Female
Follow-Up Studies
Glomerular Filtration Rate - physiology
Humans
Incidence
Independent living
Kidney - physiopathology
Magnetic Resonance Imaging
Male
Prospective Studies
Renal Insufficiency, Chronic - physiopathology - urine
Risk factors
Serum Albumin
White Matter - diagnostic imaging - pathology
Abstract
Decreased glomerular filtration rate (GFR) and albuminuria may be accompanied by brain pathology. Here we investigated whether changes in these kidney measures are linked to development of new MRI-detected infarcts and microbleeds, and progression of white matter hyperintensity volume. The study included 2671 participants from the population-based AGES-Reykjavik Study (mean age 75, 58.7% women). GFR was estimated from serum creatinine, and albuminuria was assessed by urinary albumin-to-creatinine ratio. Brain MRI was acquired at baseline (2002-2006) and 5 years later (2007-2011). New MRI-detected infarcts and microbleeds were counted on the follow-up scans. White matter hyperintensity progression was estimated as percent change in white matter hyperintensity volumes between the two exams. Participants with a large eGFR decline (over 3 ml/min/1.73m2 per year) had more incident subcortical infarcts (odds ratio 1.53; 95% confidence interval 1.05, 2.22), and more marked progression of white matter hyperintensity volume (difference: 8%; 95% confidence interval: 4%, 12%), compared to participants without a large decline. Participants with incident albuminuria (over 30 mg/g) had 21% more white matter hyperintensity volume progression (95% confidence interval: 14%, 29%) and 1.86 higher odds of developing new deep microbleeds (95% confidence interval 1.16, 2.98), compared to participants without incident albuminuria. The findings were independent of cardiovascular risk factors. Changes in kidney measures were not associated with occurrence of cortical infarcts. Thus, larger changes in eGFR and albuminuria are associated with increased risk for developing manifestations of cerebral small vessel disease. Individuals with larger changes in these kidney measures should be considered as a high risk population for accelerated brain pathology.
PubMed ID
29960746 View in PubMed
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Cardiac and Carotid Markers Link With Accelerated Brain Atrophy: The AGES-Reykjavik Study.

https://arctichealth.org/en/permalink/ahliterature276094
Source
Arterioscler Thromb Vasc Biol. 2016 Sep 8;
Publication Type
Article
Date
Sep-8-2016
Author
Behnam Sabayan
Mark A van Buchem
Sigurdur Sigurdsson
Qian Zhang
Osorio Meirelles
Tamara B Harris
Vilmundur Gudnason
Andrew E Arai
Lenore J Launer
Source
Arterioscler Thromb Vasc Biol. 2016 Sep 8;
Date
Sep-8-2016
Language
English
Publication Type
Article
Abstract
Pathologies in the heart-brain axis might, independently or in combination, accelerate the process of brain parenchymal loss. We aimed to investigate the association of serum N-terminal brain natriuretic peptide (NT-proBNP), as a marker of cardiac dysfunction, and carotid intima media thickness (CIMT), as a marker of carotid atherosclerosis burden, with structural brain changes.
In the longitudinal population-based AGES-Reykjavik study, we included 2430 subjects (mean age, 74.6 years; 41.4% men) with baseline data on NT-proBNP and CITM (assessed by ultrasound imaging). Participants underwent a high-resolution brain magnetic resonance imaging at baseline and 5 years later to assess total brain (TBV), gray matter, and white matter volumes. Each unit higher log-transformed NT-proBNP was associated with 3.6 mL (95% confidence interval [CI], -6.0 to -1.1) decline in TBV and 3.5 mL (95% CI, -5.7 to -1.3) decline in gray matter volume. Likewise, each millimeter higher CIMT was associated with 10.8 mL (95% CI, -17.3 to -4.2) decline in TBV and 8.6 mL (95% CI, -14.4 to -2.8) decline in gray matter volume. There was no association between NT-proBNP and CIMT and changes in white matter volume. Compared with participants with low NT-proBNP and CIMT, participants with both high NT-proBNP and CIMT had 3.8 mL (95% CI, -6.0 to -1.6) greater decline in their TBV and 4 mL (95% CI, -6.0 to -2.0) greater decline in GMW. These associations were independent of sociodemographic and cardiovascular factors.
Older subjects with both cardiac dysfunction and carotid atherosclerosis are at an increased risk for brain parenchymal loss. Accumulated pathologies in the heart-brain axis might accelerate brain atrophy.
PubMed ID
27609370 View in PubMed
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Physical activity and incidence of sarcopenia: the population-based AGES-Reykjavik Study.

