4 research outputs found
New insights into the genetic etiology of Alzheimer's disease and related dementias
- Author
- Aaltonen L.
- Aaltonen V.
- Aarsland Dag
- Aavikko M.
- Abalos M.S.
- Abdelnour Carla
- Abner E.
- Abraham R.
- Adams H.
- Adams P.M.
- Adarmes-GĂłmez A.
- Adarmes-GĂłmez A.D.
- Aguilera N.
- Aguilera N.
- Aguirre A.
- Ahmad S.
- Akinyemi R.O.
- Al-Chalabi A.
- AlarcĂłn-MartĂn Emilio
- Albert M.S.
- Albin R.L.
- Alcolea Daniel
- Alegret Montserrat
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- Allende I.R.
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- Publication venue
- Publication date
- 01/01/2022
- Field of study
Get PDFCharacterization of the genetic landscape of Alzheimer's disease (AD) and related dementias (ADD) provides a unique opportunity for a better understanding of the associated pathophysiological processes. We performed a two-stage genome-wide association study totaling 111,326 clinically diagnosed/'proxy' AD cases and 677,663 controls. We found 75 risk loci, of which 42 were new at the time of analysis. Pathway enrichment analyses confirmed the involvement of amyloid/tau pathways and highlighted microglia implication. Gene prioritization in the new loci identified 31 genes that were suggestive of new genetically associated processes, including the tumor necrosis factor alpha pathway through the linear ubiquitin chain assembly complex. We also built a new genetic risk score associated with the risk of future AD/dementia or progression from mild cognitive impairment to AD/dementia. The improvement in prediction led to a 1.6- to 1.9-fold increase in AD risk from the lowest to the highest decile, in addition to effects of age and the APOE Δ4 allele
Comparison of arterial spin labeling registration strategies in the multi-center GENetic frontotemporal dementia initiative (GENFI)
- Author
- Borroni B. (Barbara)
- Cash D.M. (David M)
- Castelo Branco M. (Miguel)
- Finger E. (Elizabeth)
- Galimberti D. (Daniela)
- Golay A. (Alain)
- Graff M.J. (Maud J.L.)
- Groot P.F. (Paul F.C.)
- Laforce R. (Robert)
- MacIntosh B.J. (Bradley J)
- Masellis M. (Mario)
- Mutsaerts H.-J. (Henk-Jan)
- Osch M.J.v. (Matthias J.P. van)
- Ourselin S. (Sebastien)
- Petr J. (Jan)
- Pizzini F.B. (Francesca B.)
- Rohrer J.D. (Jonathan D)
- Rowe J.B. (James)
- Sorbi S. (Sandro)
- Swieten J.v. (John van)
- Tagliavini F. (Fabrizio)
- Thomas D.L. (David L)
- Vita E.d. (Enrico de)
- Publication venue
- 'Wiley'
- Publication date
- 01/01/2017
- Field of study
No full textPurpose: To compare registration strategies to align arterial spin labeling (ASL) with 3D T1-weighted (T1w) images, with the goal of reducing the between-subject variability of cerebral blood flow (CBF) images. Materials and Methods: Multi-center 3T ASL data were collected at eight sites with four different sequences in the multi-center GENetic Frontotemporal dementia Initiative (GENFI) study. In a total of 48 healthy controls, we compared the following image registration options: (I) which images to use for registration (perfusion-weighted images [PWI] to the segmented gray matter (GM) probability map (pGM) (CBF-pGM) or M0 to T1w (M0-T1w); (II) which transformation to use (rigid-body or non-rigid); and (III) whether to mask or not (no masking, M0-based FMRIB software library Brain Extraction Tool [BET] masking). In addition to visual comparison, we quantified image similarity using the Pearson correlation coefficient (CC), and used the Mann-Whitney U rank sum test. Results: CBF-pGM outperformed M0-T1w (CC