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The -629C>A polymorphism in the CETP gene does not explain the association of TaqIB polymorphism with risk and age of myocardial infarction in Icelandic men.

https://arctichealth.org/en/permalink/ahliterature53840
Source
Atherosclerosis. 2001 Nov;159(1):187-92
Publication Type
Article
Date
Nov-2001
Author
G. Eiriksdottir
M K Bolla
B. Thorsson
G. Sigurdsson
S E Humphries
V. Gudnason
Author Affiliation
Molecular Genetics Laboratory, Hjartavernd, Icelandic Heart Association, Lagmuli 9, 108, Reykjavik, Iceland. gudny@hjarta.is
Source
Atherosclerosis. 2001 Nov;159(1):187-92
Date
Nov-2001
Language
English
Publication Type
Article
Keywords
Aged
Carrier Proteins - genetics
Gene Frequency
Genotype
Glycoproteins
Homozygote
Humans
Iceland
Linkage Disequilibrium
Lipids - blood
Lipoproteins, HDL Cholesterol - blood
Male
Myocardial Infarction - blood - genetics
Polymerase Chain Reaction
Polymorphism, Genetic
Promoter Regions (Genetics) - genetics
Prospective Studies
Research Support, Non-U.S. Gov't
Risk factors
Abstract
The aim of this study was to examine whether the well-established effect of the common TaqIB polymorphism in intron 1 of the gene for cholesterol ester transfer protein (CETP) on high density lipoprotein cholesterol (HDL-C) concentration and increased risk of myocardial infarction (MI), could be explained by the recently identified -629C>A functional polymorphism in the promoter. Non-fatal MI cases (388 male) and a control group of 794 healthy men were recruited from the 30 year long prospective Reykjavik Study. In the healthy men the frequency of the TaqIB B2 allele was 0.47 (95% CI: 0.44-0.50) and there was a strong allelic association with the -629A allele (D=-0.21, P
PubMed ID
11689220 View in PubMed
Less detail

Age-related loss of proximal femoral strength in elderly men and women: the Age Gene/Environment Susceptibility Study--Reykjavik.

https://arctichealth.org/en/permalink/ahliterature128686
Source
Bone. 2012 Mar;50(3):743-8
Publication Type
Article
Date
Mar-2012
Author
T F Lang
S. Sigurdsson
G. Karlsdottir
D. Oskarsdottir
A. Sigmarsdottir
J. Chengshi
J. Kornak
T B Harris
G. Sigurdsson
B Y Jonsson
K. Siggeirsdottir
G. Eiriksdottir
V. Gudnason
J H Keyak
Author Affiliation
Department of Radiology and Biomedical Imaging, University of California, San Francisco, CA 94143-0946, USA. thomas.lang@ucsf.edu
Source
Bone. 2012 Mar;50(3):743-8
Date
Mar-2012
Language
English
Publication Type
Article
Keywords
Aged
Aged, 80 and over
Aging - physiology
Bone Density - physiology
Disease Susceptibility
Female
Femur - physiology - radiography
Hip Fractures - etiology - physiopathology - radiography
Humans
Male
Sex Factors
Abstract
The risk of hip fracture rises rapidly with age, and is particularly high in women. This increase in fracture risk reflects both the age-related change in the risk of falling and decrements in the strength of the proximal femur. To better understand the extent to which proximal femoral density, structure and strength change with age as a function of gender, we have carried out a longitudinal analysis of proximal femoral volumetric quantitative computed tomographic (vQCT) images in men and women, analyzing changes in trabecular and cortical bone properties, and using subject-specific finite element modeling (FEM) to estimate changes in bone strength. In the AGES-Reykjavik Study vQCT scans of the hip were performed at a baseline visit in 2002-2006 and at a second visit 5.05±0.25 years later. From these, 223 subjects (111 men, 112 women, aged 68-87 years) were randomly selected. The subjects were evaluated for longitudinal changes in three bone variables assessed in a region similar to the total femur region quantified by DXA: areal bone mineral density (aBMD), trabecular volumetric bone mineral density (tBMD) and the ratio of cortical to total tissue volume (cvol/ivol). They were also evaluated for changes in bone strength using FEM models of the left proximal femur. Models were analyzed under single-limb stance loading (F(Stance)), which approximates normal physiologic loading of the hip, as well as a load approximating a fall onto the posterolateral aspect of the greater trochanter (F(Fall)). We computed five-year absolute and percentage changes in aBMD, tBMD, cvol/ivol, F(Fall) and F(Stance). The Mann-Whitney Test was employed to compare changes in bone variables between genders and the Wilcoxon Signed Rank Test was used to compare changes in bone strength between loading conditions. Multiple (linear) regression was employed to determine the association of changes in F(Fall) and F(Stance) with baseline age and five-year weight loss. Both men and women showed declines in indices of proximal femoral density and structure (aBMD: men -3.9±6.0%, women -6.1±6.2%; tBMD: men -14.8±20.3%, women -23.9±26.8%; cvol/ivol: men -2.6±4.6%, women -4.7±4.8%, gender difference: p
Notes
Cites: J Clin Densitom. 2009 Jul-Sep;12(3):330-619577939
Cites: Ann N Y Acad Sci. 2010 Mar;1192:57-6520392218
Cites: J Bone Miner Res. 2010 Mar;25(3):482-9119594320
Cites: J Bone Miner Res. 2010 May;25(5):994-100119874201
Cites: Bone. 2011 Jun 1;48(6):1239-4521419886
Cites: J Bone Miner Res. 2000 Apr;15(4):710-2010780863
Cites: J Biomech. 2000 Feb;33(2):209-1410653034
Cites: Bone. 2006 Jul;39(1):152-816459156
Cites: Osteoporos Int. 2000;11(7):592-911069193
Cites: Med Eng Phys. 2001 Apr;23(3):165-7311410381
Cites: Med Eng Phys. 2001 Nov;23(9):657-6411755810
Cites: J Am Geriatr Soc. 2003 Dec;51(12):1740-714687352
Cites: J Bone Miner Res. 2004 Jun;19(6):1006-1215125798
Cites: Arch Intern Med. 1998 May 11;158(9):990-69588432
Cites: J Biomech. 1998 Feb;31(2):125-339593205
Cites: J Bone Miner Res. 2004 Dec;19(12):1945-5415537436
Cites: Lancet. 2005 Jul 9-15;366(9480):129-3516005335
Cites: Clin Orthop Relat Res. 2005 Aug;(437):219-2816056052
Cites: Osteoporos Int. 2006;17(9):1329-3616767524
Cites: J Bone Miner Res. 2006 Aug;21(8):1197-20616869717
Cites: Bone. 2006 Sep;39(3):644-5116790372
Cites: Bone. 2007 Jan;40(1):169-7416876496
Cites: Bone. 2007 Mar;40(3):662-7317175209
Cites: Am J Epidemiol. 2007 May 1;165(9):1076-8717351290
Cites: J Bone Miner Res. 2008 Aug;23(8):1326-3318348697
Cites: J Bone Miner Res. 2009 Mar;24(3):475-8319049327
PubMed ID
22178403 View in PubMed
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Are bone turnover markers associated with volumetric bone density, size, and strength in older men and women? The AGES-Reykjavik study.

