03227nas a2200457 4500008004100000022001400041245006200055210006100117260001500178300001000193490000700203520200900210653000902219653002202228653001302250653001102263653002202274653001102296653001402307653000902321653003202330653001702362653001802379653001402397653002502411100002702436700002302463700001802486700002202504700002202526700002302548700001702571700002502588700002102613700002202634700002002656700001802676700001502694700002402709856003602733 2014 eng d a1526-632X00aVitamin D and the risk of dementia and Alzheimer disease.0 aVitamin D and the risk of dementia and Alzheimer disease c2014 Sep 2 a920-80 v833 a

OBJECTIVE: To determine whether low vitamin D concentrations are associated with an increased risk of incident all-cause dementia and Alzheimer disease.

METHODS: One thousand six hundred fifty-eight elderly ambulatory adults free from dementia, cardiovascular disease, and stroke who participated in the US population-based Cardiovascular Health Study between 1992-1993 and 1999 were included. Serum 25-hydroxyvitamin D (25(OH)D) concentrations were determined by liquid chromatography-tandem mass spectrometry from blood samples collected in 1992-1993. Incident all-cause dementia and Alzheimer disease status were assessed during follow-up using National Institute of Neurological and Communicative Disorders and Stroke/Alzheimer's Disease and Related Disorders Association criteria.

RESULTS: During a mean follow-up of 5.6 years, 171 participants developed all-cause dementia, including 102 cases of Alzheimer disease. Using Cox proportional hazards models, the multivariate adjusted hazard ratios (95% confidence interval [CI]) for incident all-cause dementia in participants who were severely 25(OH)D deficient (<25 nmol/L) and deficient (≥25 to <50 nmol/L) were 2.25 (95% CI: 1.23-4.13) and 1.53 (95% CI: 1.06-2.21) compared to participants with sufficient concentrations (≥50 nmol/L). The multivariate adjusted hazard ratios for incident Alzheimer disease in participants who were severely 25(OH)D deficient and deficient compared to participants with sufficient concentrations were 2.22 (95% CI: 1.02-4.83) and 1.69 (95% CI: 1.06-2.69). In multivariate adjusted penalized smoothing spline plots, the risk of all-cause dementia and Alzheimer disease markedly increased below a threshold of 50 nmol/L.

CONCLUSION: Our results confirm that vitamin D deficiency is associated with a substantially increased risk of all-cause dementia and Alzheimer disease. This adds to the ongoing debate about the role of vitamin D in nonskeletal conditions.

10aAged10aAlzheimer Disease10aDementia10aFemale10aFollow-Up Studies10aHumans10aIncidence10aMale10aProportional Hazards Models10aRisk Factors10aUnited States10aVitamin D10aVitamin D Deficiency1 aLittlejohns, Thomas, J1 aHenley, William, E1 aLang, Iain, A1 aAnnweiler, Cedric1 aBeauchet, Olivier1 aChaves, Paulo, H M1 aFried, Linda1 aKestenbaum, Bryan, R1 aKuller, Lewis, H1 aLanga, Kenneth, M1 aLopez, Oscar, L1 aKos, Katarina1 aSoni, Maya1 aLlewellyn, David, J uhttps://chs-nhlbi.org/node/701702522nas a2200337 4500008004100000022001400041245007600055210006900131260000900200300001300209490000700222520154400229100002201773700001501795700002701810700002201837700002701859700002101886700001901907700002301926700002501949700002101974700002001995700002102015700002202036700002302058700001802081700002502099700002402124856003602148 2016 ENG d a1875-890800aVitamin D and Memory Decline: Two Population-Based Prospective Studies.0 aVitamin D and Memory Decline Two PopulationBased Prospective Stu c2016 a1099-1080 v503 a

BACKGROUND: Vitamin D deficiency has been linked with dementia risk, cognitive decline, and executive dysfunction. However, the association with memory remains largely unknown.

OBJECTIVE: To investigate whether low serum 25-hydroxyvitamin D (25(OH)D) concentrations are associated with memory decline.

METHODS: We used data on 1,291 participants from the US Cardiovascular Health Study (CHS) and 915 participants from the Dutch Longitudinal Aging Study Amsterdam (LASA) who were dementia-free at baseline, had valid vitamin D measurements, and follow-up memory assessments. The Benton Visual Retention Test (in the CHS) and Rey's Auditory Verbal Learning Test (in the LASA) were used to assess visual and verbal memory, respectively.

RESULTS: In the CHS, those moderately and severely deficient in serum 25(OH)D changed -0.03 SD (95% CI: -0.06 to 0.01) and -0.10 SD (95% CI: -0.19 to -0.02) per year respectively in visual memory compared to those sufficient (p = 0.02). In the LASA, moderate and severe deficiency in serum 25(OH)D was associated with a mean change of 0.01 SD (95% CI: -0.01 to 0.02) and -0.01 SD (95% CI: -0.04 to 0.02) per year respectively in verbal memory compared to sufficiency (p = 0.34).

CONCLUSIONS: Our findings suggest an association between severe vitamin D deficiency and visual memory decline but no association with verbal memory decline. They warrant further investigation in prospective studies assessing different memory subtypes.

