Decrease of dehydrogenase activity of cerebral glyceraldehyde-3-phosphate dehydrogenase in different animal models of Alzheimer's disease.

[1]  E. Heuland,et al.  Motor impulsivity in APP-SWE mice: a model of Alzheimer's disease , 2006, Behavioural pharmacology.

[2]  A. Sawa,et al.  GAPDH as a sensor of NO stress. , 2006, Biochimica et biophysica acta.

[3]  D. Butterfield,et al.  Identification of nitrated proteins in Alzheimer's disease brain using a redox proteomics approach , 2006, Neurobiology of Disease.

[4]  R. Cumming,et al.  Amyloid‐β induces disulfide bonding and aggregation of GAPDH in Alzheimer's disease , 2005 .

[5]  L. Jen,et al.  Amyloid beta peptide causes chronic glial cell activation and neuro‐degeneration after intravitreal injection , 2005, Neuropathology and applied neurobiology.

[6]  G. Laviola,et al.  Aspects of spatial memory and behavioral disinhibition in Tg2576 transgenic mice as a model of Alzheimer’s disease , 2005, Behavioural Brain Research.

[7]  E. Arutyunova,et al.  Oxidation of glyceraldehyde-3-phosphate dehydrogenase enhances its binding to nucleic acids. , 2003, Biochemical and biophysical research communications.

[8]  J. Mazzola,et al.  Subcellular localization of human glyceraldehyde-3-phosphate dehydrogenase is independent of its glycolytic function. , 2003, Biochimica et biophysica acta.

[9]  Yu-Min Kuo,et al.  APP Transgenic Mice Tg2576 Accumulate Aβ Peptides That Are Distinct from the Chemically Modified and Insoluble Peptides Deposited in Alzheimer's Disease Senile Plaques† , 2002 .

[10]  J. Mazzola,et al.  Reduction of glyceraldehyde‐3‐phosphate dehydrogenase activity in Alzheimer's disease and in Huntington's disease fibroblasts , 2001, Journal of neurochemistry.

[11]  T. Saido,et al.  Reply to: 'Clearance of amyloid β-peptide from brain: transport or metabolism?' , 2000, Nature Medicine.

[12]  K. Titani,et al.  Glutamine synthetase, hemoglobin alpha-chain, and macrophage migration inhibitory factor binding to amyloid beta-protein: their identification in rat brain by a novel affinity chromatography and in Alzheimer's disease brain by immunoprecipitation. , 2000, Biochimica et biophysica acta.

[13]  T. Saido,et al.  Identification of the major Aβ1–42-degrading catabolic pathway in brain parenchyma: Suppression leads to biochemical and pathological deposition , 2000, Nature Medicine.

[14]  V. Muronetz,et al.  Antibodies to the nonnative forms of d-glyceraldehyde-3-phosphate dehydrogenase: identification, purification, and influence on the renaturation of the enzyme. , 1999, Archives of biochemistry and biophysics.

[15]  M A Sirover,et al.  New insights into an old protein: the functional diversity of mammalian glyceraldehyde-3-phosphate dehydrogenase. , 1999, Biochimica et biophysica acta.

[16]  V. Muronetz,et al.  Mildly oxidized GAPDH: the coupling of the dehydrogenase and acyl phosphatase activities , 1999, FEBS letters.

[17]  D. Chuang,et al.  Nuclear Translocation of Glyceraldehyde‐3‐Phosphate Dehydrogenase Isoforms During Neuronal Apoptosis , 1999, Journal of neurochemistry.

[18]  G. Wenk,et al.  Peripheral administration of novel anti-inflammatories can attenuate the effects of chronic inflammation within the CNS , 1999, Brain Research.

[19]  Í. Lopes-Cendes,et al.  Brain glyceraldehyde-3-phosphate dehydrogenase activity in human trinucleotide repeat disorders. , 1998, Archives of neurology.

[20]  J. Blass,et al.  Tissue transglutaminase-catalyzed formation of high-molecular-weight aggregates in vitro is favored with long polyglutamine domains: a possible mechanism contributing to CAG-triplet diseases. , 1998, Archives of biochemistry and biophysics.

[21]  A. Roses,et al.  Transglutaminase-catalyzed inactivation of glyceraldehyde 3-phosphate dehydrogenase and alpha-ketoglutarate dehydrogenase complex by polyglutamine domains of pathological length. , 1997, Proceedings of the National Academy of Sciences of the United States of America.

[22]  J. Trojanowski,et al.  Amyloid β-Protein (Aβ) 1–40 But Not Aβ1–42 Contributes to the Experimental Formation of Alzheimer Disease Amyloid Fibrils in Rat Brain , 1997, The Journal of Neuroscience.

[23]  A. Matsumoto,et al.  The β‐amyloid epitope masking activity in human brain is identified as albumin , 1997 .

[24]  S. Snyder,et al.  Glyceraldehyde-3-phosphate dehydrogenase: nuclear translocation participates in neuronal and nonneuronal cell death. , 1997, Proceedings of the National Academy of Sciences of the United States of America.

[25]  K. Islam,et al.  Carboxyl-terminal fragments of beta-amyloid precursor protein bind to microtubules and the associated protein tau. , 1997, The American journal of pathology.

