MRI-derived brain iron, grey matter volume, and risk of dementia and Parkinson's disease: Observational and genetic analysis in the UK Biobank cohort
Iron overload is observed in neurodegenerative diseases, especially Alzheimer's disease (AD) and Parkinson's disease (PD). Homozygotes for the iron-overload (haemochromatosis) causing HFE p.C282Y variant have increased risk of dementia and PD. Whether brain iron deposition is causal or sec...
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| Published in | Neurobiology of disease Vol. 197; p. 106539 |
|---|---|
| Main Authors | , , , , , , , , , |
| Format | Journal Article |
| Language | English |
| Published |
United States
Elsevier Inc
01.07.2024
Elsevier |
| Subjects | |
| Online Access | Get full text |
| ISSN | 0969-9961 1095-953X 1095-953X |
| DOI | 10.1016/j.nbd.2024.106539 |
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| Abstract | Iron overload is observed in neurodegenerative diseases, especially Alzheimer's disease (AD) and Parkinson's disease (PD). Homozygotes for the iron-overload (haemochromatosis) causing HFE p.C282Y variant have increased risk of dementia and PD. Whether brain iron deposition is causal or secondary to the neurodegenerative processes in the general population is unclear.
We analysed 39,533 UK Biobank participants of European genetic ancestry with brain MRI data. We studied brain iron estimated by R2* and quantitative susceptibility mapping (QSM) in 8 subcortical regions: accumbens, amygdala, caudate, hippocampus, pallidum, putamen, substantia nigra, and thalamus. We performed genome-wide associations studies (GWAS) and used Mendelian Randomization (MR) methods to estimate the causal effect of brain iron on grey matter volume, and risk of AD, non-AD and PD. We also used MR to test whether genetic liability to AD or PD causally increased brain iron (R2* and QSM).
In GWAS of R2* and QSM we replicated 83% of previously reported genetic loci and identified 174 further loci across all eight brain regions. Higher genetically predicted brain iron, using both R2* and QSM, was associated with lower grey matter volumes in the caudate, putamen and thalamus (e.g., Beta-putamenQSM: −0.37, p = 2*10–46). Higher genetically predicted thalamus R2* was associated with increased risk of non-AD dementia (OR 1.36(1.16;1.60), p = 2*10–4) but not AD (p > 0.05). In males, genetically predicted putamen R2* increased non-AD dementia risk, but not in females. Higher genetically predicted iron in the caudate, putamen, and substantia nigra was associated with an increased risk of PD (Odds Ratio QSM ∼ substantia-nigra 1.21(1.07;1.37), p = 0.003). Genetic liability to AD or PD was not associated with R2* or QSM in the dementia or PD-associated regions.
Our genetic analysis supports a causal effect of higher iron deposition in specific subcortical brain regions for Parkinson's disease, grey matter volume, and non-Alzheimer's dementia.
•Genetic evidence supports a causal relationship between higher brain iron with lower grey matter volumes in specific areas.•Higher genetically predicted thalamus R2* increased risk of non-Alzheimer's dementia only.•Higher genetically predicted iron in the caudate, putamen, and substantia nigra increased risk of Parkinson's disease.•Higher iron deposition in specific subcortical brain regions caused non-Alzheimer's dementia and Parkinson's disease. |
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| AbstractList | Iron overload is observed in neurodegenerative diseases, especially Alzheimer's disease (AD) and Parkinson's disease (PD). Homozygotes for the iron-overload (haemochromatosis) causing HFE p.C282Y variant have increased risk of dementia and PD. Whether brain iron deposition is causal or secondary to the neurodegenerative processes in the general population is unclear.
We analysed 39,533 UK Biobank participants of European genetic ancestry with brain MRI data. We studied brain iron estimated by R2* and quantitative susceptibility mapping (QSM) in 8 subcortical regions: accumbens, amygdala, caudate, hippocampus, pallidum, putamen, substantia nigra, and thalamus. We performed genome-wide associations studies (GWAS) and used Mendelian Randomization (MR) methods to estimate the causal effect of brain iron on grey matter volume, and risk of AD, non-AD and PD. We also used MR to test whether genetic liability to AD or PD causally increased brain iron (R2* and QSM).
In GWAS of R2* and QSM we replicated 83% of previously reported genetic loci and identified 174 further loci across all eight brain regions. Higher genetically predicted brain iron, using both R2* and QSM, was associated with lower grey matter volumes in the caudate, putamen and thalamus (e.g., Beta-putamenQSM: −0.37, p = 2*10–46). Higher genetically predicted thalamus R2* was associated with increased risk of non-AD dementia (OR 1.36(1.16;1.60), p = 2*10–4) but not AD (p > 0.05). In males, genetically predicted putamen R2* increased non-AD dementia risk, but not in females. Higher genetically predicted iron in the caudate, putamen, and substantia nigra was associated with an increased risk of PD (Odds Ratio QSM ∼ substantia-nigra 1.21(1.07;1.37), p = 0.003). Genetic liability to AD or PD was not associated with R2* or QSM in the dementia or PD-associated regions.