https://arctichealth.org/en/permalink/ahliterature268064
Source
Osteoporos Int. 2015 Dec 2;
Publication Type
Article
Date
Dec-2-2015
Author
E A Marques
V. Gudnason
G. Sigurdsson
T. Lang
F. Johannesdottir
K. Siggeirsdottir
L. Launer
G. Eiriksdottir
T B Harris
Source
Osteoporos Int. 2015 Dec 2;
Date
Dec-2-2015
Language
English
Publication Type
Article
Abstract
Association between serum bone formation and resorption markers and bone mineral, structural, and strength variables derived from quantitative computed tomography (QCT) in a population-based cohort of 1745 older adults was assessed. The association was weak for lumbar spine and femoral neck areal and volumetric bone mineral density.
The aim of this study was to examine the relationship between levels of bone turnover markers (BTMs; osteocalcin (OC), C-terminal cross-linking telopeptide of type I collagen (CTX), and procollagen type 1N propeptide (P1NP)) and quantitative computed tomography (QCT)-derived bone density, geometry, and strength indices in the lumbar spine and femoral neck (FN).
A total of 1745 older individuals (773 men and 972 women, aged 66-92 years) from the Age, Gene/Environment Susceptibility (AGES)-Reykjavik cohort were studied. QCT was performed in the lumbar spine and hip to estimate volumetric trabecular, cortical, and integral bone mineral density (BMD), areal BMD, bone geometry, and bone strength indices. Association between BTMs and QCT variables were explored using multivariable linear regression.
Major findings showed that all BMD measures, FN cortical index, and compressive strength had a low negative correlation with the BTM levels in both men and women. Correlations between BTMs and bone size parameters were minimal or not significant. No associations were found between BTMs and vertebral cross-sectional area in women. BTMs alone accounted for only a relatively small percentage of the bone parameter variance (1-10 %).
Serum CTX, OC, and P1NP were weakly correlated with lumbar spine and FN areal and volumetric BMD and strength measures. Most of the bone size indices were not associated with BTMs; thus, the selected bone remodeling markers do not reflect periosteal bone formation. These results confirmed the limited ability of the most sensitive established BTMs to predict bone structural integrity in older adults.
PubMed ID
26630978 View in PubMed
Less detail

Association of bone turnover markers with volumetric bone loss, periosteal apposition, and fracture risk in older men and women: the AGES-Reykjavik longitudinal study.