https://arctichealth.org/en/permalink/ahliterature272829
Source
Age Ageing. 2016 May 17;
Publication Type
Article
Date
May-17-2016
Author
Donja M Mijnarends
Annemarie Koster
Jos M G A Schols
Judith M M Meijers
Ruud J G Halfens
Vilmundur Gudnason
Gudny Eiriksdottir
Kristin Siggeirsdottir
Sigurdur Sigurdsson
Pálmi V Jónsson
Osorio Meirelles
Tamara Harris
Source
Age Ageing. 2016 May 17;
Date
May-17-2016
Language
English
Publication Type
Article
Abstract
the prevalence of sarcopenia increases with age. Physical activity might slow the rate of muscle loss and therewith the incidence of sarcopenia.
to examine the association of physical activity with incident sarcopenia over a 5-year period.
data from the population-based Age, Gene/Environment, Susceptibility-Reykjavik Study were used.
people residing in the Reykjavik area at the start of the study.
the study included people aged 66-93 years (n = 2309).
the amount of moderate-vigorous physical activity (MVPA) was assessed by a self-reported questionnaire. Sarcopenia was identified using the European Working Group on Sarcopenia in Older People algorithm, including muscle mass (computed tomography imaging), grip strength (computerised dynamometer) and gait speed (6 m).
mean age of the participants was 74.9 ± 4.7 years. The prevalence of sarcopenia was 7.3% at baseline and 16.8% at follow-up. The incidence proportion of sarcopenia over 5 years was 14.8% in the least-active individuals and 9.0% in the most-active individuals. Compared with the least-active participants, those reporting a moderate-high amount of MVPA had a significantly lower likelihood of incident sarcopenia (OR = 0.64, 95% CI 0.45-0.91). Participants with a high amount of MVPA had higher baseline levels of muscle mass, strength and walking speed, but baseline MVPA was not associated with the rate of muscle loss.
a higher amount of MVPA seems to contribute to counteracting the development of sarcopenia. To delay the onset of sarcopenia and its potential adverse outcomes, attention should be paid to increasing physical activity levels in older adults.
PubMed ID
27189729 View in PubMed
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Proximal Femur Volumetric Bone Mineral Density and Mortality: 13 Years of Follow-Up of the AGES-Reykjavik Study.

https://arctichealth.org/en/permalink/ahliterature290729
Source
J Bone Miner Res. 2017 Jun; 32(6):1237-1242
Publication Type
Journal Article
Date
Jun-2017
Author
Elisa A Marques
Martine Elbejjani
Vilmundur Gudnason
Gunnar Sigurdsson
Thomas Lang
Sigurdur Sigurdsson
Thor Aspelund
Osorio Meirelles
Kristin Siggeirsdottir
Lenore Launer
Gudny Eiriksdottir
Tamara B Harris
Author Affiliation
National Institute on Aging, Intramural Research Program, Laboratory of Epidemiology and Population Sciences, Bethesda, MD, USA.
Source
J Bone Miner Res. 2017 Jun; 32(6):1237-1242
Date
Jun-2017
Language
English
Publication Type
Journal Article
Keywords
Aged
Bone Density - physiology
Bone Resorption - mortality - pathology - physiopathology
Cancellous Bone - pathology - physiopathology
Cortical Bone - pathology - physiopathology
Demography
Female
Femur - pathology - physiopathology
Follow-Up Studies
Humans
Male
Mortality
Organ Size
Risk factors
Abstract
Bone mineral density (BMD) has been linked to mortality, but little is known about the independent contribution of each endosteal bone compartment and also the rate of bone loss to risk of mortality. We examined the relationships between (1) baseline trabecular and cortical volumetric BMD (vBMD) at the proximal femur, and (2) the rate of trabecular and cortical bone loss and all-cause mortality in older adults from the AGES-Reykjavik study. The analysis of trabecular and cortical vBMD and mortality was based on the baseline cohort of 4654 participants (aged =66 years) with a median follow-up of 9.4 years; the association between rate of bone loss and mortality was based on 2653 participants with bone loss data (median follow-up of 5.6 years). Analyses employed multivariable Cox-proportional models to estimate hazard ratios (HRs) with time-varying fracture status; trabecular and cortical variables were included together in all models. Adjusted for important confounders, Cox models showed that participants in the lowest quartile of trabecular vBMD had an increased risk of mortality compared to participants in other quartiles (HR?=?1.12; 95% confidence interval (CI), 1.01 to 1.25); baseline cortical vBMD was not related to mortality (HR?=?1.08; 95% CI, 0.97 to 1.20). After adjustment for time-dependent fracture status, results were attenuated and not statistically significant. A faster loss (quartile 1 versus quartiles 2-4) in both trabecular and cortical bone was associated with higher mortality risk (HR?=?1.37 and 1.33, respectively); these associations were independent of major potential confounders including time-dependent incident fractures (HR?=?1.32 and 1.34, respectively). Overall, data suggest that faster bone losses over time in both the trabecular and cortical bone compartments are associated with mortality risk and that measurements of change in bone health may be more informative than single-point measurements in explaining mortality differences in older adults. © 2017 American Society for Bone and Mineral Research.
Notes
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PubMed ID
28276125 View in PubMed
Less detail