Our genetic analysis supports a causal effect of higher iron deposition in specific subcortical brain regions for Parkinson's disease, grey matter volume, and non-Alzheimer's dementia.
•Genetic evidence supports a causal relationship between higher brain iron with lower grey matter volumes in specific areas.•Higher genetically predicted thalamus R2* increased risk of non-Alzheimer's dementia only.•Higher genetically predicted iron in the caudate, putamen, and substantia nigra increased risk of Parkinson's disease.•Higher iron deposition in specific subcortical brain regions caused non-Alzheimer's dementia and Parkinson's disease. Iron overload is observed in neurodegenerative diseases, especially Alzheimer's disease (AD) and Parkinson's disease (PD). Homozygotes for the iron-overload (haemochromatosis) causing HFE p.C282Y variant have increased risk of dementia and PD. Whether brain iron deposition is causal or secondary to the neurodegenerative processes in the general population is unclear.BACKGROUNDIron overload is observed in neurodegenerative diseases, especially Alzheimer's disease (AD) and Parkinson's disease (PD). Homozygotes for the iron-overload (haemochromatosis) causing HFE p.C282Y variant have increased risk of dementia and PD. Whether brain iron deposition is causal or secondary to the neurodegenerative processes in the general population is unclear.We analysed 39,533 UK Biobank participants of European genetic ancestry with brain MRI data. We studied brain iron estimated by R2* and quantitative susceptibility mapping (QSM) in 8 subcortical regions: accumbens, amygdala, caudate, hippocampus, pallidum, putamen, substantia nigra, and thalamus. We performed genome-wide associations studies (GWAS) and used Mendelian Randomization (MR) methods to estimate the causal effect of brain iron on grey matter volume, and risk of AD, non-AD and PD. We also used MR to test whether genetic liability to AD or PD causally increased brain iron (R2* and QSM).METHODSWe analysed 39,533 UK Biobank participants of European genetic ancestry with brain MRI data. We studied brain iron estimated by R2* and quantitative susceptibility mapping (QSM) in 8 subcortical regions: accumbens, amygdala, caudate, hippocampus, pallidum, putamen, substantia nigra, and thalamus. We performed genome-wide associations studies (GWAS) and used Mendelian Randomization (MR) methods to estimate the causal effect of brain iron on grey matter volume, and risk of AD, non-AD and PD. We also used MR to test whether genetic liability to AD or PD causally increased brain iron (R2* and QSM).In GWAS of R2* and QSM we replicated 83% of previously reported genetic loci and identified 174 further loci across all eight brain regions. Higher genetically predicted brain iron, using both R2* and QSM, was associated with lower grey matter volumes in the caudate, putamen and thalamus (e.g., Beta-putamenQSM: -0.37, p = 2*10-46). Higher genetically predicted thalamus R2* was associated with increased risk of non-AD dementia (OR 1.36(1.16;1.60), p = 2*10-4) but not AD (p > 0.05). In males, genetically predicted putamen R2* increased non-AD dementia risk, but not in females. Higher genetically predicted iron in the caudate, putamen, and substantia nigra was associated with an increased risk of PD (Odds Ratio QSM ∼ substantia-nigra 1.21(1.07;1.37), p = 0.003). Genetic liability to AD or PD was not associated with R2* or QSM in the dementia or PD-associated regions.FINDINGSIn GWAS of R2* and QSM we replicated 83% of previously reported genetic loci and identified 174 further loci across all eight brain regions. Higher genetically predicted brain iron, using both R2* and QSM, was associated with lower grey matter volumes in the caudate, putamen and thalamus (e.g., Beta-putamenQSM: -0.37, p = 2*10-46). Higher genetically predicted thalamus R2* was associated with increased risk of non-AD dementia (OR 1.36(1.16;1.60), p = 2*10-4) but not AD (p > 0.05). In males, genetically predicted putamen R2* increased non-AD dementia risk, but not in females. Higher genetically predicted iron in the caudate, putamen, and substantia nigra was associated with an increased risk of PD (Odds Ratio QSM ∼ substantia-nigra 1.21(1.07;1.37), p = 0.003). Genetic liability to AD or PD was not associated with R2* or QSM in the dementia or PD-associated