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Alison Goate
Researcher at Icahn School of Medicine at Mount Sinai
Publications - 781
Citations - 98332
Alison Goate is an academic researcher from Icahn School of Medicine at Mount Sinai. The author has contributed to research in topics: Genome-wide association study & Alzheimer's disease. The author has an hindex of 136, co-authored 721 publications receiving 85846 citations. Previous affiliations of Alison Goate include St Mary's Hospital & Brown University.
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Journal ArticleDOI
Segregation of functional networks is associated with cognitive resilience in Alzheimer's disease.
Michael Ewers,Michael Ewers,Ying Luan,Lukas Frontzkowski,Julia Neitzel,Anna Rubinski,Martin Dichgans,Martin Dichgans,Jason Hassenstab,Brian A. Gordon,Jasmeer P. Chhatwal,Johannes Levin,Johannes Levin,Peter R. Schofield,Peter R. Schofield,Tammie L.S. Benzinger,John C. Morris,Alison Goate,Alison Goate,Celeste M. Karch,Anne M. Fagan,Eric McDade,Ricardo F. Allegri,Sarah B. Berman,Helena C. Chui,Carlos Cruchaga,Marty Farlow,Neill R. Graff-Radford,Mathias Jucker,Mathias Jucker,Jae-Hong Lee,Ralph N. Martins,Hiroshi Mori,Richard J. Perrin,Chengjie Xiong,Martin N. Rossor,Nick C. Fox,Antoinette O'Connor,Stephen Salloway,Adrian Danek,Katharina Buerger,Katharina Buerger,Randall J. Bateman,Christian G. Habeck,Yaakov Stern,Nicolai Franzmeier,Alzheimer’s Disease Neuroimaging Initiative +46 more
TL;DR: In this paper, the authors found that higher segregation of the brain's connectome into distinct functional networks represents a functional mechanism underlying cognitive resilience in Alzheimer's disease using resting-state functional MRI and the alternate index of modularity Q as predictors of cognitive resilience.
Journal ArticleDOI
No association found between Alzheimer's disease and a mitochondrial tRNA glutamine gene variant ☆
TL;DR: A large sample of patients with sporadic late-onset dementia of the Alzheimer type (DAT) and age-matched controls for a mitochondrial tRNA(Gln) variant previously reported to be associated with increased risk of developing Alzheimer's disease (AD) are screened.
Journal ArticleDOI
A 3p26-3p25 Genetic Linkage Finding for DSM-IV Major Depression in Heavy Smoking Families
Michele L. Pergadia,Anne L. Glowinski,Naomi R. Wray,Arpana Agrawal,Scott F. Saccone,Anu Loukola,Ulla Broms,Tellervo Korhonen,Brenda W.J.H. Penninx,Julia D. Grant,Elliot C. Nelson,Anjali K. Henders,Andrew J. Schrage,Yi-Ling Chou,Kaisu Keskitalo-Vuokko,Qin Zhu,Scott D. Gordon,Jacqueline M. Vink,Eco J. C. de Geus,Stuart MacGregor,Jimmy Z. Liu,Gonneke Willemsen,Sarah E. Medland,Dorret I. Boomsma,Grant W. Montgomery,John P. Rice,Alison Goate,Andrew C. Heath,Jaakko Kaprio,Nicholas G. Martin,Pamela A. F. Madden +30 more
TL;DR: Genome-wide significant linkage was detected for major depressive disorder on chromosome 3p in a sample ascertained for smoking, and a linkage peak at this location was also observed in an independent study of major depressive Disorder.
Journal ArticleDOI
Age-specific incidence rates for dementia and alzheimer disease in NIA-LOAD/NCRAD and EFIGA families: National Institute on Aging Genetics Initiative for late-onset Alzheimer disease/National Cell Repository for Alzheimer disease (NIA-LOAD/NCRAD) and Estudio Familiar de Influencia Genetica en Alzheimer (EFIGA)
Badri N. Vardarajan,Kelley Faber,Thomas D. Bird,David A. Bennett,Roger N. Rosenberg,Bradley F. Boeve,Neill R. Graff-Radford,Alison Goate,Martin R. Farlow,Robert A. Sweet,Rafael Lantigua,Martin Medrano,Ruth Ottman,Daniel J. Schaid,Tatiana Foroud,Richard Mayeux +15 more
TL;DR: The incidence rates for familial dementia and LOAD in the NIA-LOAD/NCRAD and EFIGA families are significantly higher than population-based estimates and can be explained by segregation of Alzheimer disease-related genes in these families or shared environmental risks.
Journal ArticleDOI
Sequencing of exons 16 and 17 of the β-amyloid precursor protein gene in 14 families with early onset Alzheimer's disease fails to reveal mutations in the β-amyloid sequence
Fiona Crawford,John Hardy,Michael Mullan,Alison Goate,David Hughes,Liana Fidani,P Roques,Martin N. Rossor,Marie-Christine Chartier-Harlin +8 more
TL;DR: Direct sequencing of exons 16 and 17 of the beta-amyloid precursor protein gene in 14 families with familial early onset Alzheimer's disease without the known pathogenic mutation (APP717) failed to reveal other mutations within the Beta-Amyloid sequence in this form of the disorder.