https://arctichealth.org/en/permalink/ahliterature273828
Source
Osteoporos Int. 2016 Jun 24;
Publication Type
Article
Date
Jun-24-2016
Author
E A Marques
V. Gudnason
T. Lang
G. Sigurdsson
S. Sigurdsson
T. Aspelund
K. Siggeirsdottir
L. Launer
G. Eiriksdottir
T B Harris
Source
Osteoporos Int. 2016 Jun 24;
Date
Jun-24-2016
Language
English
Publication Type
Article
Abstract
Association between serum bone formation and resorption markers and cortical and trabecular bone loss and the concurrent periosteal apposition in a population-based cohort of 1069 older adults was assessed. BTM levels moderately reflect the cellular events at the endosteal and periosteal surfaces but are not associated with fracture risk.
We assessed whether circulating bone formation and resorption markers (BTM) were individual predictors for trabecular and cortical bone loss, periosteal expansion, and fracture risk in older adults aged 66 to 93 years from the AGES-Reykjavik study.
The sample for the quantitative computed tomography (QCT)-derived cortical and trabecular BMD and periosteal expansion analysis consisted of 1069 participants (474 men and 595 women) who had complete baseline (2002 to 2006) and follow-up (2007 to 2011) hip QCT scans and serum baseline BTM. During the median follow-up of 11.7 years (range 5.4-12.5), 54 (11.4 %) men and 182 (30.6 %) women sustained at least one fracture of any type.
Increase in BTM levels was associated with faster cortical and trabecular bone loss at the femoral neck and proximal femur in men and women. Higher BTM levels were positively related with periosteal expansion rate at the femoral neck in men. Markers were not associated with fracture risk.
This data corroborates the notion from few previous studies that both envelopes are metabolically active and that BTM levels may moderately reflect the cellular events at the endosteal and periosteal surfaces. However, our results do not support the routine use of BTM to assess fracture risk in older men and women. In light of these findings, further studies are justified to examine whether systemic markers of bone turnover might prove useful in monitoring skeletal remodeling events and the effects of current osteoporosis drugs at the periosteum.
PubMed ID
27341810 View in PubMed
Less detail

Association of bone turnover markers with volumetric bone loss, periosteal apposition, and fracture risk in older men and women: the AGES-Reykjavik longitudinal study.