regions.Our genetic analysis supports a causal effect of higher iron deposition in specific subcortical brain regions for Parkinson's disease, grey matter volume, and non-Alzheimer's dementia.INTERPRETATIONOur genetic analysis supports a causal effect of higher iron deposition in specific subcortical brain regions for Parkinson's disease, grey matter volume, and non-Alzheimer's dementia. Iron overload is observed in neurodegenerative diseases, especially Alzheimer's disease (AD) and Parkinson's disease (PD). Homozygotes for the iron-overload (haemochromatosis) causing HFE p.C282Y variant have increased risk of dementia and PD. Whether brain iron deposition is causal or secondary to the neurodegenerative processes in the general population is unclear. We analysed 39,533 UK Biobank participants of European genetic ancestry with brain MRI data. We studied brain iron estimated by R2* and quantitative susceptibility mapping (QSM) in 8 subcortical regions: accumbens, amygdala, caudate, hippocampus, pallidum, putamen, substantia nigra, and thalamus. We performed genome-wide associations studies (GWAS) and used Mendelian Randomization (MR) methods to estimate the causal effect of brain iron on grey matter volume, and risk of AD, non-AD and PD. We also used MR to test whether genetic liability to AD or PD causally increased brain iron (R2* and QSM). In GWAS of R2* and QSM we replicated 83% of previously reported genetic loci and identified 174 further loci across all eight brain regions. Higher genetically predicted brain iron, using both R2* and QSM, was associated with lower grey matter volumes in the caudate, putamen and thalamus (e.g., Beta-putamenQSM: -0.37, p = 2*10-46). Higher genetically predicted thalamus R2* was associated with increased risk of non-AD dementia (OR 1.36(1.16;1.60), p = 2*10-4) but not AD (p > 0.05). In males, genetically predicted putamen R2* increased non-AD dementia risk, but not in females. Higher genetically predicted iron in the caudate, putamen, and substantia nigra was associated with an increased risk of PD (Odds Ratio QSM ∼ substantia-nigra 1.21(1.07;1.37), p = 0.003). Genetic liability to AD or PD was not associated with R2* or QSM in the dementia or PD-associated regions. Our genetic analysis supports a causal effect of higher iron deposition in specific subcortical brain regions for Parkinson's disease, grey matter volume, and non-Alzheimer's dementia. Background: Iron overload is observed in neurodegenerative diseases, especially Alzheimer's disease (AD) and Parkinson's disease (PD). Homozygotes for the iron-overload (haemochromatosis) causing HFE p.C282Y variant have increased risk of dementia and PD. Whether brain iron deposition is causal or secondary to the neurodegenerative processes in the general population is unclear. Methods: We analysed 39,533 UK Biobank participants of European genetic ancestry with brain MRI data. We studied brain iron estimated by R2* and quantitative susceptibility mapping (QSM) in 8 subcortical regions: accumbens, amygdala, caudate, hippocampus, pallidum, putamen, substantia nigra, and thalamus. We performed genome-wide associations studies (GWAS) and used Mendelian Randomization (MR) methods to estimate the causal effect of brain iron on grey matter volume, and risk of AD, non-AD and PD. We also used MR to test whether genetic liability to AD or PD causally increased brain iron (R2* and QSM). Findings: In GWAS of R2* and QSM we replicated 83% of previously reported genetic loci and identified 174 further loci across all eight brain regions. Higher genetically predicted brain iron, using both R2* and QSM, was associated with lower grey matter volumes in the caudate, putamen and thalamus (e.g., Beta-putamenQSM: −0.37, p = 2*10–46). Higher genetically predicted thalamus R2* was associated with increased risk of non-AD dementia (OR 1.36(1.16;1.60), p = 2*10–4) but not AD (p > 0.05). In males, genetically predicted putamen R2* increased non-AD dementia risk, but not in females. Higher genetically predicted iron in the caudate, putamen, and substantia nigra was associated with an increased risk of PD (Odds Ratio QSM ∼ substantia-nigra 1.21(1.07;1.37), p = 0.003). Genetic liability to AD or PD was not associated with R2* or QSM in the dementia or PD-associated regions. Interpretation: Our genetic analysis supports a causal effect of higher iron deposition in specific subcortical brain regions for Parkinson's disease, grey matter volume, and non-Alzheimer's dementia. |