1 aKuźma, Elżbieta1 aSoni, Maya1 aLittlejohns, Thomas, J1 aRanson, Janice, M1 avan Schoor, Natasja, M1 aDeeg, Dorly, J H1 aComijs, Hannie1 aChaves, Paulo, H M1 aKestenbaum, Bryan, R1 aKuller, Lewis, H1 aLopez, Oscar, L1 aBecker, James, T1 aLanga, Kenneth, M1 aHenley, William, E1 aLang, Iain, A1 aUkoumunne, Obioha, C1 aLlewellyn, David, J uhttps://chs-nhlbi.org/node/699902884nas a2200277 4500008004100000022001400041245005400055210005300109260000900162300001300171490000700184520211400191100002702305700001802332700002302350700001802373700002202391700002202413700002302435700002502458700002102483700002202504700002002526700002402546856003602570 2016 eng d a1932-620300aVitamin D and Risk of Neuroimaging Abnormalities.0 aVitamin D and Risk of Neuroimaging Abnormalities c2016 ae01548960 v113 a

Vitamin D deficiency has been linked with an increased risk of incident all-cause dementia and Alzheimer's disease. The aim of the current study was to explore the potential mechanisms underlying these associations by determining whether low vitamin D concentrations are associated with the development of incident cerebrovascular and neurodegenerative neuroimaging abnormalities. The population consisted of 1,658 participants aged ≥65 years from the US-based Cardiovascular Health Study who were free from prevalent cardiovascular disease, stroke and dementia at baseline in 1992-93. Serum 25-hydroxyvitamin D (25(OH)D) concentrations were determined by liquid chromatography-tandem mass spectrometry from blood samples collected at baseline. The first MRI scan was conducted between 1991-1994 and the second MRI scan was conducted between 1997-1999. Change in white matter grade, ventricular grade and presence of infarcts between MRI scan one and two were used to define neuroimaging abnormalities. During a mean follow-up of 5.0 years, serum 25(OH)D status was not significantly associated with the development of any neuroimaging abnormalities. Using logistic regression models, the multivariate adjusted odds ratios (95% confidence interval) for worsening white matter grade in participants who were severely 25(OH)D deficient (<25 nmol/L) and deficient (≥25-50 nmol/L) were 0.76 (0.35-1.66) and 1.09 (0.76-1.55) compared to participants with sufficient concentrations (≥50 nmol/L). The multivariate adjusted odds ratios for ventricular grade in participants who were severely 25(OH)D deficient and deficient were 0.49 (0.20-1.19) and 1.12 (0.79-1.59) compared to those sufficient. The multivariate adjusted odds ratios for incident infarcts in participants who were severely 25(OH)D deficient and deficient were 1.95 (0.84-4.54) and 0.73 (0.47-1.95) compared to those sufficient. Overall, serum vitamin D concentrations could not be shown to be associated with the development of cerebrovascular or neurodegenerative neuroimaging abnormalities in Cardiovascular Health Study participants.

1 aLittlejohns, Thomas, J1 aKos, Katarina1 aHenley, William, E1 aLang, Iain, A1 aAnnweiler, Cedric1 aBeauchet, Olivier1 aChaves, Paulo, H M1 aKestenbaum, Bryan, R1 aKuller, Lewis, H1 aLanga, Kenneth, M1 aLopez, Oscar, L1 aLlewellyn, David, J uhttps://chs-nhlbi.org/node/712602627nas a2200277 4500008004100000022001400041245009500055210006900150260001600219520176300235100002201998700001702020700002702037700002102064700002202085700001802107700002502125700002102150700002502171700002102196700002002217700002702237700002502264700002402289856003602313 2017 eng d a1546-415600aCoronary Artery Bypass Graft Surgery and Dementia Risk in the Cardiovascular Health Study.0 aCoronary Artery Bypass Graft Surgery and Dementia Risk in the Ca c2017 Mar 033 a

INTRODUCTION: The association between history of coronary artery bypass graft surgery (CABG) and dementia risk remains unclear.

METHODS: We conducted a prospective cohort analysis using data on 3155 elderly adults free from prevalent dementia from the US population-based Cardiovascular Health Study (CHS) with adjudicated incident all-cause dementia, Alzheimer disease (AD), vascular dementia (VaD), and mixed dementia.

RESULTS: In the CHS, the hazard ratio (HR) for all-cause dementia was 1.93 [95% confidence interval (CI), 1.36-2.74] for those with CABG history compared with those with no CABG history after adjustment for potential confounders. Similar HRs were observed for AD (HR=1.71; 95% CI, 0.98-2.98), VaD (HR=1.42; 95% CI, 0.56-3.65), and mixed dementia (HR=2.73; 95% CI, 1.55-4.80). The same pattern of results was observed when these CHS findings were pooled with a prior prospective study, the pooled HRs were 1.96 (95% CI, 1.42-2.69) for all-cause dementia, 1.71 (95% CI, 1.04-2.79) for AD and 2.20 (95% CI, 0.78-6.19) for VaD.

DISCUSSION: Our results suggest CABG history is associated with long-term dementia risk. Further investigation is warranted to examine the causal mechanisms which may explain this relationship or whether the association reflects differences in coronary artery disease severity.This is an open-access article distributed under the terms of the Creative Commons Attribution-Non Commercial-No Derivatives License 4.0 (CCBY-NC-ND), where it is permissible to download and share the work provided it is properly cited. The work cannot be changed in any way or used commercially without permission from the journal. http://creativecommons.org/licenses/by-nc-nd/4.0/.

1 aKuźma, Elżbieta1 aAirdrie, Jac1 aLittlejohns, Thomas, J1 aLourida, Ilianna1 aThompson-Coon, Jo1 aLang, Iain, A1 aScrobotovici, Monica1 aThacker, Evan, L1 aFitzpatrick, Annette1 aKuller, Lewis, H1 aLopez, Oscar, L1 aLongstreth, William, T1 aUkoumunne, Obioha, C1 aLlewellyn, David, J uhttps://chs-nhlbi.org/node/7348