https://arctichealth.org/en/permalink/ahliterature291359
Source
Osteoporos Int. 2016 12; 27(12):3485-3494
Publication Type
Journal Article
Research Support, N.I.H., Extramural
Research Support, Non-U.S. Gov't
Research Support, N.I.H., Intramural
Date
12-2016
Author
E A Marques
V Gudnason
T Lang
G Sigurdsson
S Sigurdsson
T Aspelund
K Siggeirsdottir
L Launer
G Eiriksdottir
T B Harris
Author Affiliation
Laboratory of Epidemiology and Population Sciences, Intramural Research Program, National Institute on Aging, National Institutes of Health, Bethesda, MD, USA. elisa.marques@nih.gov.
Source
Osteoporos Int. 2016 12; 27(12):3485-3494
Date
12-2016
Language
English
Publication Type
Journal Article
Research Support, N.I.H., Extramural
Research Support, Non-U.S. Gov't
Research Support, N.I.H., Intramural
Keywords
Aged
Aged, 80 and over
Biomarkers - blood
Bone Density
Bone remodeling
Female
Femur Neck - pathology
Fractures, Bone - epidemiology
Humans
Iceland
Longitudinal Studies
Male
Abstract
Association between serum bone formation and resorption markers and cortical and trabecular bone loss and the concurrent periosteal apposition in a population-based cohort of 1069 older adults was assessed. BTM levels moderately reflect the cellular events at the endosteal and periosteal surfaces but are not associated with fracture risk.
We assessed whether circulating bone formation and resorption markers (BTM) were individual predictors for trabecular and cortical bone loss, periosteal expansion, and fracture risk in older adults aged 66 to 93 years from the AGES-Reykjavik study.
The sample for the quantitative computed tomography (QCT)-derived cortical and trabecular BMD and periosteal expansion analysis consisted of 1069 participants (474 men and 595 women) who had complete baseline (2002 to 2006) and follow-up (2007 to 2011) hip QCT scans and serum baseline BTM. During the median follow-up of 11.7 years (range 5.4-12.5), 54 (11.4 %) men and 182 (30.6 %) women sustained at least one fracture of any type.
Increase in BTM levels was associated with faster cortical and trabecular bone loss at the femoral neck and proximal femur in men and women. Higher BTM levels were positively related with periosteal expansion rate at the femoral neck in men. Markers were not associated with fracture risk.
This data corroborates the notion from few previous studies that both envelopes are metabolically active and that BTM levels may moderately reflect the cellular events at the endosteal and periosteal surfaces. However, our results do not support the routine use of BTM to assess fracture risk in older men and women. In light of these findings, further studies are justified to examine whether systemic markers of bone turnover might prove useful in monitoring skeletal remodeling events and the effects of current osteoporosis drugs at the periosteum.
Notes
Cites: Crit Rev Eukaryot Gene Expr. 2009;19(3):219-33 PMID 19883366
Cites: Bone. 2005 Feb;36(2):311-6 PMID 15780957
Cites: Am J Epidemiol. 2007 May 1;165(9):1076-87 PMID 17351290
Cites: Bone. 2002 Aug;31(2):313-8 PMID 12151084
Cites: J Bone Miner Res. 2003 Feb;18(2):312-8 PMID 12568408
Cites: J Bone Miner Res. 2003 Jun;18(6):949-54 PMID 12817746
Cites: Bone. 2015 Dec;81:1-6 PMID 26112819
Cites: Bone. 2005 Jan;36(1):13-21 PMID 15663998
Cites: J Bone Miner Res. 1998 Feb;13(2):297-302 PMID 9495524
Cites: Bone. 2011 Dec;49(6):1232-41 PMID 21920485
Cites: Ann Rheum Dis. 2008 Sep;67(9):1249-55 PMID 18065499
Cites: Nat Rev Rheumatol. 2012 Jun 05;8(7):379-89 PMID 22664836
Cites: J Bone Miner Res. 2014 Apr;29(4):1015-24 PMID 24014423
Cites: J Clin Endocrinol Metab. 2008 Jul;93(7):2622-32 PMID 18460567
Cites: J Bone Miner Res. 2004 Mar;19(3):386-93 PMID 15040826
Cites: Calcif Tissue Int. 2014 May;94(5):560-7 PMID 24590144
Cites: Bone. 2012 Mar;50(3):628-37 PMID 22154841
Cites: J Bone Miner Res. 2010 Feb;25(2):393-403 PMID 19961336
Cites: Bone. 2002 Jun;30(6):807-9 PMID 12052445
Cites: Osteoporos Int. 2016 May;27(5):1765-76 PMID 26630978
Cites: Osteoporos Int. 2015 Feb;26(2):617-27 PMID 25224294
Cites: J Bone Miner Res. 1999 Sep;14(9):1614-21 PMID 10469291
Cites: Bone. 2011 Dec;49(6):1125-30 PMID 21872686
Cites: Joint Bone Spine. 2012 Jan;79(1):26-31 PMID 21723772
Cites: J Bone Miner Res. 2005 Apr;20(4):579-87 PMID 15765176
Cites: Lancet. 2010 May 15;375(9727):1729-36 PMID 20472174
Cites: J Bone Miner Res. 1992 Dec;7(12):1475-82 PMID 1481733
Cites: Osteoporos Int. 2003;14 Suppl 3:S2-8 PMID 12730770
Cites: J Bone Miner Res. 2009 Dec;24(12):2032-8 PMID 19453262
Cites: Osteoporos Int. 2003 Apr;14(2):141-5 PMID 12730775
Cites: Osteoporos Int. 2011 Feb;22(2):391-420 PMID 21184054
Cites: Eur J Epidemiol. 2007;22(9):631-9 PMID 17653601
Cites: Bone. 2006 Sep;39(3):644-51 PMID 16790372
Cites: Clin Chim Acta. 2005 Jun;356(1-2):67-75 PMID 15936304
Cites: Nutr J. 2012 Mar 13;11:12 PMID 22413931
Cites: J Bone Miner Res. 2000 Dec;15(12):2473-8 PMID 11127212
Cites: Crit Rev Biomed Eng. 2006;34(3):215-71 PMID 16930125
Cites: J Bone Miner Res. 2013 Oct;28(10 ):2165-76 PMID 23609070
PubMed ID
27341810 View in PubMed
Less detail

Associations between Proportion of Plasma Phospholipid Fatty Acids, Depressive Symptoms and Major Depressive Disorder. Cross-Sectional Analyses from the AGES Reykjavik Study.