| ArticleNumber | 106539 |
| Author | Zweibaum, David Tian, Qu Ding, Jun Melzer, David Atkins, Janice L. Qian, Yong Williamson, Daniel S. Casanova, Francesco Ferrucci, Luigi Pilling, Luke C. |
| AuthorAffiliation | a Department of Clinical and Biomedical Sciences, University of Exeter, Magdalen Road, Exeter, Devon EX1 2LU, UK b Translational Gerontology Branch Longitudinal Studies Section, National Institute on Aging, 251 Bayview Blvd., Suite 100, Baltimore, MD 21224, USA c Department of Medical Imaging, University of Exeter, Magdalen Road, Exeter, Devon EX1 2LU, UK |
| AuthorAffiliation_xml | – name: b Translational Gerontology Branch Longitudinal Studies Section, National Institute on Aging, 251 Bayview Blvd., Suite 100, Baltimore, MD 21224, USA – name: a Department of Clinical and Biomedical Sciences, University of Exeter, Magdalen Road, Exeter, Devon EX1 2LU, UK – name: c Department of Medical Imaging, University of Exeter, Magdalen Road, Exeter, Devon EX1 2LU, UK |
| Author_xml | – sequence: 1 givenname: Francesco surname: Casanova fullname: Casanova, Francesco organization: Department of Clinical and Biomedical Sciences, University of Exeter, Magdalen Road, Exeter, Devon EX1 2LU, UK – sequence: 2 givenname: Qu surname: Tian fullname: Tian, Qu organization: Translational Gerontology Branch Longitudinal Studies Section, National Institute on Aging, 251 Bayview Blvd., Suite 100, Baltimore, MD 21224, USA – sequence: 3 givenname: Daniel S. surname: Williamson fullname: Williamson, Daniel S. organization: Department of Clinical and Biomedical Sciences, University of Exeter, Magdalen Road, Exeter, Devon EX1 2LU, UK – sequence: 4 givenname: Yong surname: Qian fullname: Qian, Yong organization: Translational Gerontology Branch Longitudinal Studies Section, National Institute on Aging, 251 Bayview Blvd., Suite 100, Baltimore, MD 21224, USA – sequence: 5 givenname: David surname: Zweibaum fullname: Zweibaum, David organization: Translational Gerontology Branch Longitudinal Studies Section, National Institute on Aging, 251 Bayview Blvd., Suite 100, Baltimore, MD 21224, USA – sequence: 6 givenname: Jun surname: Ding fullname: Ding, Jun organization: Translational Gerontology Branch Longitudinal Studies Section, National Institute on Aging, 251 Bayview Blvd., Suite 100, Baltimore, MD 21224, USA – sequence: 7 givenname: Janice L. surname: Atkins fullname: Atkins, Janice L. organization: Department of Clinical and Biomedical Sciences, University of Exeter, Magdalen Road, Exeter, Devon EX1 2LU, UK – sequence: 8 givenname: David surname: Melzer fullname: Melzer, David organization: Department of Clinical and Biomedical Sciences, University of Exeter, Magdalen Road, Exeter, Devon EX1 2LU, UK – sequence: 9 givenname: Luigi surname: Ferrucci fullname: Ferrucci, Luigi email: ferruccilu@mail.nih.gov organization: Translational Gerontology Branch Longitudinal Studies Section, National Institute on Aging, 251 Bayview Blvd., Suite 100, Baltimore, MD 21224, USA – sequence: 10 givenname: Luke C. surname: Pilling fullname: Pilling, Luke C. email: L.Pilling@exeter.ac.uk organization: Department of Clinical and Biomedical Sciences, University of Exeter, Magdalen Road, Exeter, Devon EX1 2LU, UK |
| BackLink | https://www.ncbi.nlm.nih.gov/pubmed/38789058$$D View this record in MEDLINE/PubMed |
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| Cites_doi | 10.1093/brain/114.4.1953 10.3389/fnagi.2021.743754 10.1056/NEJMe2213120 10.1002/gepi.22522 10.1038/s41593-022-01074-w 10.1016/j.ejmp.2023.102590 10.1016/j.acra.2013.09.018 10.3390/ijms23137267 10.3233/JAD-201080 10.1038/ng.3190 10.1016/j.neuroimage.2015.12.045 10.1093/aje/kwx246 10.1016/j.bbagen.2008.08.005 10.1016/j.nbd.2015.08.007 10.1038/s41588-018-0184-y 10.3389/fnins.2021.618435 10.1002/jmri.21563 10.1016/j.neuroimage.2012.05.049 10.1038/s41586-018-0579-z 10.1155/2014/581256 10.1038/ng.3211 10.1016/S0140-6736(23)00287-8 10.1016/S1474-4422(14)70117-6 10.1038/s41380-019-0375-7 10.1038/s41588-019-0358-2 10.1016/S1474-4422(19)30320-5 10.1148/radiol.2021210116 |
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| Keywords | Parkinson's Genetics Iron Grey matter Dementia |
