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  • 1
    Online Resource
    Online Resource
    The AGES-Reykjavik Study suggests that change in kidney measures is associated with subclinical brain pathology in older community-dwelling persons
    Elsevier BV ; 2018
    In:  Kidney International Vol. 94, No. 3 ( 2018-09), p. 608-615
    Details
    In: Kidney International, Elsevier BV, Vol. 94, No. 3 ( 2018-09), p. 608-615
    Type of Medium: Online Resource
    ISSN: 0085-2538
    URL: Article
    DOI: 10.1016/j.kint.2018.04.022
    Language: English
    Publisher: Elsevier BV
    Publication Date: 2018
    detail.hit.zdb_id: 2007940-0
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  • 2
    Online Resource
    Online Resource
    Contributions of Cerebral Blood Flow to Associations Between Blood Pressure Levels and Cognition: The Age, Gene/Environment Susceptibility-Reykjavik Study
    Ovid Technologies (Wolters Kluwer Health) ; 2021
    In:  Hypertension Vol. 77, No. 6 ( 2021-06), p. 2075-2083
    Details
    In: Hypertension, Ovid Technologies (Wolters Kluwer Health), Vol. 77, No. 6 ( 2021-06), p. 2075-2083
    Abstract: Cerebral hypoperfusion leads to adverse sequalae including dementia. Midlife higher blood pressure (BP) can lead to low cerebral blood flow (CBF), but older persons may need higher BP to maintain cerebral perfusion. We investigated the associations among late-life BP, CBF, and cognition. Data are from 2498 participants with a mean age of 79.8 (SD, 4.7) years of the second exam of the AGES (Age, Gene/Environment Susceptibility)–Reykjavik Study. BP was measured, and phase-contrast (PC) magnetic resonance imaging was acquired to estimate total brain CBF PC . Cognitive outcomes included verbal and working memory, processing speed, mild cognitive impairment, and all-cause dementia. Relationships among late-life BP, CBF PC , and cognition were assessed with regression models, controlling for socio-demographics, BP level at midlife (at a mean age of 49.6 [SD, 5.9] years), cardiovascular factors, and total brain volume. In fully adjusted models, each mm Hg increase in late-life diastolic BP was associated with a −0.082 mL/min per 100 mL (95% CI −0.123 to −0.041) lower CBF PC . In contrast, each mm Hg increase in late-life systolic BP or pulse pressure was associated with a 0.027 mL/min per 100 mL (95% CI, 0.0065–0.048) and 0.061 mL/min per 100 mL (95% CI, 0.038–0.084) higher late-life CBF PC , respectively. Higher CBF PC was significantly related to higher cognitive scores for psychomotor speed, verbal, and working memory and to a lower odd of mild cognitive impairment or dementia, irrespective of late-life BP level. Higher late-life diastolic BP and systolic BP were differentially associated with CBF PC . Our findings suggest CBF is an important correlate of late-life cognition, independent of BP level.
