Lisa Doil
Celera Corporation
6 Papers
84 Citations
Lisa Doil is an academic researcher from Celera Corporation. The author has contributed to research in topics: Single-nucleotide polymorphism & Haplotype. The author has an hindex of 6, co-authored 6 publications.
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Papers
Association of late-onset Alzheimer's disease with genetic variation in multiple members of the GAPD gene family
Yonghong Li,Petra Nowotny,Peter Holmans,Scott Smemo,John S. K. Kauwe,Anthony L. Hinrichs,Kristina Tacey,Lisa Doil,Ryan van Luchene,Veronica Garcia,Charles M. Rowland,Steven J. Schrodi,Diane Leong,Goran Gogic,Joanne Chan,Anibal Cravchik,David A. Ross,Kit Lau,Shirley Kwok,Sheng-Yung Chang,Joseph J. Catanese,John J. Sninsky,Thomas J. White,John Hardy,John Powell,Simon Lovestone,John C. Morris,Leon J. Thal,Michael John Owen,Julie Williams,Alison Goate,Andrew Grupe +31 more
TL;DR: A large-scale single-nucleotide polymorphism (SNP)-based association study across the region of linkage on chromosome 12 in multiple case-control series raises the possibility that GAPD genes are AD risk factors, a hypothesis that is consistent with the role of GAPD in neuronal apoptosis.
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Association of ABCA1 with late-onset Alzheimer's disease is not observed in a case-control study.
Yonghong Li,Kristina Tacey,Lisa Doil,Ryan van Luchene,Veronica Garcia,Charles M. Rowland,Steven J. Schrodi,Diane Leong,Kit Lau,Joe Catanese,John J. Sninsky,Petra Nowotny,Peter Holmans,John Hardy,John Powell,Simon Lovestone,Leon J. Thal,Michael John Owen,Julie Williams,Alison Goate,Andrew Grupe +20 more
TL;DR: Genetic association of ABCA1 or the ATP-binding cassette A1 transporter with late-onset Alzheimer's disease (LOAD) has recently been proposed for a haplotype comprised of three single nucleotide polymorphisms (SNPs), but this study was unable to replicate the published association, using either single markers or multiple marker haplotypes.
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Alpha-T-catenin is expressed in human brain and interacts with the Wnt signaling pathway but is not responsible for linkage to chromosome 10 in Alzheimer's disease
Victoria L. Busby,Steven Goossens,Petra Nowotny,Gillian Hamilton,Scott Smemo,Denise Harold,D. Turic,Luke Jehu,Amanda J. Myers,Meredith Womick,Daniel Woo,Danielle Compton,Lisa Doil,Kristina Tacey,Kit Lau,Safa Al-Saraj,Richard Killick,Stuart Pickering-Brown,Pamela Moore,Paul Hollingworth,Nicola Archer,Catherine Foy,Sarah Walter,C. Lendon,Takeshi Iwatsubo,John C. Morris,Joanne Norton,David M. A. Mann,Barbara Janssens,John Hardy,Michael Conlon O'Donovan,Lesley Jones,Julie Williams,Peter Holmans,Michael John Owen,Andrew Grupe,John Powell,Jolanda van Hengel,Alison Goate,Frans van Roy,Simon Lovestone +40 more
TL;DR: It is concluded that CTNNA3 is unlikely to account for the AD susceptibility locus on chromosome 10, and like other α-catenins, it inhibits Wnt signaling and is therefore also a functional candidate.
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Genetic association of the APP binding protein 2 gene (APBB2) with late onset Alzheimer disease
Yonghong Li,Paul Hollingworth,Pamela Moore,Catherine Foy,Nicola Archer,John Powell,Petra Nowotny,Peter Holmans,Michael Conlon O'Donovan,Kristina Tacey,Lisa Doil,Ryan van Luchene,Veronica Garcia,Charles M. Rowland,Kit Lau,Joseph J. Cantanese,John J. Sninsky,John Hardy,Leon J. Thal,John C. Morris,Alison Goate,Simon Lovestone,Michael John Owen,Julie Williams,Andrew Grupe +24 more
TL;DR: The data raise the possibility that genetic variations in APBB2 may affect LOAD susceptibility, and two SNPs, located in a region conserved between the human and mouse genome, showed a significant interaction with age of disease onset.
Association studies between risk for late-onset Alzheimer's disease and variants in insulin degrading enzyme.
Petra Nowotny,Anthony L. Hinrichs,Scott Smemo,John S. K. Kauwe,Taylor J. Maxwell,Peter Holmans,Marian L. Hamshere,D. Turic,Luke Jehu,Paul Hollingworth,Pamela Moore,Leslie Bryden,Amanda J. Myers,Lisa Doil,Kristina Tacey,Alison M. Gibson,Ian G. McKeith,Robert H. Perry,Christopher Morris,Leon J. Thal,John C. Morris,Michael Conlon O'Donovan,Simon Lovestone,Andrew Grupe,John Hardy,Michael John Owen,Julie Williams,Alison Goate +27 more
TL;DR: It is concluded that common variants or haplotypes of these variants in IDE are not major risk factors for LOAD, and these weak associations observed in the series were in the opposite direction to the results in previous studies.