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| References | Peters, Connor, Meadowcroft (bb0100) 2015; 81 Langkammer, Schweser, Krebs (bb0075) 2012; 62 Adams, Jeffrey, Ryan (bb0005) 2023; 401 Daugherty, Raz (bb0040) 2016; 128 Zhou, Nielsen, Fritsche (bb0145) 2018; 50 Gustavo Cuna, Schulz, Tuzzi (bb0060) 2023; 110 Bycroft, Freeman, Petkova (bb0030) 2018; 562 Ayton, Lei (bb0015) 2014; 2014 Fry, Littlejohns, Sudlow (bb0050) 2017; 186 Casanova, Tian, Atkins (bb0035) 2024; 61 Han, Fan, Wu (bb0065) 2021; 13 Ward, Dexter, Crichton (bb0140) 2022; 23 Ayton, Wang, Diouf (bb0020) 2020; 25 Lee, Cho, Lee, Kim, Roh, Lee (bb0080) 2021; 301 Nalls, Blauwendraat, Vallerga (bb0095) 2019; 18 Loh, Tucker, Bulik-Sullivan (bb0085) 2015; 47 Snyder, Connor (bb0120) 2009; 1790 Ravanfar, Loi, Syeda (bb0105) 2021; 15 Wallis, Paley, Graham (bb0125) 2008; 28 Rossi, Ruottinen, Saunamaki, Elovaara, Dastidar (bb0110) 2014; 21 Bulik-Sullivan, Loh, Finucane (bb0025) 2015; 47 Ward, Zucca, Duyn, Crichton, Zecca (bb0135) 2014; 13 Kunkle, Grenier-Boley, Sims (bb0070) 2019; 51 Wang, Martins-Bach, Alfaro-Almagro (bb0130) 2022; 25 Atkins, Pilling, Heales (bb0010) 2021; 79 Dexter, Carayon, Javoy-Agid (bb0045) 1991; 114 Mounier, Kutalik (bb0090) 2023; 47 Sanderson, Glymour, Holmes (bb0115) 2022 Galasko, Simuni (bb0055) 2022; 387 Fry (10.1016/j.nbd.2024.106539_bb0050) 2017; 186 Sanderson (10.1016/j.nbd.2024.106539_bb0115) 2022 Wallis (10.1016/j.nbd.2024.106539_bb0125) 2008; 28 Han (10.1016/j.nbd.2024.106539_bb0065) 2021; 13 Bycroft (10.1016/j.nbd.2024.106539_bb0030) 2018; 562 Atkins (10.1016/j.nbd.2024.106539_bb0010) 2021; 79 Ravanfar (10.1016/j.nbd.2024.106539_bb0105) 2021; 15 Ward (10.1016/j.nbd.2024.106539_bb0135) 2014; 13 Kunkle (10.1016/j.nbd.2024.106539_bb0070) 2019; 51 Bulik-Sullivan (10.1016/j.nbd.2024.106539_bb0025) 2015; 47 Ayton (10.1016/j.nbd.2024.106539_bb0020) 2020; 25 Nalls (10.1016/j.nbd.2024.106539_bb0095) 2019; 18 Lee (10.1016/j.nbd.2024.106539_bb0080) 2021; 301 Daugherty (10.1016/j.nbd.2024.106539_bb0040) 2016; 128 Mounier (10.1016/j.nbd.2024.106539_bb0090) 2023; 47 Ayton (10.1016/j.nbd.2024.106539_bb0015) 2014; 2014 Loh (10.1016/j.nbd.2024.106539_bb0085) 2015; 47 Peters (10.1016/j.nbd.2024.106539_bb0100) 2015; 81 Adams (10.1016/j.nbd.2024.106539_bb0005) 2023; 401 Zhou (10.1016/j.nbd.2024.106539_bb0145) 2018; 50 Dexter (10.1016/j.nbd.2024.106539_bb0045) 1991; 114 Rossi (10.1016/j.nbd.2024.106539_bb0110) 2014; 21 Ward (10.1016/j.nbd.2024.106539_bb0140) 2022; 23 Casanova (10.1016/j.nbd.2024.106539_bb0035) 2024; 61 Gustavo Cuna (10.1016/j.nbd.2024.106539_bb0060) 2023; 110 Snyder (10.1016/j.nbd.2024.106539_bb0120) 2009; 1790 Wang (10.1016/j.nbd.2024.106539_bb0130) 2022; 25 Galasko (10.1016/j.nbd.2024.106539_bb0055) 2022; 387 Langkammer (10.1016/j.nbd.2024.106539_bb0075) 2012; 62 |
| References_xml | – volume: 21 start-page: 64 year: 2014 end-page: 71 ident: bb0110 article-title: Imaging brain iron and diffusion patterns: a follow-up study of Parkinson’s disease in the initial stages publication-title: Acad. Radiol. – volume: 47 start-page: 284 year: 2015 end-page: 290 ident: bb0085 article-title: Efficient Bayesian mixed-model analysis increases association power in large cohorts publication-title: Nat. Genet. – volume: 79 start-page: 1203 year: 2021 end-page: 1211 ident: bb0010 article-title: Hemochromatosis mutations, brain Iron imaging, and dementia in the UK biobank cohort publication-title: J. Alzheimers Dis. – volume: 62 start-page: 1593 year: 2012 end-page: 1599 ident: bb0075 article-title: Quantitative susceptibility mapping (QSM) as a means to measure brain iron? A post mortem validation study publication-title: Neuroimage – volume: 25 start-page: 818 year: 2022 end-page: 831 ident: bb0130 article-title: Phenotypic and genetic associations of quantitative magnetic susceptibility in UK biobank brain imaging publication-title: Nat. Neurosci. – start-page: 2 year: 2022 ident: bb0115 article-title: Mendelian randomization publication-title: Nat. Rev. Meth. Prim. – volume: 15 year: 2021 ident: bb0105 article-title: Systematic review: quantitative susceptibility mapping (QSM) of brain Iron profile in neurodegenerative diseases publication-title: Front. Neurosci. – volume: 13 year: 2021 ident: bb0065 article-title: Parkinson’s disease dementia: synergistic effects of alpha-Synuclein, tau, Beta-amyloid, and