N-truncated Abeta starting with position four: early intraneuronal accumulation and rescue of toxicity using NT4X-167, a novel monoclonal antibody

[1]  A. Paetau,et al.  N-truncated Abeta starting with position four: early intraneuronal accumulation and rescue of toxicity using NT4X-167, a novel monoclonal antibody , 2013, Acta Neuropathologica Communications.

[2]  T. Bayer,et al.  N-truncated amyloid β (Aβ) 4-42 forms stable aggregates and induces acute and long-lasting behavioral deficits , 2013, Acta Neuropathologica.

[3]  K. Reymann,et al.  Structural basis of β-amyloid-dependent synaptic dysfunctions. , 2012, Angewandte Chemie.

[4]  Oliver Wirths,et al.  Motor deficits, neuron loss, and reduced anxiety coinciding with axonal degeneration and intraneuronal Aβ aggregation in the 5XFAD mouse model of Alzheimer's disease , 2012, Neurobiology of Aging.

[5]  B. Strooper,et al.  The toxic Aβ oligomer and Alzheimer's disease: an emperor in need of clothes , 2012, Nature Neuroscience.

[6]  K. Blennow,et al.  Pyroglutamate Amyloid β (Aβ) Aggravates Behavioral Deficits in Transgenic Amyloid Mouse Model for Alzheimer Disease , 2012, The Journal of Biological Chemistry.

[7]  H. Scheidt,et al.  Dynamics of Amyloid β Fibrils Revealed by Solid-state NMR* , 2011, The Journal of Biological Chemistry.

[8]  T. Bayer,et al.  Pyroglutamate Amyloid-β (Aβ): A Hatchet Man in Alzheimer Disease* , 2011, The Journal of Biological Chemistry.

[9]  K. Reymann,et al.  Selective Hippocampal Neurodegeneration in Transgenic Mice Expressing Small Amounts of Truncated Aβ Is Induced by Pyroglutamate–Aβ Formation , 2011, The Journal of Neuroscience.

[10]  C. Broeckhoven,et al.  Potent amyloidogenicity and pathogenicity of Aβ43 , 2011, Nature Neuroscience.

[11]  H. Scheidt,et al.  Solid-state NMR spectroscopic investigation of Aβ protofibrils: implication of a β-sheet remodeling upon maturation into terminal amyloid fibrils. , 2011, Angewandte Chemie.

[12]  S. Weggen,et al.  Presenilin‐1 but not amyloid precursor protein mutations present in mouse models of Alzheimer’s disease attenuate the response of cultured cells to γ‐secretase modulators regardless of their potency and structure , 2011, Journal of neurochemistry.

[13]  D. Selkoe.  Alzheimer's disease. , 2011, Cold Spring Harbor perspectives in biology.

[14]  T. Bayer,et al.  Identification of low molecular weight pyroglutamate A{beta} oligomers in Alzheimer disease: a novel tool for therapy and diagnosis. , 2010, The Journal of biological chemistry.

[15]  T. Bayer,et al.  Overexpression of Glutaminyl Cyclase, the Enzyme Responsible for Pyroglutamate Aβ Formation, Induces Behavioral Deficits, and Glutaminyl Cyclase Knock-out Rescues the Behavioral Phenotype in 5XFAD Mice* , 2010, The Journal of Biological Chemistry.

[16]  T. Bayer,et al.  Intracellular Aβ triggers neuron loss in the cholinergic system of the APP/PS1KI mouse model of Alzheimer's disease , 2010, Neurobiology of Aging.

[17]  K. Blennow,et al.  Mass spectrometric characterization of brain amyloid beta isoform signatures in familial and sporadic Alzheimer’s disease , 2010, Acta Neuropathologica.

[18]  Judianne Davis,et al.  Structural conversion of neurotoxic amyloid-β(1–42) oligomers to fibrils , 2010, Nature Structural &Molecular Biology.

[19]  Rie Teraoka,et al.  A Mouse Model of Amyloid β Oligomers: Their Contribution to Synaptic Alteration, Abnormal Tau Phosphorylation, Glial Activation, and Neuronal Loss In Vivo , 2010, The Journal of Neuroscience.

[20]  T. Bayer,et al.  Intracellular Accumulation of Amyloid-Beta – A Predictor for Synaptic Dysfunction and Neuron Loss in Alzheimer's Disease , 2010, Front. Ag. Neurosci..

[21]  Jin-Moo Lee,et al.  Amyloid seeds formed by cellular uptake, concentration, and aggregation of the amyloid-beta peptide , 2009, Proceedings of the National Academy of Sciences.

[22]  T. Bayer,et al.  Pyroglutamate Abeta pathology in APP/PS1KI mice, sporadic and familial Alzheimer’s disease cases , 2009, Journal of Neural Transmission.

[23]  D. Holtzman,et al.  The Role of Apolipoprotein E in Alzheimer's Disease , 2009, Neuron.

[24]  B. Winblad,et al.  Aβ43 is more frequent than Aβ40 in amyloid plaque cores from Alzheimer disease brains , 2009, Journal of neurochemistry.