improvement 47.2% ± 22.0%; P < 0.001), and the non-rigid transformation outperformed rigid-body (20.6% ± 5.3%; P < 0.001). Masking only improved the M0-T1w rigid-body registration (14.5% ± 15.5%; P = 0.007). Conclusion: The choice of image registration strategy impacts ASL group analyses. The non-rigid transformation is promising but requires validation. CBF-pGM rigid-body registration without masking can be used as a default strategy. In patients with expansive perfusion deficits, M0-T1w may outperform CBF-pGM in sequences with high effective spatial resolution. BET-masking only improves M0-T1w registration when the M0 image has sufficient contrast
2017 Cardiovascular and Stroke Endpoint Definitions for Clinical Trials
- Author
- A. Michael Lincoff
- Akshay S. Desai
- Albers
- Alexandra J. Lansky
- Alpert
- Ana Szarfman
- Andrew Farb
- Anna Park
- Benjamin M. Scirica
- Bernard R. Chaitman
- Billy Dunn
- Bram Zuckerman
- Braunwald
- Bron Kisler
- Burgess
- C. Michael Gibson
- Cathy A. Sila
- Chaitman
- Charles Jaffe
- Cheri Janning
- Christopher J. White
- Christopher M. OâConnor
- Cutlip
- David A. Morrow
- David L. DeMets
- Donald E. Cutlip
- Douglas Peddicord
- Easton
- Eldrin F. Lewis
- Ellis F. Unger
- Gore
- Granger
- H.M. James Hung
- Heather D. Fitter
- Hicks
- Hylton V. Joffe
- Ilan Irony
- James E. Tcheng
- John J.V. McMurray
- John Lawrence
- John R. Marler
- John R. Teerlink
- Jonathan G. Levine
- Kachikwu Illoh
- Karen A. Hicks
- Karnegis
- Keller
- Kenneth J. Cavanaugh
- Kenneth Rosenfield
- Kenneth W. Mahaffey
- Lansky
- Laura Mauri
- Leonard Sacks
- Lori Ann Wachter
- Mahaffey
- Marc A. Pfeffer
- MariJo Mencini
- Martin J. Landray
- Mary T. Thanh Hai
- McKee
- Melki
- Michael J. Domanski
- Michael R. Jaff
- Moussa
- Mozaffarian
- Norman L. Stockbridge
- Okumura
- Paul Burton
- Rachel E. Brown Kichline
- Ralph B. DâAgostino
- Rhonda Bartley
- Robert J. Temple
- Roxana Mehran
- Sacco
- Scott D. Solomon
- Shari L. Targum
- Skali
- Solomon
- Stephen D. Wiviott
- Steve Bai
- Steven E. Nissen
- Steven R. Steinhubl
- Steven S. Brooks
- Stuart J. Pocock
- Thom
- Thomas Shook
- Thygesen
- Thygesen
- Van Swieten
- Yale Mitchel
- Publication venue
- 'Elsevier BV'
- Publication date
- Field of study
No full textNew insights into the genetic etiology of Alzheimerâs disease and related dementias
- Publication venue
- 'Springer Science and Business Media LLC'
- Publication date
- 01/01/2022
- Field of study
No full textCharacterization of the genetic landscape of Alzheimerâs disease (AD) and related dementias (ADD) provides a unique opportunity for a better understanding of the associated pathophysiological processes. We performed a two-stage genome-wide association study totaling 111,326 clinically diagnosed/âproxyâ AD cases and 677,663 controls. We found 75 risk loci, of which 42 were new at the time of analysis. Pathway enrichment analyses confirmed the involvement of amyloid/tau pathways and highlighted microglia implication. Gene prioritization in the new loci identified 31 genes that were suggestive of new genetically associated processes, including the tumor necrosis factor alpha pathway through the linear ubiquitin chain assembly complex. We also built a new genetic risk score associated with the risk of future AD/dementia or progression from mild cognitive impairment to AD/dementia. The improvement in prediction led to a 1.6- to 1.9-fold increase in AD risk from the lowest to the highest decile, in addition to effects of age and the APOE Δ4 allele. © 2022, The Author(s)