Iron publication-title: Front. Aging Neurosci. – volume: 186 start-page: 1026 year: 2017 end-page: 1034 ident: bb0050 article-title: Comparison of sociodemographic and health-related characteristics of UK biobank participants with those of the general population publication-title: Am. J. Epidemiol. – volume: 301 start-page: 682 year: 2021 end-page: 691 ident: bb0080 article-title: Differential effect of Iron and myelin on susceptibility MRI in the substantia Nigra publication-title: Radiology – volume: 81 start-page: 49 year: 2015 end-page: 65 ident: bb0100 article-title: The relationship between iron dyshomeostasis and amyloidogenesis in Alzheimer’s disease: two sides of the same coin publication-title: Neurobiol. Dis. – volume: 128 start-page: 11 year: 2016 end-page: 20 ident: bb0040 article-title: Accumulation of iron in the putamen predicts its shrinkage in healthy older adults: a multi-occasion longitudinal study publication-title: Neuroimage – volume: 61 start-page: 435 year: 2024 end-page: 442 ident: bb0035 article-title: Serum iron and risk of dementia: Mendelian randomization analysis in UK biobank publication-title: J. Med. Genet. – volume: 110 year: 2023 ident: bb0060 article-title: Simulated and experimental phantom data for multi-center quality assurance of quantitative susceptibility maps at 3 T, 7 T and 9.4 T publication-title: Phys. Med. – volume: 47 start-page: 314 year: 2023 end-page: 331 ident: bb0090 article-title: Bias correction for inverse variance weighting Mendelian randomization publication-title: Genet. Epidemiol. – volume: 401 start-page: 1811 year: 2023 end-page: 1821 ident: bb0005 article-title: Haemochromatosis publication-title: Lancet – volume: 2014 year: 2014 ident: bb0015 article-title: Nigral iron elevation is an invariable feature of Parkinson’s disease and is a sufficient cause of neurodegeneration publication-title: Biomed. Res. Int. – volume: 51 start-page: 414 year: 2019 end-page: 430 ident: bb0070 article-title: Genetic meta-analysis of diagnosed Alzheimer’s disease identifies new risk loci and implicates Abeta, tau, immunity and lipid processing publication-title: Nat. Genet. – volume: 387 start-page: 2087 year: 2022 end-page: 2088 ident: bb0055 article-title: Lack of benefit of Iron chelation in early Parkinson’s disease publication-title: N. Engl. J. Med. – volume: 25 start-page: 2932 year: 2020 end-page: 2941 ident: bb0020 article-title: Brain iron is associated with accelerated cognitive decline in people with Alzheimer pathology publication-title: Mol. Psychiatry – volume: 23 year: 2022 ident: bb0140 article-title: Iron, Neuroinflammation and Neurodegeneration publication-title: Int. J. Mol. Sci. – volume: 28 start-page: 1061 year: 2008 end-page: 1067 ident: bb0125 article-title: MRI assessment of basal ganglia iron deposition in Parkinson’s disease publication-title: J. Magn. Reson. Imaging – volume: 562 start-page: 203 year: 2018 end-page: 209 ident: bb0030 article-title: The UK biobank resource with deep phenotyping and genomic data publication-title: Nature – volume: 18 start-page: 1091 year: 2019 end-page: 1102 ident: bb0095 article-title: Identification of novel risk loci, causal insights, and heritable risk for Parkinson’s disease: a meta-analysis of genome-wide association studies publication-title: Lancet Neurol. – volume: 50 start-page: 1335 year: 2018 end-page: 1341 ident: bb0145 article-title: Efficiently controlling for case-control imbalance and sample relatedness in large-scale genetic association studies publication-title: Nat. Genet. – volume: 114 start-page: 1953 year: 1991 end-page: 1975 ident: bb0045 article-title: Alterations in the levels of iron, ferritin and other trace metals in Parkinson’s disease and other neurodegenerative diseases affecting the basal ganglia publication-title: Brain – volume: 1790 start-page: 606 year: 2009 end-page: 614 ident: bb0120 article-title: Iron, the substantia nigra and related neurological disorders publication-title: Biochim. Biophys. Acta – volume: 47 start-page: 291 year: 2015 end-page: 295 ident: bb0025 article-title: LD score regression distinguishes confounding from polygenicity in genome-wide association studies publication-title: Nat. Genet. – volume: 13 start-page: 1045 year: 2014 end-page: 1060 ident: bb0135 article-title: The role of iron in brain ageing and