[25]  T. Bayer,et al.  Intraneuronal pyroglutamate-Abeta 3–42 triggers neurodegeneration and lethal neurological deficits in a transgenic mouse model , 2009, Acta Neuropathologica.

[26]  Marie-Claude Potier,et al.  Classification and basic pathology of Alzheimer disease , 2009, Acta Neuropathologica.

[27]  B. Roques,et al.  Aminopeptidase A contributes to the N‐terminal truncation of amyloid β‐peptide , 2009, Journal of neurochemistry.

[28]  T. Bayer,et al.  Transient intraneuronal Aβ rather than extracellular plaque pathology correlates with neuron loss in the frontal cortex of APP/PS1KI mice , 2008, Acta Neuropathologica.

[29]  Hans-Ulrich Demuth,et al.  Glutaminyl cyclase inhibition attenuates pyroglutamate Aβ and Alzheimer's disease–like pathology , 2008, Nature Medicine.

[30]  B. Kriem,et al.  N-truncated amyloid-β oligomers induce learning impairment and neuronal apoptosis , 2008, Neurobiology of Aging.

[31]  W. K. Cullen,et al.  Amyloid β Protein Dimer-Containing Human CSF Disrupts Synaptic Plasticity: Prevention by Systemic Passive Immunization , 2008, The Journal of Neuroscience.

[32]  G. Schellenberg,et al.  Clinical and neuropathological features of the arctic APP gene mutation causing early-onset Alzheimer disease. , 2008, Archives of neurology.

[33]  R. D'Hooge,et al.  Lipids revert inert Aβ amyloid fibrils to neurotoxic protofibrils that affect learning in mice , 2007, The EMBO Journal.

[34]  Y. Ishii,et al.  Evidence of fibril-like β-sheet structures in a neurotoxic amyloid intermediate of Alzheimer's β-amyloid , 2007, Nature Structural &Molecular Biology.

[35]  D. Selkoe,et al.  Aβ Oligomers – a decade of discovery , 2007, Journal of neurochemistry.

[36]  D. Selkoe,et al.  Soluble protein oligomers in neurodegeneration: lessons from the Alzheimer's amyloid β-peptide , 2007, Nature Reviews Molecular Cell Biology.

[37]  R. Hepler,et al.  Solution State Characterization of Amyloid β-Derived Diffusible Ligands , 2006 .

[38]  M. Ohno,et al.  Intraneuronal β-Amyloid Aggregates, Neurodegeneration, and Neuron Loss in Transgenic Mice with Five Familial Alzheimer's Disease Mutations: Potential Factors in Amyloid Plaque Formation , 2006, The Journal of Neuroscience.

[39]  T. Hoffmann,et al.  Inhibition of glutaminyl cyclase alters pyroglutamate formation in mammalian cells. , 2006, Biochimica et biophysica acta.

[40]  C. Ballard,et al.  Quantification of Alzheimer pathology in ageing and dementia: age‐related accumulation of amyloid‐β(42) peptide in vascular dementia , 2006, Neuropathology and applied neurobiology.

[41]  M. Gallagher,et al.  A specific amyloid-β protein assembly in the brain impairs memory , 2006, Nature.

[42]  Michela Gallagher,et al.  A specific amyloid-beta protein assembly in the brain impairs memory. , 2006, Nature.

[43]  R. Hepler,et al.  Solution state characterization of amyloid beta-derived diffusible ligands. , 2006, Biochemistry.

[44]  G. Bitan,et al.  Neurotoxic protein oligomers — what you see is not always what you get , 2005, Amyloid : the international journal of experimental and clinical investigation : the official journal of the International Society of Amyloidosis.

[45]  T. Bayer,et al.  A modified β‐amyloid hypothesis: intraneuronal accumulation of the β‐amyloid peptide – the first step of a fatal cascade , 2004, Journal of neurochemistry.

[46]  T. Bayer,et al.  Massive CA1/2 neuronal loss with intraneuronal and N-terminal truncated Abeta42 accumulation in a novel Alzheimer transgenic model. , 2004, The American journal of pathology.

[47]  T. Hoffmann,et al.  Glutaminyl cyclases unfold glutamyl cyclase activity under mild acid conditions , 2004, FEBS letters.

[48]  C. Almeida,et al.  Oligomerization of Alzheimer's β-Amyloid within Processes and Synapses of Cultured Neurons and Brain , 2004, The Journal of Neuroscience.

[49]  H. Steinbusch,et al.  Hippocampal neuron loss exceeds amyloid plaque load in a transgenic mouse model of Alzheimer's disease. , 2004, The American journal of pathology.

[50]  A. Delacourte,et al.  Truncated beta‐amyloid peptide species in pre‐clinical Alzheimer's disease as new targets for the vaccination approach , 2003, Journal of neurochemistry.

[51]  R. Leapman,et al.  A structural model for Alzheimer's β-amyloid fibrils based on experimental constraints from solid state NMR , 2002, Proceedings of the National Academy of Sciences of the United States of America.

