Biblio
Found 47 results
Author [ Keyword] Title Type Year Filters: Author is Norton, Joanne and First Letter Of Title is A [Clear All Filters]
“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.”, Neuromolecular Med, vol. 5, no. 2, pp. 133-46, 2004.
, “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.”, Neuromolecular Med, vol. 5, no. 2, pp. 133-46, 2004.
, “Analysis of neurodegenerative Mendelian genes in clinically diagnosed Alzheimer Disease.”, PLoS Genet, vol. 13, no. 11, p. e1007045, 2017.
, “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.”, Neuromolecular Med, vol. 5, no. 2, pp. 133-46, 2004.
, “Analysis of neurodegenerative Mendelian genes in clinically diagnosed Alzheimer Disease.”, PLoS Genet, vol. 13, no. 11, p. e1007045, 2017.
, “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.”, Neuromolecular Med, vol. 5, no. 2, pp. 133-46, 2004.
, “Analysis of neurodegenerative Mendelian genes in clinically diagnosed Alzheimer Disease.”, PLoS Genet, vol. 13, no. 11, p. e1007045, 2017.
, “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.”, Neuromolecular Med, vol. 5, no. 2, pp. 133-46, 2004.
, “Analysis of neurodegenerative Mendelian genes in clinically diagnosed Alzheimer Disease.”, PLoS Genet, vol. 13, no. 11, p. e1007045, 2017.
, “Analysis of neurodegenerative Mendelian genes in clinically diagnosed Alzheimer Disease.”, PLoS Genet, vol. 13, no. 11, p. e1007045, 2017.
, “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.”, Neuromolecular Med, vol. 5, no. 2, pp. 133-46, 2004.
, “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.”, Neuromolecular Med, vol. 5, no. 2, pp. 133-46, 2004.
, “Analysis of neurodegenerative Mendelian genes in clinically diagnosed Alzheimer Disease.”, PLoS Genet, vol. 13, no. 11, p. e1007045, 2017.
, “Analysis of neurodegenerative Mendelian genes in clinically diagnosed Alzheimer Disease.”, PLoS Genet, vol. 13, no. 11, p. e1007045, 2017.
, “Analysis of neurodegenerative Mendelian genes in clinically diagnosed Alzheimer Disease.”, PLoS Genet, vol. 13, no. 11, p. e1007045, 2017.
, “Analysis of neurodegenerative Mendelian genes in clinically diagnosed Alzheimer Disease.”, PLoS Genet, vol. 13, no. 11, p. e1007045, 2017.
, “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.”, Neuromolecular Med, vol. 5, no. 2, pp. 133-46, 2004.
, “Analysis of neurodegenerative Mendelian genes in clinically diagnosed Alzheimer Disease.”, PLoS Genet, vol. 13, no. 11, p. e1007045, 2017.
, “Analysis of neurodegenerative Mendelian genes in clinically diagnosed Alzheimer Disease.”, PLoS Genet, vol. 13, no. 11, p. e1007045, 2017.
, “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.”, Neuromolecular Med, vol. 5, no. 2, pp. 133-46, 2004.
, “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.”, Neuromolecular Med, vol. 5, no. 2, pp. 133-46, 2004.
, “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.”, Neuromolecular Med, vol. 5, no. 2, pp. 133-46, 2004.
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