neurodegenerative disorders publication-title: Lancet Neurol. – volume: 114 start-page: 1953 issue: Pt 4 year: 1991 ident: 10.1016/j.nbd.2024.106539_bb0045 article-title: Alterations in the levels of iron, ferritin and other trace metals in Parkinson’s disease and other neurodegenerative diseases affecting the basal ganglia publication-title: Brain doi: 10.1093/brain/114.4.1953 – volume: 13 year: 2021 ident: 10.1016/j.nbd.2024.106539_bb0065 article-title: Parkinson’s disease dementia: synergistic effects of alpha-Synuclein, tau, Beta-amyloid, and Iron publication-title: Front. Aging Neurosci. doi: 10.3389/fnagi.2021.743754 – volume: 387 start-page: 2087 issue: 22 year: 2022 ident: 10.1016/j.nbd.2024.106539_bb0055 article-title: Lack of benefit of Iron chelation in early Parkinson’s disease publication-title: N. Engl. J. Med. doi: 10.1056/NEJMe2213120 – volume: 47 start-page: 314 issue: 4 year: 2023 ident: 10.1016/j.nbd.2024.106539_bb0090 article-title: Bias correction for inverse variance weighting Mendelian randomization publication-title: Genet. Epidemiol. doi: 10.1002/gepi.22522 – volume: 61 start-page: 435 year: 2024 ident: 10.1016/j.nbd.2024.106539_bb0035 article-title: Serum iron and risk of dementia: Mendelian randomization analysis in UK biobank publication-title: J. Med. Genet. – volume: 25 start-page: 818 issue: 6 year: 2022 ident: 10.1016/j.nbd.2024.106539_bb0130 article-title: Phenotypic and genetic associations of quantitative magnetic susceptibility in UK biobank brain imaging publication-title: Nat. Neurosci. doi: 10.1038/s41593-022-01074-w – volume: 110 year: 2023 ident: 10.1016/j.nbd.2024.106539_bb0060 article-title: Simulated and experimental phantom data for multi-center quality assurance of quantitative susceptibility maps at 3 T, 7 T and 9.4 T publication-title: Phys. Med. doi: 10.1016/j.ejmp.2023.102590 – volume: 21 start-page: 64 issue: 1 year: 2014 ident: 10.1016/j.nbd.2024.106539_bb0110 article-title: Imaging brain iron and diffusion patterns: a follow-up study of Parkinson’s disease in the initial stages publication-title: Acad. Radiol. doi: 10.1016/j.acra.2013.09.018 – volume: 23 issue: 13 year: 2022 ident: 10.1016/j.nbd.2024.106539_bb0140 article-title: Iron, Neuroinflammation and Neurodegeneration publication-title: Int. J. Mol. Sci. doi: 10.3390/ijms23137267 – volume: 79 start-page: 1203 issue: 3 year: 2021 ident: 10.1016/j.nbd.2024.106539_bb0010 article-title: Hemochromatosis mutations, brain Iron imaging, and dementia in the UK biobank cohort publication-title: J. Alzheimers Dis. doi: 10.3233/JAD-201080 – volume: 47 start-page: 284 issue: 3 year: 2015 ident: 10.1016/j.nbd.2024.106539_bb0085 article-title: Efficient Bayesian mixed-model analysis increases association power in large cohorts publication-title: Nat. Genet. doi: 10.1038/ng.3190 – volume: 128 start-page: 11 year: 2016 ident: 10.1016/j.nbd.2024.106539_bb0040 article-title: Accumulation of iron in the putamen predicts its shrinkage in healthy older adults: a multi-occasion longitudinal study publication-title: Neuroimage doi: 10.1016/j.neuroimage.2015.12.045 – volume: 186 start-page: 1026 issue: 9 year: 2017 ident: 10.1016/j.nbd.2024.106539_bb0050 article-title: Comparison of sociodemographic and health-related characteristics of UK biobank participants with those of the general population publication-title: Am. J. Epidemiol. doi: 10.1093/aje/kwx246 – volume: 1790 start-page: 606 issue: 7 year: 2009 ident: 10.1016/j.nbd.2024.106539_bb0120 article-title: Iron, the substantia nigra and related neurological disorders publication-title: Biochim. Biophys. Acta doi: 10.1016/j.bbagen.2008.08.005 – volume: 81 start-page: 49 year: 2015 ident: 10.1016/j.nbd.2024.106539_bb0100 article-title: The relationship between iron dyshomeostasis and amyloidogenesis in Alzheimer’s disease: two sides of the same coin publication-title: Neurobiol. Dis. doi: 10.1016/j.nbd.2015.08.007 – volume: 50 start-page: 1335 issue: 9 year: 2018 ident: 10.1016/j.nbd.2024.106539_bb0145 article-title: Efficiently controlling for case-control imbalance and sample relatedness in large-scale genetic association studies publication-title: Nat. Genet. doi: 10.1038/s41588-018-0184-y – volume: 15 year: 2021 ident: 10.1016/j.nbd.2024.106539_bb0105 article-title: Systematic review: quantitative susceptibility mapping (QSM) of brain