Proximal Femur Volumetric Bone Mineral Density and Mortality: 13 Years of Follow-Up of the AGES-Reykjavik Study.

https://arctichealth.org/en/permalink/ahliterature280745
Source
J Bone Miner Res. 2017 Mar 09;
Publication Type
Article
Date
Mar-09-2017
Author
Elisa A Marques
Martine Elbejjani
Vilmundur Gudnason
Gunnar Sigurdsson
Thomas Lang
Sigurdur Sigurdsson
Thor Aspelund
Osorio Meirelles
Kristin Siggeirsdottir
Lenore Launer
Gudny Eiriksdottir
Tamara B Harris
Source
J Bone Miner Res. 2017 Mar 09;
Date
Mar-09-2017
Language
English
Publication Type
Article
Abstract
Bone mineral density (BMD) has been linked to mortality, but little is known about the independent contribution of each endosteal bone compartment and also the rate of bone loss to risk of mortality. We examined the relationships between (1) baseline trabecular and cortical volumetric BMD (vBMD) at the proximal femur, and (2) the rate of trabecular and cortical bone loss and all-cause mortality in older adults from the AGES-Reykjavik study. The analysis of trabecular and cortical vBMD and mortality was based on the baseline cohort of 4654 participants (aged =66 years) with a median follow-up of 9.4 years; the association between rate of bone loss and mortality was based on 2653 participants with bone loss data (median follow-up of 5.6 years). Analyses employed multivariable Cox-proportional models to estimate hazard ratios (HRs) with time-varying fracture status; trabecular and cortical variables were included together in all models. Adjusted for important confounders, Cox models showed that participants in the lowest quartile of trabecular vBMD had an increased risk of mortality compared to participants in other quartiles (HR?=?1.12; 95% confidence interval (CI), 1.01 to 1.25); baseline cortical vBMD was not related to mortality (HR?=?1.08; 95% CI, 0.97 to 1.20). After adjustment for time-dependent fracture status, results were attenuated and not statistically significant. A faster loss (quartile 1 versus quartiles 2-4) in both trabecular and cortical bone was associated with higher mortality risk (HR?=?1.37 and 1.33, respectively); these associations were independent of major potential confounders including time-dependent incident fractures (HR?=?1.32 and 1.34, respectively). Overall, data suggest that faster bone losses over time in both the trabecular and cortical bone compartments are associated with mortality risk and that measurements of change in bone health may be more informative than single-point measurements in explaining mortality differences in older adults. © 2017 American Society for Bone and Mineral Research.
PubMed ID
28276125 View in PubMed
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Space and location of cerebral microbleeds, cognitive decline, and dementia in the community.

https://arctichealth.org/en/permalink/ahliterature282194
Source
Neurology. 2017 May 03;
Publication Type
Article
Date
May-03-2017
Author
Jie Ding
Sigurður Sigurðsson
Pálmi V Jónsson
Gudny Eiriksdottir
Osorio Meirelles
Olafur Kjartansson
Oscar L Lopez
Mark A van Buchem
Vilmundur Gudnason
Lenore J Launer
Source
Neurology. 2017 May 03;
Date
May-03-2017
Language
English
Publication Type
Article
Abstract
To assess the association of the number and anatomic location of cerebral microbleeds (CMBs), visible indicators of microvascular damage on MRI, with incident cognitive disease in the general population of older people.
In the longitudinal population-based Age, Gene/Environment Susceptibility (AGES)-Reykjavik Study, 2,602 participants 66 to 93 years of age and free of prevalent dementia underwent brain MRI and cognitive testing of verbal memory, processing speed, and executive function at baseline and a mean of 5.2 years later. Adjudicated incident dementia cases were diagnosed according to international guidelines.
In the multiple linear regression models adjusted for demographic, genetic, cardiovascular risk, and other cerebrovascular MRI markers, the presence of CMBs located in deep or mixed (deep and lobar) areas was associated with a greater decline in all 3 cognitive domains. Mixed CMBs were the strongest correlate for decline in memory and speed. Compared to those with no CMBs, participants with =3 CMBs had a steeper decline in a composite measure of global cognitive function, memory, and speed. Among those with =3 deep or mixed CMBs, associations were strongest for memory; the association with speed was strongest in those having =3 strictly lobar CMBs. People with =3 CMBs, regardless of their locations, had a higher incidence of all-cause dementia and vascular dementia.
Mixed or a higher load of CMBs, with some specificity for location, is associated with accelerated cognitive decline in older people. These findings suggest a role for hypertensive vasculopathy and the combined effect of hypertensive and cerebral amyloid angiopathy in the pathogenesis of cognitive deterioration.
PubMed ID
28468844 View in PubMed
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7 records – page 1 of 1.