A Novel Origin for Granulovacuolar Degeneration in Aging and Alzheimer’s Disease: Parallels to Stress Granules

[1]  T. Maeda,et al.  Stress granules , 2012, Cell cycle.

[2]  J. Kuret,et al.  Granulovacuolar degeneration (GVD) bodies of Alzheimer's disease (AD) resemble late‐stage autophagic organelles , 2011, Neuropathology and applied neurobiology.

[3]  D. Neary,et al.  Granular expression of prolyl-peptidyl isomerase PIN1 is a constant and specific feature of Alzheimer’s disease pathology and is independent of tau, Aβ and TDP-43 pathology , 2011, Acta Neuropathologica.

[4]  J. Simpkins,et al.  Estrogen-induced activation of extracellular signal-regulated kinase signaling triggers dendritic resident mRNA translation , 2010, Neuroscience.

[5]  M. A. Desbats,et al.  RNA granules: The good, the bad and the ugly , 2010, Cellular Signalling.

[6]  T. Yamawaki,et al.  Immunopositivity for ESCRT-III subunit CHMP2B in granulovacuolar degeneration of neurons in the Alzheimer's disease hippocampus , 2010, Neuroscience Letters.

[7]  R. Parker,et al.  Eukaryotic stress granules: the ins and outs of translation. , 2009, Molecular cell.

[8]  W. Scheper,et al.  The unfolded protein response is activated in pretangle neurons in Alzheimer's disease hippocampus. , 2009, The American journal of pathology.

[9]  H. Saito,et al.  Formation of stress granules inhibits apoptosis by suppressing stress-responsive MAPK pathways , 2008, Nature Cell Biology.

[10]  J. Shabanowitz,et al.  Codependent functions of RSK2 and the apoptosis-promoting factor TIA-1 in stress granule assembly and cell survival. , 2008, Molecular cell.

[11]  Kathryn Ziegler-Graham,et al.  Worldwide variation in the doubling time of Alzheimer's disease incidence rates , 2008, Alzheimer's & Dementia.

[12]  L. J. Eldik,et al.  Suppression of acute proinflammatory cytokine and chemokine upregulation by post-injury administration of a novel small molecule improves long-term neurologic outcome in a mouse model of traumatic brain injury , 2008, Journal of Neuroinflammation.

[13]  A. Nunomura,et al.  Sublethal RNA Oxidation as a Mechanism for Neurodegenerative Disease , 2008, International journal of molecular sciences.

[14]  P. Anderson,et al.  Stress granules: the Tao of RNA triage. , 2008, Trends in biochemical sciences.

[15]  Kathryn Ziegler-Graham,et al.  Forecasting the global burden of Alzheimer’s disease , 2007, Alzheimer's & Dementia.

[16]  R. Berry,et al.  Relation of hippocampal phospho-SAPK/JNK granules in Alzheimer’s disease and tauopathies to granulovacuolar degeneration bodies , 2006, Acta Neuropathologica.

[17]  W. Markesbery,et al.  Decreased RNA, and Increased RNA Oxidation, in Ribosomes from Early Alzheimer’s Disease , 2006, Neurochemical Research.

[18]  J. Kuret,et al.  Casein kinase-1 isoforms differentially associate with neurofibrillary and granulovacuolar degeneration lesions , 2006, Acta Neuropathologica.

[19]  Xiongwei Zhu,et al.  Ribosomal RNA in Alzheimer Disease Is Oxidized by Bound Redox-active Iron* , 2005, Journal of Biological Chemistry.

[20]  D. Weil,et al.  The translational regulator CPEB1 provides a link between dcp1 bodies and stress granules , 2005, Journal of Cell Science.

[21]  G. Kroemer,et al.  Regulation of cytoplasmic stress granules by apoptosis-inducing factor , 2004, Journal of Cell Science.

[22]  H. Braak,et al.  Up-regulation of phosphorylated/activated p70 S6 kinase and its relationship to neurofibrillary pathology in Alzheimer's disease. , 2003, The American journal of pathology.

[23]  T. Arendt,et al.  Inverse association of Pin1 and tau accumulation in Alzheimer's disease hippocampus , 2002, Acta Neuropathologica.