    Type of Medium: Online Resource
    ISSN: 0194-911X , 1524-4563
    URL: Article
    DOI: 10.1161/HYPERTENSIONAHA.120.16894
    Language: English
    Publisher: Ovid Technologies (Wolters Kluwer Health)
    Publication Date: 2021
    detail.hit.zdb_id: 2094210-2
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  • 3
    Online Resource
    Online Resource
    Comparison of midlife offspring cohorts based on family history of Alzheimer’s Disease: multi‐domain risk factors and cognitive function
    Wiley ; 2022
    In:  Alzheimer's & Dementia Vol. 18, No. S11 ( 2022-12)
    Details
    In: Alzheimer's & Dementia, Wiley, Vol. 18, No. S11 ( 2022-12)
    Abstract: Maintaining healthy clinical indicators and behavior is positively related to cognitive protection from midlife. However, limited population‐based studies have explored the role of family history on these factors in midlife. Therefore, we examined cognitive‐related risk factors in two midlife cohorts from the same source population in the Age, Gene/Environment Susceptibility‐Reykjavik Study. Method We included 446 offspring (aged 61, 49% women) from the random sample (RS) without Alzheimer’s Disease (AD) and 499 offspring (aged 63, 49% women) to AD cases at baseline and during follow up from the main study. Accordingly, we labeled the offspring with and without AD family history as offspring AD and offspring RS, respectively. Clinical factors included BMI, systolic (SBP) and diastolic blood pressure (DBP), cholesterol, fasting glucose, inflammatory factors, and medication. Socio‐behavioral factors included education, smoking, problems of doing usual activities. Cognitive function was evaluated by MMSE and STROOP. To address the potential correlation between siblings within one family, we compared these characteristics with the random effects intercept mixed model by family ID. We also did a sensitivity analysis by comparing people under age 65 to assess reverse causation for specific traits. All models were adjusted for age and sex. Fasting glucose, triglycerides, and inflammatory factors were log‐transformed due to skewness. We consider p 〈 0.05 as statistically significant. Result As shown in the table, socio‐behavioral factors, cognitive function, or most clinical characteristics did not differ in the two groups. The Offspring AD had 2.71‐unit lower SBP and 0.03‐unit higher log(glucose) (3% increased glucose) than the RS (p 〈 0.05). The sensitivity analysis among people under age 65 showed a similar pattern, except for the insignificant difference in fasting glucose between offspring AD and RS. Conclusion In general, there was no difference in AD‐related health profile among midlife offspring with and without AD family history. This analysis of standard cardiovascular and cognitive impairment‐related risk factors suggests that these variables alone will not help identify at‐risk individuals for later‐life cognitive impairment.
    Type of Medium: Online Resource
    ISSN: 1552-5260 , 1552-5279
    URL: Issue
    URL: Article
    DOI: 10.1002/alz.v18.S11
    DOI: 10.1002/alz.063881
    Language: English
    Publisher: Wiley
    Publication Date: 2022
    detail.hit.zdb_id: 2201940-6
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  • 4
    Online Resource
    Online Resource
    Proximal Femur Volumetric Bone Mineral Density and Mortality: 13 Years of Follow‐Up of the AGES‐Reykjavik Study
    Wiley ; 2017
    In:  Journal of Bone and Mineral Research Vol. 32, No. 6 ( 2017-06), p. 1237-1242
    Details
    In: Journal of Bone and Mineral Research, Wiley, Vol. 32, No. 6 ( 2017-06), p. 1237-1242
    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.
    Type of Medium: Online Resource
    ISSN: 0884-0431 , 1523-4681
    URL: Issue
    URL: Article
    DOI: 10.1002/jbmr.v32.6
    DOI: 10.1002/jbmr.3104
    RVK:
    XA 52230
    Language: English
    Publisher: Wiley
    Publication Date: 2017
    detail.hit.zdb_id: 2008867-X
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  • 5
    Online Resource
    Online Resource
    Physical activity and incidence of sarcopenia: the population-based AGES—Reykjavik Study
    Oxford University Press (OUP) ; 2016
    In:  Age and Ageing Vol. 45, No. 5 ( 2016-09), p. 614-620
    Details
    In: Age and Ageing, Oxford University Press (OUP), Vol. 45, No. 5 ( 2016-09), p. 614-620
    Type of Medium: Online Resource
    ISSN: 0002-0729 , 1468-2834
    URL: Article
    DOI: 10.1093/ageing/afw090
    Language: English
    Publisher: Oxford University Press (OUP)
    Publication Date: 2016
    detail.hit.zdb_id: 2065766-3
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  • 6
    Online Resource
    Online Resource
    Cardiac and Carotid Markers Link With Accelerated Brain Atrophy : The AGES–Reykjavik Study (Age, Gene/Environment Susceptibility–Reykjavik)
    Ovid Technologies (Wolters Kluwer Health) ; 2016
    In:  Arteriosclerosis, Thrombosis, and Vascular Biology Vol. 36, No. 11 ( 2016-11), p. 2246-2251
    Details
    In: Arteriosclerosis, Thrombosis, and Vascular Biology, Ovid Technologies (Wolters Kluwer Health), Vol. 36, No. 11 ( 2016-11), p. 2246-2251
    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. Approach and Results— In the longitudinal population-based AGES–Reykjavik study (Age, Gene/Environment Susceptibility–Reykjavik), 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. Conclusions— 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.