https://arctichealth.org/en/permalink/ahliterature290027
Source
J Nutr Health Aging. 2018; 22(3):354-360
Publication Type
Journal Article
Date
2018
Author
C M Imai
T I Halldorsson
T Aspelund
G Eiriksdottir
L J Launer
I Thorsdottir
T B Harris
V Gudnason
I A Brouwer
I Gunnarsdottir
Author Affiliation
Ingibjorg Gunnarsdottir, Unit for Nutrition Research, Landspitali-The National University Hospital of Iceland and Faculty of Food Science and Nutrition, School of Health Sciences, University of Iceland, Eiriksgata 29, 101 Reykjavik, Iceland, ingigun@hi.is.
Source
J Nutr Health Aging. 2018; 22(3):354-360
Date
2018
Language
English
Publication Type
Journal Article
Abstract
Deficits in n-3 fatty acids may be associated with depression. However, data are scarce from older adults who are at greater risk of poor dietary intake and of developing depression.
To investigate proportion of plasma phospholipid fatty acids with respect to depressive symptoms and major depressive disorder in community dwelling older adults.
Cross-sectional analyses of 1571 participants in the Age, Gene/Environment Susceptibility (AGES)-Reykjavik Study aged 67-93 years. Depressive symptoms were measured using the 15-item Geriatric Depression Scale (GDS-15). Major depressive disorder was assessed according to Diagnostic and Statistical Manual of Mental Disorders (DSM-IV) criteria using the Mini-International Neuropsychiatric Interview (MINI).
Depressive symptoms were observed in 195 (12.4%) subjects and there were 27 (1.7%) cases of major depressive disorder. Participants with depressive symptoms were less educated, more likely to be smokers, less physically active and consumed cod liver oil less frequently. Difference in GDS-15 scores by tertiles of n-3 fatty acid proportion was not significant. Proportion of long chain n-3 fatty acids (Eicosapentaenoic- + Docosahexaenoic acid) were inversely related to major depressive disorder, (tertile 2 vs. tertile 1) OR: 0.31 (95% CI: 0.11, 0.86); tertile 3 vs. tertile 1, OR: 0.45 (95% CI: 0.17, 1.21).
In our cross sectional analyses low proportions of long chain n-3 fatty acids in plasma phospholipids appear to be associated with increased risk of major depressive disorder. However, the results from this study warrant further investigation in prospective setting with sufficiently long follow-up.
Notes
Cites: Am J Psychiatry. 2004 Mar;161(3):567-9 PMID 14992986
Cites: J Am Coll Cardiol. 2011 Nov 8;58(20):2047-67 PMID 22051327
Cites: Psychosom Med. 2007 Apr;69(3):217-24 PMID 17401057
Cites: Am J Epidemiol. 2007 May 1;165(9):1076-87 PMID 17351290
Cites: J Nutr Health Aging. 2011 Dec;15(10):809-14 PMID 22159766
Cites: Prostaglandins Leukot Essent Fatty Acids. 2010 Apr-Jun;82(4-6):295-303 PMID 20227866
Cites: J Lipid Res. 1965 Apr;6:317-9 PMID 14328439
Cites: Prostaglandins Leukot Essent Fatty Acids. 2012 Jul;87(1):11-6 PMID 22658580
Cites: Laeknabladid. 2000 May;86(5):344-8 PMID 17018929
Cites: Biol Psychiatry. 2003 Sep 1;54(5):566-72 PMID 12946885
Cites: FASEB J. 2015 Jun;29(6):2207-22 PMID 25713056
Cites: Nutr Neurosci. 2004 Apr;7(2):101-6 PMID 15281176
Cites: Eur J Clin Nutr. 2015 Apr;69(4):489-93 PMID 25585599
Cites: J Nutr. 2003 Mar;133 Suppl 3:925S-932S PMID 12612178
Cites: J Nutr. 2013 Nov;143(11):1743-52 PMID 24005610
Cites: Prev Med. 2006 Jan;42(1):4-13 PMID 16337677
Cites: J Nutr Sci. 2015 Nov 20;4:e37 PMID 26688723
Cites: Eur J Clin Nutr. 2010 Sep;64(9):958-64 PMID 20551966
Cites: Am J Epidemiol. 2012 May 15;175(10):979-87 PMID 22302121
Cites: PLoS One. 2010 May 07;5(5):e10530 PMID 20479881
Cites: Neuroscience. 2008 Aug 26;155(3):751-9 PMID 18620024
Cites: Can J Psychiatry. 2003 Apr;48(3):195-203 PMID 12728744
Cites: Mol Psychiatry. 2012 Dec;17(12):1272-82 PMID 21931319
Cites: Am J Clin Nutr. 2015 May;101(5):947-55 PMID 25787995
Cites: Biol Psychiatry. 2007 Jul 1;62(1):17-24 PMID 17188654
Cites: J Clin Psychiatry. 2011 Dec;72(12):1577-84 PMID 21939614
Cites: Am J Clin Nutr. 2008 May;87(5):1156-62 PMID 18469234
Cites: Diabetes Care. 2001 Jun;24(6):1069-78 PMID 11375373
Cites: Mol Nutr Food Res. 2010 Apr;54(4):471-88 PMID 19998381
Cites: Psychol Med. 2013 Feb;43(2):317-28 PMID 22647536
Cites: BMJ. 2009 Feb 02;338:a3079 PMID 19188214
Cites: Am J Clin Nutr. 2003 Jul;78(1):40-6 PMID 12816769
Cites: PLoS One. 2014 May 07;9(5):e96905 PMID 24805797
Cites: J Affect Disord. 2009 Nov;118(1-3):209-14 PMID 19232744
Cites: Oxid Med Cell Longev. 2014;2014:313570 PMID 24757497
Cites: Nutrients. 2013 Jul 26;5(8):2901-23 PMID 23896654
Cites: Am J Clin Nutr. 2006 Jun;83(6 Suppl):1505S-1519S PMID 16841861
Cites: Eur J Clin Nutr. 2006 Jul;60(7):882-8 PMID 16465199
Cites: J Affect Disord. 2007 Aug;101(1-3):245-9 PMID 17184843
Cites: J Lipid Res. 1986 Jan;27(1):114-20 PMID 3958609
Cites: J Biol Chem. 1957 May;226(1):497-509 PMID 13428781
Cites: J Clin Endocrinol Metab. 2013 Jun;98(6):2544-52 PMID 23585664
Cites: J Nutr. 2001 Aug;131(8):2192-6 PMID 11481416
Cites: Nutr J. 2012 Mar 13;11:12 PMID 22413931
Cites: Annu Rev Clin Psychol. 2009;5:363-89 PMID 19327033
PubMed ID
29484348 View in PubMed
Less detail

