Perturbed neurogenesis in the adult hippocampus associated with presenilin-1 A246E mutation.

[1]  J. Sweatt,et al.  Presenilin 1 familial Alzheimer's disease mutation leads to defective associative learning and impaired adult neurogenesis , 2004, Neuroscience.

[2]  J. Csernansky,et al.  Modulation of hippocampal cell proliferation, memory, and amyloid plaque deposition in APPsw (Tg2576) mutant mice by isolation stress , 2004, Neuroscience.

[3]  Lin Xie,et al.  Enhanced neurogenesis in Alzheimer's disease transgenic (PDGF-APPSw,Ind) mice. , 2004, Proceedings of the National Academy of Sciences of the United States of America.

[4]  P. Hof,et al.  The presenilin-1 familial Alzheimer disease mutant P117L impairs neurogenesis in the hippocampus of adult mice , 2004, Experimental Neurology.

[5]  R. Klein,et al.  Notch activation induces apoptosis in neural progenitor cells through a p53-dependent pathway. , 2004, Developmental biology.

[6]  J. Aster,et al.  Multiple niches for Notch in cancer: context is everything. , 2004, Current opinion in genetics & development.

[7]  Lin Xie,et al.  Increased hippocampal neurogenesis in Alzheimer's disease , 2003, Proceedings of the National Academy of Sciences of the United States of America.

[8]  D. Selkoe,et al.  Notch and Presenilin: regulated intramembrane proteolysis links development and degeneration. , 2003, Annual review of neuroscience.

[9]  R. Felling,et al.  Enhanced neurogenesis following stroke , 2003, Journal of neuroscience research.

[10]  C. Walsh,et al.  Increased neuronal production, enlarged forebrains and cytoarchitectural distortions in beta-catenin overexpressing transgenic mice. , 2003, Cerebral cortex.

[11]  Hans Clevers,et al.  You Wnt some, you lose some: oncogenes in the Wnt signaling pathway. , 2003, Current opinion in genetics & development.

[12]  Y. Lu,et al.  Expression of Inducible Nitric Oxide Synthase after Focal Cerebral Ischemia Stimulates Neurogenesis in the Adult Rodent Dentate Gyrus , 2003, The Journal of Neuroscience.

[13]  M. Mattson,et al.  Disruption of neurogenesis by amyloid β‐peptide, and perturbed neural progenitor cell homeostasis, in models of Alzheimer's disease , 2002, Journal of neurochemistry.

[14]  Edward H. Koo,et al.  Presenilin Couples the Paired Phosphorylation of β-Catenin Independent of Axin Implications for β-Catenin Activation in Tumorigenesis , 2002, Cell.

[15]  Anjen Chenn,et al.  Regulation of Cerebral Cortical Size by Control of Cell Cycle Exit in Neural Precursors , 2002, Science.

[16]  P. Hof,et al.  Overexpression of Wild Type But Not an FAD Mutant Presenilin-1 Promotes Neurogenesis in the Hippocampus of Adult Mice , 2002, Neurobiology of Disease.

[17]  D. van der Kooy,et al.  Notch pathway molecules are essential for the maintenance, but not the generation, of mammalian neural stem cells. , 2002, Genes & development.

[18]  N. L. Hayes,et al.  Dynamics of cell proliferation in the adult dentate gyrus of two inbred strains of mice. , 2002, Brain research. Developmental brain research.

[19]  F. Gage,et al.  Functional neurogenesis in the adult hippocampus , 2002, Nature.

[20]  J. Shioi,et al.  Presenilin-1 is expressed in neural progenitor cells in the hippocampus of adult mice , 2002, Neuroscience Letters.

[21]  M. Staufenbiel,et al.  Amyloid-Associated Neuron Loss and Gliogenesis in the Neocortex of Amyloid Precursor Protein Transgenic Mice , 2002, The Journal of Neuroscience.

[22]  Hui Zheng,et al.  Loss of presenilin 1 is associated with enhanced β-catenin signaling and skin tumorigenesis , 2001, Proceedings of the National Academy of Sciences of the United States of America.

[23]  G. Fishell,et al.  Spatiotemporal selectivity of response to Notch1 signals in mammalian forebrain precursors. , 2001, Development.

[24]  Hui Zheng,et al.  Presenilin 1 Negatively Regulates β-Catenin/T Cell Factor/Lymphoid Enhancer Factor-1 Signaling Independently of β-Amyloid Precursor Protein and Notch Processing , 2001, The Journal of cell biology.

[25]  G. Rajkowska,et al.  Enhancement of Hippocampal Neurogenesis by Lithium , 2000, Journal of neurochemistry.

[26]  P. Polakis.  Wnt signaling and cancer. , 2000, Genes & development.