    Type of Medium: Online Resource
    ISSN: 1079-5642 , 1524-4636
    URL: Article
    DOI: 10.1161/ATVBAHA.116.308018
    Language: English
    Publisher: Ovid Technologies (Wolters Kluwer Health)
    Publication Date: 2016
    detail.hit.zdb_id: 1494427-3
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  • 7
    Online Resource
    Online Resource
    Abstract WP169: Midlife to Late-Life Changes in Blood Pressure and Cerebral Blood Flow in Old Age: the AGES-Reykjavik Study
    Ovid Technologies (Wolters Kluwer Health) ; 2018
    In:  Stroke Vol. 49, No. Suppl_1 ( 2018-01-22)
    Details
    In: Stroke, Ovid Technologies (Wolters Kluwer Health), Vol. 49, No. Suppl_1 ( 2018-01-22)
    Abstract: Introduction: Adverse changes in blood pressure (BP) over the life course can lead to adverse cerebrovascular outcomes, including reduced blood flow. In this life-course, longitudinal, population-based study, we investigated the link between midlife to late life changes in BP and cerebral blood flow (CBF) in old age. Methods: From the Age, Gene/Environment Susceptibility (AGES)–Reykjavik Study (2002-2011), 2491 individuals (mean age (SD): midlife 49.7 (6.1) and late-life 79.8 (4.7) years old) were included. BP was measured at three different time points: 1 in mid-life, and 2 in late-life measured 5 years apart (mean follow-up time 30.1 years). With linear mixed models, annual changes in BP were estimated for each participant (mmHg/year). Participants were categorized in tertiles of changes in systolic, pulse pressure and diastolic BP. Total CBF was measured in the last late-life visit with the Phase-Contrast MRI and standardized for brain parenchymal volume (mL/min/100mL). Results: Overall, each mmHg/year increase in systolic BP was associated with 3.2 mL/min/100 mL (95% CI: 0.7-5.7)) higher CBF. Mean (SE) CBF in low, middle and high tertiles of change in systolic BP were 56.0 (0.4), 56.6 (0.4) and 57.5 (0.4) mL/min/100mL respectively (P for trend: 0.01). A similar increase in total CBF was observed for an increase in pulse pressure: each mmHg/year increase in pulse pressure was associated with 6.3 mL/min/100mL (95% CI: 3.8-8.7) higher total CBF. In contrast, an increase in diastolic BP was linked with lower CBF: each mmHg/year increase in diastolic BP was associated with 6.3 mL/min/100mL (95% CI: 3.3-9.4) lower CBF. Mean (SE) CBF in low, middle and high tertiles of changes in diastolic BP were 57.3 (0.4), 57.3 (0.4) and 55.5 (0.4) mL/min/100mL respectively (P for trend: 〈 0.001). All these associations were independent of sociodemographic and cardiovascular factors and antihypertensive medications. Conclusion: In an over 30 years of midlife to late-life follow up, we observed that individuals with increasing systolic BP and pulse pressure have higher CBF in old age. Conversely, increase in diastolic BP is associated with lower CBF. The mechanisms behind the link between long-term BP alterations and CBF need to be elucidated.
    Type of Medium: Online Resource
    ISSN: 0039-2499 , 1524-4628
    URL: Article
    DOI: 10.1161/str.49.suppl_1.WP169
    RVK:
    XA 10000
    Language: English
    Publisher: Ovid Technologies (Wolters Kluwer Health)
    Publication Date: 2018
    detail.hit.zdb_id: 1467823-8
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