Associations of current and remitted major depressive disorder with brain atrophy: the AGES-Reykjavik Study.

https://arctichealth.org/en/permalink/ahliterature123910
Source
Psychol Med. 2013 Feb;43(2):317-28
Publication Type
Article
Date
Feb-2013
Author
M I Geerlings
S. Sigurdsson
G. Eiriksdottir
M E Garcia
T B Harris
T. Sigurdsson
V. Gudnason
L J Launer
Author Affiliation
University Medical Center Utrecht, Julius Center for Health Sciences and Primary Care, The Netherlands. m.geerlings@umcutrecht.nl
Source
Psychol Med. 2013 Feb;43(2):317-28
Date
Feb-2013
Language
English
Publication Type
Article
Keywords
Age of Onset
Aged
Aged, 80 and over
Atrophy - epidemiology - pathology
Brain - pathology
Cohort Studies
Cross-Sectional Studies
Dementia - diagnosis
Depressive Disorder, Major - diagnosis - epidemiology - pathology
Female
Humans
Iceland - epidemiology
Interview, Psychological
Linear Models
Magnetic Resonance Imaging - methods
Male
Recurrence
Remission, Spontaneous
Abstract
To examine whether lifetime DSM-IV diagnosis of major depressive disorder (MDD), including age at onset and number of episodes, is associated with brain atrophy in older persons without dementia.
Within the population-based Age, Gene/Environment Susceptibility (AGES)-Reykjavik Study, 4354 persons (mean age 76 ? 5 years, 58% women) without dementia had a 1.5-T brain magnetic resonance imaging (MRI) scan. Automated brain segmentation total and regional brain volumes were calculated. History of MDD, including age at onset and number of episodes, and MDD in the past 2 weeks was diagnosed according to DSM-IV criteria using the Mini-International Neuropsychiatric Interview (MINI).
Of the total sample, 4.5% reported a lifetime history of MDD; 1.5% had a current diagnosis of MDD (including 75% with a prior history of depression) and 3.0% had a past but no current diagnosis (remission). After adjusting for multiple covariates, compared to participants never depressed, those with current MDD (irrespective of past) had more global brain atrophy [B = -1.25%, 95% confidence interval (CI) -2.05 to -0.44], including more gray- and white-matter atrophy in most lobes, and also more atrophy of the hippocampus and thalamus. Participants with current, first-onset MDD also had more brain atrophy (B = -1.62%, 95% CI -3.30 to 0.05) whereas those remitted did not (B = 0.06%, 95% CI -0.54 to 0.66).
In older persons without dementia, current MDD, irrespective of prior history, but not remitted MDD was associated with widespread gray- and white-matter brain atrophy. Prospective studies should examine whether MDD is a consequence of, or contributes to, brain volume loss and development of dementia.
PubMed ID
22647536 View in PubMed
Less detail

Cerebral microbleeds, retinopathy, and dementia: the AGES-Reykjavik Study.