[27]  M. Handler,et al.  Presenilin-1 regulates neuronal differentiation during neurogenesis. , 2000, Development.

[28]  J Galceran,et al.  Hippocampus development and generation of dentate gyrus granule cells is regulated by LEF1. , 2000, Development.

[29]  B. Yankner,et al.  Proteolytic release and nuclear translocation of Notch-1 are induced by presenilin-1 and impaired by pathogenic presenilin-1 mutations. , 1999, Proceedings of the National Academy of Sciences of the United States of America.

[30]  M. Frosch,et al.  Presenilin 1 Facilitates the Constitutive Turnover of β-Catenin: Differential Activity of Alzheimer’s Disease–Linked PS1 Mutants in the β-Catenin–Signaling Pathway , 1999, The Journal of Neuroscience.

[31]  Iva Greenwald,et al.  Presenilin is required for activity and nuclear access of Notch in Drosophila , 1999, Nature.

[32]  M. Fortini,et al.  Neurogenic phenotypes and altered Notch processing in Drosophila Presenilin mutants , 1999, Nature.

[33]  Gurparkash Singh,et al.  Mutant Human Presenilin 1 Protects presenilin 1 Null Mouse against Embryonic Lethality and Elevates Aβ1–42/43 Expression , 1998, Neuron.

[34]  D. Borchelt,et al.  An Alzheimer's Disease-Linked PS1 Variant Rescues the Developmental Abnormalities of PS1-Deficient Embryos , 1998, Neuron.

[35]  Hugo Vanderstichele,et al.  Deficiency of presenilin-1 inhibits the normal cleavage of amyloid precursor protein , 1998, Nature.

[36]  B. Sommer,et al.  Neuronal Localization of Presenilin-1 and Association with Amyloid Plaques and Neurofibrillary Tangles in Alzheimer’s Disease , 1997, The Journal of Neuroscience.

[37]  S. Tonegawa,et al.  Skeletal and CNS Defects in Presenilin-1-Deficient Mice , 1997, Cell.

[38]  C. Haass,et al.  Human presenilin-1, but not familial Alzheimer's disease (FAD) mutants, facilitate Caenorhabditis elegans Notch signalling independently of proteolytic processing. , 1997, Genes and function.

[39]  A. Levey,et al.  Light and Electron Microscopic Localization of Presenilin-1 in Primate Brain , 1997, The Journal of Neuroscience.

[40]  I. Greenwald,et al.  Assessment of normal and mutant human presenilin function in Caenorhabditis elegans. , 1996, Proceedings of the National Academy of Sciences of the United States of America.

[41]  J. Hardy,et al.  Increased amyloid-β42(43) in brains of mice expressing mutant presenilin 1 , 1996, Nature.

[42]  G. Schellenberg,et al.  Secreted amyloid β–protein similar to that in the senile plaques of Alzheimer's disease is increased in vivo by the presenilin 1 and 2 and APP mutations linked to familial Alzheimer's disease , 1996, Nature Medicine.

[43]  S. Sorbi.  Molecular genetics of Alzheimer’s disease , 1993, Aging.

[44]  M. Miller,et al.  Bromodeoxyuridine immunohistochemical determination of the lengths of the cell cycle and the DNA-synthetic phase for an anatomically defined population , 1989, Journal of neurocytology.

[45]  J. Silver,et al.  Regulation of Thy-1 gene expression in transgenic mice , 1987, Cell.

[46]  L. Xie,et al.  Alzheimer病トランスジェニック(PDGF‐APPSw,Ind)マウス , 2004 .

[47]  B. de Strooper,et al.  Presenilin couples the paired phosphorylation of beta-catenin independent of axin: implications for beta-catenin activation in tumorigenesis. , 2002, Cell.

[48]  K. Herrup,et al.  Re-expression of cell cycle proteins induces neuronal cell death during Alzheimer's disease. , 2002, Journal of Alzheimer's disease : JAD.

[49]  M. Mattson,et al.  Disruption of neurogenesis in the subventricular zone of adult mice, and in human cortical neuronal precursor cells in culture, by amyloid beta-peptide: implications for the pathogenesis of Alzheimer's disease. , 2002, Neuromolecular medicine.

[50]  I. Vincent,et al.  Constitutive Wee1 activity in adult brain neurons with M phase-type alterations in Alzheimer neurodegeneration. , 2001, Journal of Alzheimer's disease : JAD.

[51]  J. Hardy,et al.  Secreted amyloid beta-protein similar to that in the senile plaques of Alzheimer's disease is increased in vivo by the presenilin 1 and 2 and APP mutations linked to familial Alzheimer's disease. , 1996, Nature medicine.