[24]  R. Mohs,et al.  Consortium to establish a registry for Alzheimer's disease (CERAD) clinical and neuropsychological assessment of Alzheimer's disease. , 2002, Psychopharmacology bulletin.

[25]  A. Nunomura,et al.  Oxidative Damage Is the Earliest Event in Alzheimer Disease , 2001, Journal of neuropathology and experimental neurology.

[26]  K. Jellinger,et al.  Activation of caspase-3 in single neurons and autophagic granules of granulovacuolar degeneration in Alzheimer's disease. Evidence for apoptotic cell death. , 1999, The American journal of pathology.

[27]  N. Holbrook,et al.  Activation of neuronal extracellular receptor kinase (ERK) in Alzheimer disease links oxidative stress to abnormal phosphorylation. , 1999, Neuroreport.

[28]  M. Smith,et al.  Re-entry into the cell cycle: a mechanism for neurodegeneration in Alzheimer disease. , 1999, Medical hypotheses.

[29]  George Perry,et al.  RNA Oxidation Is a Prominent Feature of Vulnerable Neurons in Alzheimer’s Disease , 1999, The Journal of Neuroscience.

[30]  D. Dickson,et al.  Mitotic phosphoepitopes precede paired helical filaments in Alzheimer’s disease , 1998, Neurobiology of Aging.

[31]  C. Proud,et al.  Activation of Microtubule‐Associated Protein Kinase (Erk) and p70 S6 Kinase by D2 Dopamine Receptors , 1998, Journal of neurochemistry.

[32]  J. Trojanowski,et al.  Editorial on Consensus Recommendations for the Postmortem Diagnosis of Alzheimer Disease from the National Institute on Aging and the Reagan Institute Working Group on Diagnostic Criteria for the Neuropathological Assessment of Alzheimer Disease , 1997, Journal of neuropathology and experimental neurology.

[33]  John Q. Trojanowski,et al.  Consensus Recommendations for the Postmortem Diagnosis of Alzheimer’s Disease , 1997, Neurobiology of Aging.

[34]  M. Smith,et al.  Abnormal expression of the cell cycle regulators P16 and CDK4 in Alzheimer's disease. , 1997, The American journal of pathology.

[35]  M. Adolphe,et al.  Transient mitochondrial transcript level decay in oxidative stressed chondrocytes , 1994, Journal of cellular physiology.

[36]  P. Cras,et al.  Basic fibroblast growth factor binding is a marker for extracellular neurofibrillary tangles in Alzheimer disease. , 1991, The journal of histochemistry and cytochemistry : official journal of the Histochemistry Society.

[37]  S. M. Sumi,et al.  The Consortium to Establish a Registry for Alzheimer's Disease (CERAD) , 1991, Neurology.

[38]  C. Marotta,et al.  Alzheimer's disease brain: alterations in RNA levels and in a ribonuclease-inhibitor complex. , 1984, Science.

[39]  D. Neary,et al.  Alterations in protein synthetic capability of nerve cells in Alzheimer's disease. , 1981, Journal of neurology, neurosurgery, and psychiatry.

[40]  D. Mann,et al.  Granulovacuolar degeneration in pyramidal cells of the hippocampus , 1978, Acta Neuropathologica.

[41]  M. Ball Topographic distribution of neurofibrillary tangles and granulovacuolar degeneration in hippocampal cortex of aging and demented patients. A quantitative study , 1978, Acta Neuropathologica.

[42]  R. Castellani,et al.  Alzheimer disease. , 2010, Disease-a-month : DM.

[43]  J. Saver,et al.  A Quantitative Study , 2005 .

[44]  D. Dickson,et al.  Phosphorylated tau immunoreactivity of granulovacuolar bodies (GVB) of Alzheimer's disease: localization of two amino terminal tau epitopes in GVB , 2004, Acta Neuropathologica.

[45]  H. Braak,et al.  Neuropathological stageing of Alzheimer-related changes , 2004, Acta Neuropathologica.

[46]  Xiongwei Zhu,et al.  Abortive apoptosis in Alzheimer's disease , 2001, Acta Neuropathologica.