Probing sporadic and familial Alzheimer’s disease using induced pluripotent stem cells

[1]  S. Angulo,et al.  Retraction Notice to: Directed Conversion of Alzheimer’s Disease Patient Skin Fibroblasts into Functional Neurons , 2014, Cell.

[2]  K. Irvine,et al.  Regulation of Drosophila glial cell proliferation by Merlin-Hippo signaling , 2011, Development.

[3]  Blake Byers,et al.  LRRK2 mutant iPSC-derived DA neurons demonstrate increased susceptibility to oxidative stress. , 2011, Cell stem cell.

[4]  F. Gage,et al.  Cell-Surface Marker Signatures for the Isolation of Neural Stem Cells, Glia and Neurons Derived from Human Pluripotent Stem Cells , 2011, PloS one.

[5]  C. Carson,et al.  The ROCK Inhibitor Y-27632 Improves Recovery of Human Embryonic Stem Cells after Fluorescence-Activated Cell Sorting with Multiple Cell Surface Markers , 2010, PloS one.

[6]  G. Daley,et al.  Differential modeling of fragile X syndrome by human embryonic stem cells and induced pluripotent stem cells. , 2010, Cell stem cell.

[7]  Christopher Lawrence,et al.  DEGENERATION , 2020, Side Effects May Include Strangers.

[8]  Kerry A. Mullaney,et al.  Alzheimer’s-related endosome dysfunction in Down syndrome is Aβ-independent but requires APP and is reversed by BACE-1 inhibition , 2009, Proceedings of the National Academy of Sciences.

[9]  James A. Thomson,et al.  Induced pluripotent stem cells from a spinal muscular atrophy patient , 2009, Nature.

[10]  F. Gage,et al.  YAP regulates neural progenitor cell number via the TEA domain transcription factor. , 2008, Genes & development.

[11]  Paul H Lerou,et al.  Generation of human-induced pluripotent stem cells , 2008, Nature Protocols.

[12]  T. Ichisaka,et al.  Induction of Pluripotent Stem Cells from Adult Human Fibroblasts by Defined Factors , 2007, Cell.

[13]  T. Graf Faculty Opinions recommendation of Induction of pluripotent stem cells from adult human fibroblasts by defined factors. , 2007 .

[14]  J. Trojanowski,et al.  Tau-mediated neurodegeneration in Alzheimer's disease and related disorders , 2007, Nature Reviews Neuroscience.

[15]  L. Mucke,et al.  Reducing Endogenous Tau Ameliorates Amyloid ß-Induced Deficits in an Alzheimer's Disease Mouse Model , 2007, Science.

[16]  D. Campion,et al.  APP locus duplication in a Finnish family with dementia and intracerebral haemorrhage , 2007, Journal of Neurology, Neurosurgery, and Psychiatry.

[17]  H. Soininen,et al.  CSF phosphorylated tau protein correlates with neocortical neurofibrillary pathology in Alzheimer's disease. , 2006, Brain : a journal of neurology.

[18]  Ahmad Salehi,et al.  Increased App Expression in a Mouse Model of Down's Syndrome Disrupts NGF Transport and Causes Cholinergic Neuron Degeneration , 2006, Neuron.

[19]  L. Fratiglioni,et al.  Role of genes and environments for explaining Alzheimer disease. , 2006, Archives of general psychiatry.

[20]  R. Nixon Endosome function and dysfunction in Alzheimer's disease and other neurodegenerative diseases , 2005, Neurobiology of Aging.

[21]  R. Tanzi,et al.  Twenty Years of the Alzheimer’s Disease Amyloid Hypothesis: A Genetic Perspective , 2005, Cell.

[22]  Lippincott Williams Wilkins,et al.  CSF tau protein phosphorylated at threonine 231 correlates with cognitive decline in MCI subjects , 2004, Neurology.

[23]  Jiang-Ning Zhou,et al.  Regional alteration of synapsin I in the hippocampal formation of Alzheimer’s disease patients , 2004, Acta Neuropathologica.

[24]  J. Cho,et al.  Primed phosphorylation of tau at Thr231 by glycogen synthase kinase 3β (GSK3β) plays a critical role in regulating tau's ability to bind and stabilize microtubules , 2003, Journal of neurochemistry.

[25]  H. Hanafusa,et al.  Refractory nature of normal human diploid fibroblasts with respect to oncogene-mediated transformation , 2003, Proceedings of the National Academy of Sciences of the United States of America.

[26]  J. Cho,et al.  Glycogen synthase kinase 3beta phosphorylates tau at both primed and unprimed sites. Differential impact on microtubule binding. , 2003, The Journal of biological chemistry.

[27]  H. Arai,et al.  CSF tau protein phosphorylated at threonine 231 correlates with cognitive decline in MCI subjects , 2002, Neurology.

[28]  C. van Broeckhoven,et al.  Endocytic disturbances distinguish among subtypes of alzheimer's disease and related disorders , 2001, Annals of neurology.

[29]  Laurence H. Pearl,et al.  Crystal Structure of Glycogen Synthase Kinase 3β Structural Basis for Phosphate-Primed Substrate Specificity and Autoinhibition , 2001, Cell.

[30]  K. Mizuseki,et al.  Induction of Midbrain Dopaminergic Neurons from ES Cells by Stromal Cell–Derived Inducing Activity , 2000, Neuron.

[31]  B T Hyman,et al.  Endocytic pathway abnormalities precede amyloid beta deposition in sporadic Alzheimer's disease and Down syndrome: differential effects of APOE genotype and presenilin mutations. , 2000, The American journal of pathology.

[32]  D. Alkon,et al.  Peripheral markers in testing pathophysiological hypotheses and diagnosing Alzheimer's disease , 1998, FASEB journal : official publication of the Federation of American Societies for Experimental Biology.

[33]  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.

[34]  B. Yankner,et al.  β-Amyloid fibrils induce tau phosphorylation and loss of microtubule binding , 1995, Neuron.

[35]  L. Mucke,et al.  Alzheimer-type neuropathology in transgenic mice overexpressing V717F β-amyloid precursor protein , 1995, Nature.

[36]  B. Winblad,et al.  Excessive production of amyloid beta-protein by peripheral cells of symptomatic and presymptomatic patients carrying the Swedish familial Alzheimer disease mutation. , 1994, Proceedings of the National Academy of Sciences of the United States of America.

[37]  Bradley T. Hyman,et al.  Neurofibrillary tangles but not senile plaques parallel duration and severity of Alzheimer's disease , 1992, Neurology.

[38]  David A. Drachman,et al.  Synaptic loss in Alzheimer's disease and other dementias , 1989, Neurology.

[39]  A. Baer The genetic perspective , 1977 .

[40]  Glycogen Synthase Kinase 3 (cid:1) Phosphorylates Tau at Both Primed and Unprimed Sites , 2022 .