https://arctichealth.org/en/permalink/ahliterature138487
Source
Neurology. 2010 Dec 14;75(24):2221-8
Publication Type
Article
Date
Dec-14-2010
Author
C. Qiu
M F Cotch
S. Sigurdsson
P V Jonsson
M K Jonsdottir
S. Sveinbjrnsdottir
G. Eiriksdottir
R. Klein
T B Harris
M A van Buchem
V. Gudnason
L J Launer
Author Affiliation
Laboratory of Epidemiology, Demography and Biometry, National Institute on Aging, Bethesda, MD, USA. chengxuan.qiu@ki.se
Source
Neurology. 2010 Dec 14;75(24):2221-8
Date
Dec-14-2010
Language
English
Publication Type
Article
Keywords
Aged
Aged, 80 and over
Aging - pathology - psychology
Brain - blood supply
Cerebral Hemorrhage - epidemiology - pathology - psychology
Cerebrovascular Circulation
Cognition
Confidence Intervals
Cross-Sectional Studies
Dementia - epidemiology - pathology - psychology
Executive Function
Female
Humans
Iceland - epidemiology
Magnetic Resonance Imaging
Male
Microcirculation
Neuropsychological Tests
Retinal Vessels - pathology
Risk factors
Abstract
To determine whether microvascular damage, indicated by cerebral microbleeds (CMBs) and retinal microvascular signs, is associated with cognitive function and dementia in older persons.
This is a cross-sectional study of 3,906 participants (mean age 76 years; 58% women) in the AGES-Reykjavik Study (2002-2006). We assessed CMBs on MRI and retinal microvascular signs on digital retinal images. Composite Z scores of memory, processing speed, and executive function were derived from a battery of neurocognitive tests. Dementia and subtypes were diagnosed following international criteria. Regression models were used to relate cognitive Z scores and dementia to CMBs and retinal microvascular signs, adjusting for demographics, cardiovascular factors, and brain ischemic lesions.
People with multiple (= 2) CMBs had lower Z scores on tests of processing speed (ß-coefficient -0.16; 95% confidence interval -0.26 to -0.05) and executive function (-0.14; -0.24 to -0.04); results were strongest for having multiple CMBs located in the deep hemispheric or infratentorial areas. The odds ratio of vascular dementia was 2.32 (95% confidence interval 1.02 to 5.25) for multiple CMBs and 1.95 (1.04 to 3.62) for retinopathy. Having both CMBs and retinopathy, compared to having neither, was significantly associated with markedly slower processing speed (-0.25; -0.37 to -0.12), poorer executive function (-0.19; -0.31 to -0.07), and an increased odds ratio of vascular dementia (3.10; 1.11 to 8.62).
Having multiple CMBs or concomitant CMBs and retinopathy is associated with a profile of vascular cognitive impairment. These findings suggest that microvascular damage, as indicated by CMBs and retinopathy lesions, has functional consequences in older men and women living in the community.
Notes
Cites: Lancet Neurol. 2005 Aug;4(8):487-9916033691
Cites: Neurology. 2005 May 10;64(9):1539-4715883314
Cites: Neurology. 2006 Jan 24;66(2):165-7116434647
Cites: Stroke. 2006 Sep;37(9):2220-4116917086
Cites: Am J Epidemiol. 2007 Jan 1;165(1):78-8417041135
Cites: Am J Epidemiol. 2007 May 1;165(9):1076-8717351290
Cites: Stroke. 2007 Jul;38(7):2041-717525385
Cites: J Neuroimaging. 2007 Jul;17(3):193-20317608904
Cites: Neurology. 2008 Apr 1;70(14):1208-1418378884
Cites: Diabetes. 2008 Jun;57(6):1645-5018332097
Cites: J Neurol Neurosurg Psychiatry. 2008 Sep;79(9):1002-618270235
Cites: J Gerontol A Biol Sci Med Sci. 2008 Aug;63(8):848-5418772473
Cites: J Appl Physiol (1985). 2008 Nov;105(5):1652-6018772322
Cites: Am J Epidemiol. 2008 Nov 15;168(10):1132-918836152
Cites: Neurology. 2009 Jan 13;72(2):143-819139365
Cites: Lancet Neurol. 2009 Feb;8(2):165-7419161908
Cites: Stroke. 2009 Mar;40(3):677-8219131654
Cites: Ann Neurol. 2009 May;65(5):569-7619475677
Cites: Arch Neurol. 2009 Jun;66(6):714-2019364926
Cites: Lancet Neurol. 2009 Jul;8(7):628-3419481977
Cites: JAMA. 2009 Jun 24;301(24):2563-7019549973
Cites: Neurology. 2009 Sep 15;73(11):862-819752453
Cites: J Am Geriatr Soc. 2009 Oct;57(10):1892-619737331
Cites: Acta Neuropathol. 2010 Mar;119(3):291-30219937043
Cites: JAMA. 2002 Feb 13;287(6):742-811851541
Cites: Stroke. 2002 Jun;33(6):1487-9212052979
Cites: Neurology. 2002 Jun 11;58(11):1629-3412058090
Cites: JAMA. 2002 Jul 3;288(1):67-7412090864
Cites: J Neurol Neurosurg Psychiatry. 2004 Jan;75(1):61-7114707310
Cites: Stroke. 2004 Aug;35(8):1831-515155954
Cites: Brain. 2004 Oct;127(Pt 10):2265-7515282216
Cites: Neurology. 1984 Jul;34(7):939-446610841
Cites: Neurology. 1992 Mar;42(3 Pt 1):473-801549205
Cites: AJNR Am J Neuroradiol. 1999 Apr;20(4):637-4210319975
Cites: Arch Ophthalmol. 2004 Nov;122(11):1642-615534124
Cites: J Neurol Sci. 2005 Mar 15;229-230:37-4115760617
Cites: Brain. 2005 Sep;128(Pt 9):2034-4115947059
PubMed ID
21172845 View in PubMed
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Chromosome alterations and E-cadherin gene mutations in human lobular breast cancer.

