Lotta Forsell
Karolinska Institutet
3 Papers
1 Citations
Lotta Forsell is an academic researcher from Karolinska Institutet. The author has contributed to research in topics: Gene & Inositol trisphosphate receptor. The author has an hindex of 2, co-authored 3 publications.
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Papers
The structure of the presenilin 1 (S182) gene and identification of six novel mutations in early onset AD families
Robert Clark,Mike Hutton,Rebecca A. Fuldner,Sue Froelich,Eric Karran,Christopher Talbot,Richard Crook,Corinne Lendon,Guy Prihar,C He,Kevin M. Korenblat,Alonso Martínez,Alonso Martínez,Michelle Wragg,F. Busfield,Maria I. Behrens,Amanda J. Myers,Joanne Norton,John C. Morris,N Mehta,Chad G. Pearson,Sarah Lincoln,M Baker,Karen Duff,C Zehr,Jordi Pérez-Tur,Harry Houlden,Adriana Ruiz,Jorge Ossa,Francisco Lopera,M. Arcos,Lucia Madrigal,John Collinge,C Humphreys,T Ashworth,S Sarner,Nick C. Fox,R Harvey,A Kennedy,P Roques,Cline Rt,Phillips Ca,Venter Jc,Lotta Forsell,Karin Axelman,Lena Lilius,Janet A. Johnston,R Cowburn,Matti Viitanen,Bengt Winblad,Ken Kosik,Matti Haltia,Minna Pöyhönen,Dennis W. Dickson,David G. Mann,D Neary,Julie S. Snowden,Peter L. Lantos,Lars Lannfelt,Martin N. Rossor,George Roberts,Mark Raymond Adams,John Hardy,Alison Goate +63 more
TL;DR: This work has localized the PS-1 gene to a 75 kb region and present the structure of this gene, evidence for alternative splicing and describe six novel mutations in early onset FAD pedigrees all of which alter residues conserved in the STM26 (Presenilin 2: PS-2) gene.
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Chromosome 14–encoded Alzheimer's disease: Genetic and clinicopathological description
Matti Haltia,Matti Viitanen,Raimo Sulkava,Veli Ala‐Hurula,Minna Pöyhönen,Lev G. Goldfarb,Paul Brown,Efrat Levy,Henry Houlde,Henry Houlde,Richard Crook,Alison Goate,Robert Clark,Kevin M. Korenblat,Sunil D. Pandit,Helen Donis Keller,Lena Llius,Li Liu,Karin Axelman,Lotta Forsell,Bengt Winblad,Lars Lannfelt,John Hardy +22 more
TL;DR: A family of Finnish descent with very‐early‐onset Alzheimer's disease has been identified, and genetic analysis of this family eliminated the amyloid precursor protein gene as the pathogenic locus, but strongly implicated a locus on chromosome 14q23.4 between D 14S52 and D14S55.