[26]  C. Finch,et al.  Aging, Metabolism, and Alzheimer Disease: Review and Hypotheses , 1997, Experimental Neurology.

[27]  S. Younkin,et al.  Correlative Memory Deficits, Aβ Elevation, and Amyloid Plaques in Transgenic Mice , 1996, Science.

[28]  T. Billiar,et al.  Excessive NO production dose not account for the inhibition of hepatic gluconeogenesis in endotoxemia. , 1996, The American journal of physiology.

[29]  D. Chuang,et al.  Glyceraldehyde-3-phosphate dehydrogenase antisense oligodeoxynucleotides protect against cytosine arabinonucleoside-induced apoptosis in cultured cerebellar neurons. , 1996, Proceedings of the National Academy of Sciences of the United States of America.

[30]  D. Chuang,et al.  A role for GAPDH in apoptosis and neurodegeneration , 1996, Nature Medicine.

[31]  A. Roses,et al.  Reply to “A role for GAPDH in apoptosis and neurodegeneration” , 1996, Nature Medicine.

[32]  D. Selkoe,et al.  Antibodies to amyloid β protein (Aβ) crossreact with glyceraldehyde-3-phosphate dehydrogenase (GAPDH) , 1996, Neurobiology of Aging.

[33]  A. Roses.  From genes to mechanisms to therapies: Lessons to be learned from neurological disorders , 1996, Nature Medicine.

[34]  D. Chuang,et al.  Evidence that Glyceraldehyde‐3‐Phosphate Dehydrogenase Is Involved in Age‐Induced Apoptosis in Mature Cerebellar Neurons in Culture , 1996, Journal of neurochemistry.

[35]  J. Trojanowski,et al.  Phosphorylation of paired helical filament tau in Alzheimer's disease neurofibrillary lesions: focusing on phosphatases , 1995, FASEB journal : official publication of the Federation of American Societies for Experimental Biology.

[36]  Hiroshi Takahashi,et al.  Glyceraldehyde-3-phosphate dehydrogenase is over-expressed during apoptotic death of neuronal cultures and is recognized by a monoclonal antibody against amyloid plaques from Alzheimer's brain , 1995, Neuroscience Letters.

[37]  Y. L. Dubreuil,et al.  Inflammatory processes induce beta-amyloid precursor protein changes in mouse brain. , 1995, Proceedings of the National Academy of Sciences of the United States of America.

[38]  H. Langen,et al.  Rat Brain Glyceraldehyde‐3‐Phosphate Dehydrogenase Interacts with the Recombinant Cytoplasmic Domain of Alzheimer's β‐Amyloid Precursor Protein , 1993, Journal of neurochemistry.

[39]  G. Cole,et al.  Effects of injected Alzheimer beta-amyloid cores in rat brain. , 1991, Proceedings of the National Academy of Sciences of the United States of America.

[40]  J. Trojanowski,et al.  Antibodies to the β‐amyloid peptide cross‐react with conformational epitopes in human fibrinogen subunits from peripheral blood , 1990, FEBS letters.

[41]  B. Cool,et al.  Immunocytochemical localization of the base excision repair enzyme uracil DNA glycosylase in quiescent and proliferating normal human cells. , 1989, Cancer research.

[42]  H. Vinters,et al.  High molecular weight Alzheimer's disease amyloid peptide immunoreactivity in human serum and CSF is an immunoglobulin G. , 1987, Biochemical and biophysical research communications.

[43]  M. Macart,et al.  An improvement of the Coomassie Blue dye binding method allowing an equal sensitivity to various proteins: application to cerebrospinal fluid. , 1982, Clinica chimica acta; international journal of clinical chemistry.

[44]  M. M. Bradford.  A rapid and sensitive method for the quantitation of microgram quantities of protein utilizing the principle of protein-dye binding. , 1976, Analytical biochemistry.

[45]  U. K. Laemmli,et al.  Cleavage of Structural Proteins during the Assembly of the Head of Bacteriophage T4 , 1970, Nature.

[46]  S. Hoyer,et al.  Effects of low-level lead on glycolytic enzymes and pyruvate dehydrogenase of rat brain in vitro: relevance to sporadic Alzheimer's disease? , 2000, Journal of Neural Transmission.

[47]  T. Arendt,et al.  Activities of key glycolytic enzymes in the brains of patients with Alzheimer's disease , 1999, Journal of Neural Transmission.

[48]  B. Hyman,et al.  Microglial response to amyloid plaques in APPsw transgenic mice. , 1998, The American journal of pathology.

[49]  S. Hoyer.  Models of Alzheimer's disease: cellular and molecular aspects. , 1997, Journal of neural transmission. Supplementum.

[50]  W. Meier-Ruge,et al.  The Significance of Glucose Turnover in the Brain in the Pathogenetic Mechanisms of Alzheimer's Disease , 1996, Reviews in the neurosciences.

[51]  R. Scopes,et al.  Purification of all glycolytic enzymes from one muscle extract. , 1982, Methods in enzymology.

[52]  T. Montine,et al.  The FASEB Journal express article 10.1096/fj.04-3210fje. Published online March 3, 2005. ©2005 FASEB , 2022 .