Iron profile in neurodegenerative diseases publication-title: Front. Neurosci. doi: 10.3389/fnins.2021.618435 – start-page: 2 year: 2022 ident: 10.1016/j.nbd.2024.106539_bb0115 article-title: Mendelian randomization publication-title: Nat. Rev. Meth. Prim. – volume: 28 start-page: 1061 issue: 5 year: 2008 ident: 10.1016/j.nbd.2024.106539_bb0125 article-title: MRI assessment of basal ganglia iron deposition in Parkinson’s disease publication-title: J. Magn. Reson. Imaging doi: 10.1002/jmri.21563 – volume: 62 start-page: 1593 issue: 3 year: 2012 ident: 10.1016/j.nbd.2024.106539_bb0075 article-title: Quantitative susceptibility mapping (QSM) as a means to measure brain iron? A post mortem validation study publication-title: Neuroimage doi: 10.1016/j.neuroimage.2012.05.049 – volume: 562 start-page: 203 issue: 7726 year: 2018 ident: 10.1016/j.nbd.2024.106539_bb0030 article-title: The UK biobank resource with deep phenotyping and genomic data publication-title: Nature doi: 10.1038/s41586-018-0579-z – volume: 2014 year: 2014 ident: 10.1016/j.nbd.2024.106539_bb0015 article-title: Nigral iron elevation is an invariable feature of Parkinson’s disease and is a sufficient cause of neurodegeneration publication-title: Biomed. Res. Int. doi: 10.1155/2014/581256 – volume: 47 start-page: 291 issue: 3 year: 2015 ident: 10.1016/j.nbd.2024.106539_bb0025 article-title: LD score regression distinguishes confounding from polygenicity in genome-wide association studies publication-title: Nat. Genet. doi: 10.1038/ng.3211 – volume: 401 start-page: 1811 issue: 10390 year: 2023 ident: 10.1016/j.nbd.2024.106539_bb0005 article-title: Haemochromatosis publication-title: Lancet doi: 10.1016/S0140-6736(23)00287-8 – volume: 13 start-page: 1045 issue: 10 year: 2014 ident: 10.1016/j.nbd.2024.106539_bb0135 article-title: The role of iron in brain ageing and neurodegenerative disorders publication-title: Lancet Neurol. doi: 10.1016/S1474-4422(14)70117-6 – volume: 25 start-page: 2932 issue: 11 year: 2020 ident: 10.1016/j.nbd.2024.106539_bb0020 article-title: Brain iron is associated with accelerated cognitive decline in people with Alzheimer pathology publication-title: Mol. Psychiatry doi: 10.1038/s41380-019-0375-7 – volume: 51 start-page: 414 issue: 3 year: 2019 ident: 10.1016/j.nbd.2024.106539_bb0070 article-title: Genetic meta-analysis of diagnosed Alzheimer’s disease identifies new risk loci and implicates Abeta, tau, immunity and lipid processing publication-title: Nat. Genet. doi: 10.1038/s41588-019-0358-2 – volume: 18 start-page: 1091 issue: 12 year: 2019 ident: 10.1016/j.nbd.2024.106539_bb0095 article-title: Identification of novel risk loci, causal insights, and heritable risk for Parkinson’s disease: a meta-analysis of genome-wide association studies publication-title: Lancet Neurol. doi: 10.1016/S1474-4422(19)30320-5 – volume: 301 start-page: 682 issue: 3 year: 2021 ident: 10.1016/j.nbd.2024.106539_bb0080 article-title: Differential effect of Iron and myelin on susceptibility MRI in the substantia Nigra publication-title: Radiology doi: 10.1148/radiol.2021210116 |
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| Snippet | Iron overload is observed in neurodegenerative diseases, especially Alzheimer's disease (AD) and Parkinson's disease (PD). Homozygotes for the iron-overload... Background: Iron overload is observed in neurodegenerative diseases, especially Alzheimer's disease (AD) and Parkinson's disease (PD). Homozygotes for the... |
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| SubjectTerms | Aged Brain - diagnostic imaging Brain - metabolism Brain - pathology Cohort Studies Dementia Dementia - diagnostic imaging Dementia - genetics Dementia - pathology Female Genetics Genome-Wide Association Study Gray Matter - diagnostic imaging Gray Matter - metabolism Gray Matter - pathology Grey matter Humans Iron Iron - metabolism Magnetic Resonance Imaging Male Middle Aged Parkinson Disease - diagnostic imaging Parkinson Disease - genetics Parkinson Disease - pathology Parkinson's UK Biobank United Kingdom - epidemiology |
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| Title | MRI-derived brain iron, grey matter volume, and risk of dementia and Parkinson's disease: Observational and genetic analysis in the UK Biobank cohort |
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