https://arctichealth.org/en/permalink/ahliterature20709
Source
Br J Cancer. 1999 Dec;81(7):1103-10
Publication Type
Article
Date
Dec-1999
Author
C. Huiping
J R Sigurgeirsdottir
J G Jonasson
G. Eiriksdottir
J T Johannsdottir
V. Egilsson
S. Ingvarsson
Author Affiliation
Department of Pathology, National University Hospital, Reykjavik, Iceland.
Source
Br J Cancer. 1999 Dec;81(7):1103-10
Date
Dec-1999
Language
English
Publication Type
Article
Keywords
Breast Neoplasms - genetics
Cadherins - genetics
Chromosome Aberrations - genetics
Chromosome Disorders
Chromosome Mapping
Female
Humans
Immunohistochemistry
Loss of Heterozygosity
Mutation
Polymerase Chain Reaction
Polymorphism, Single-Stranded Conformational
Research Support, Non-U.S. Gov't
Sequence Analysis, DNA
Abstract
We have studied a set of 40 human lobular breast cancers for loss of heterozygosity (LOH) at various chromosome locations and for mutations in the coding region plus flanking intron sequences of the E-cadherin gene. We found a high frequency of LOH (100%, 31/31) at 16q21-q22.1. A significantly higher level of LOH was detected in ductal breast tumours at chromosome arms 1p, 3p, 9p, 11q, 13q and 18q compared to lobular breast tumours. Furthermore, we found a significant association between LOH at 16q containing the E-cadherin locus and lobular histological type. Six different somatic mutations were detected in the E-cadherin gene, of which three were insertions, two deletions and one splice site mutation. Mutations were found in combination with LOH of the wild type E-cadherin locus and loss of or reduced E-cadherin expression detected by immunohistochemistry. The mutations described here have not previously been reported. We compared LOH at different chromosome regions with E-cadherin gene mutations and found a significant association between LOH at 13q and E-cadherin gene mutations. A significant association was also detected between LOH at 13q and LOH at 7q and 11q. Moreover, we found a significant association between LOH at 3p and high S phase, LOH at 9p and low ER and PgR content, LOH at 17p and aneuploidy. We conclude that LOH at 16q is the most frequent chromosome alteration and E-cadherin is a typical tumour suppressor gene in lobular breast cancer.
PubMed ID
10584868 View in PubMed
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Chromosome imbalance at the 3p14 region in human breast tumours: high frequency in patients with inherited predisposition due to BRCA2.

https://arctichealth.org/en/permalink/ahliterature21599
Source
Eur J Cancer. 1998 Jan;34(1):142-7
Publication Type
Article
Date
Jan-1998
Author
J T Bergthorsson
J. Johannsdottir
A. Jonasdottir
G. Eiriksdottir
V. Egilsson
S. Ingvarsson
R B Barkardottir
A. Arason
Author Affiliation
Department of Pathology, University Hospital of Iceland, Reykjavik, Iceland.
Source
Eur J Cancer. 1998 Jan;34(1):142-7
Date
Jan-1998
Language
English
Publication Type
Article
Keywords
BRCA2 Protein
Breast Neoplasms - genetics
Chromosome Fragility
Chromosomes, Human, Pair 3 - genetics
Female
Genetic Predisposition to Disease
Humans
Loss of Heterozygosity
Middle Aged
Mutation
Neoplasm Proteins - genetics
Research Support, Non-U.S. Gov't
Transcription Factors - genetics
Abstract
Our previous studies have indicated that genetic aberrations in the 3p14 region are more frequent in malignant tumours from hereditary breast cancer patients than sporadic breast cancers. The main purpose of this study was to test if BRCA2 susceptibility alleles contribute to imbalance in the 3p14 region. We mapped allelic imbalance at 3p14 in tumours from Icelandic sisters affected with breast cancer using a set of 10 microsatellite markers (tel-D3S1295-D3S1234-D3S1300-D3S1600-D3S1233+ ++-D3S1217-D3S1261-D3S1296-D3S1210- D3S1284-cen). The patients were of known carrier status with respect to the 999del5 mutation in BRCA2 which is the most common cause of hereditary breast cancer in Iceland. Of 103 patients, 32 in the group were mutation carriers. A high degree of imbalance was observed in tumours from BRCA2 mutation carriers, ranging from 44 to 88% for individual markers. This was significantly higher than the percentage of imbalance in tumours from non-carriers, where the frequency ranged from 25 to 43%. In both groups, we noted elevated 3p14 imbalance in patients with bilateral disease. Allelic imbalance was most commonly observed near the marker D3S1210 (3p14.1-p12) and the FHIT gene (3p21.1-p14.2) for both groups. We conclude that genomic aberrations in 3p14 are especially frequent in tumours with BRCA2 gene defects, and suggest that this is caused by regional loss of chromosome stability rather than selection.
PubMed ID
9624249 View in PubMed
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