[52]  W. K. Cullen,et al.  Naturally secreted oligomers of amyloid β protein potently inhibit hippocampal long-term potentiation in vivo , 2002, Nature.

[53]  Brett Chromy,et al.  Soluble oligomers of β amyloid (1-42) inhibit long-term potentiation but not long-term depression in rat dentate gyrus , 2002, Brain Research.

[54]  D. Selkoe,et al.  Intraneuronal Aβ42 accumulation in Down syndrome brain , 2002 .

[55]  D. Selkoe,et al.  Intraneuronal Abeta42 accumulation in Down syndrome brain. , 2002, Amyloid : the international journal of experimental and clinical investigation : the official journal of the International Society of Amyloidosis.

[56]  W Blaine Stine,et al.  Soluble oligomers of beta amyloid (1-42) inhibit long-term potentiation but not long-term depression in rat dentate gyrus. , 2002, Brain research.

[57]  S. Younkin,et al.  The 'Arctic' APP mutation (E693G) causes Alzheimer's disease by enhanced Aβ protofibril formation , 2001, Nature Neuroscience.

[58]  M. Staufenbiel,et al.  Comparative Analysis of Amyloid-β Chemical Structure and Amyloid Plaque Morphology of Transgenic Mouse and Alzheimer's Disease Brains* , 2001, The Journal of Biological Chemistry.

[59]  D. Selkoe,et al.  The oligomerization of amyloid beta-protein begins intracellularly in cells derived from human brain. , 2000, Biochemistry.

[60]  T. Pillot,et al.  The nonfibrillar amyloid beta-peptide induces apoptotic neuronal cell death: involvement of its C-terminal fusogenic domain. , 2002, Journal of neurochemistry.

[61]  C. Masters,et al.  Soluble pool of Aβ amyloid as a determinant of severity of neurodegeneration in Alzheimer's disease , 1999, Annals of neurology.

[62]  J. Vandekerckhove,et al.  The Nonfibrillar Amyloid β‐Peptide Induces Apoptotic Neuronal Cell Death , 1999 .

[63]  L. Lue,et al.  Soluble Amyloid β Peptide Concentration as a Predictor of Synaptic Change in Alzheimer’s Disease , 1999 .

[64]  C. Barrow,et al.  The Aβ 3-Pyroglutamyl and 11-Pyroglutamyl Peptides Found in Senile Plaque Have Greater β-Sheet Forming and Aggregation Propensities in Vitro than Full-Length Aβ† , 1999 .

[65]  Veerle Baekelandt,et al.  Early Phenotypic Changes in Transgenic Mice That Overexpress Different Mutants of Amyloid Precursor Protein in Brain* , 1999, The Journal of Biological Chemistry.

[66]  J. Morris,et al.  Tangles and plaques in nondemented aging and “preclinical” Alzheimer's disease , 1999, Annals of neurology.

[67]  C. Barrow,et al.  The A beta 3-pyroglutamyl and 11-pyroglutamyl peptides found in senile plaque have greater beta-sheet forming and aggregation propensities in vitro than full-length A beta. , 1999, Biochemistry.

[68]  L. Lue,et al.  Soluble amyloid beta peptide concentration as a predictor of synaptic change in Alzheimer's disease. , 1999, The American journal of pathology.

[69]  E. Mandelkow,et al.  Tau in Alzheimer's disease. , 1998, Trends in cell biology.

[70]  A. Paetau,et al.  A variant of Alzheimer's disease with spastic paraparesis and unusual plaques due to deletion of exon 9 of presenilin 1 , 1998, Nature Medicine.

[71]  L S Honig,et al.  Aging and Alzheimer's disease: lessons from the Nun Study. , 1998, The Gerontologist.

[72]  T. Iwatsubo,et al.  Amino- and carboxyl-terminal heterogeneity of β-amyloid peptides deposited in human brain , 1996, Neuroscience Letters.

[73]  M. Ball,et al.  Water-soluble A(N-40, N-42) Oligomers in Normal and Alzheimer Disease Brains (*) , 1996, The Journal of Biological Chemistry.

[74]  Carl W. Cotman,et al.  Amino-terminal Deletions Enhance Aggregation of β-Amyloid Peptides in Vitro(*) , 1995, The Journal of Biological Chemistry.

[75]  D. Mann,et al.  Dominant and differential deposition of distinct β-amyloid peptide species, Aβ N3(pE), in senile plaques , 1995, Neuron.

[76]  C. Cotman,et al.  Amino-terminal deletions enhance aggregation of beta-amyloid peptides in vitro. , 1995, The Journal of biological chemistry.

[77]  D. Mann,et al.  Dominant and differential deposition of distinct beta-amyloid peptide species, A beta N3(pE), in senile plaques. , 1995, Neuron.

[78]  P. Greengard,et al.  Relative abundance of Alzheimer A beta amyloid peptide variants in Alzheimer disease and normal aging. , 1994, Proceedings of the National Academy of Sciences of the United States of America.

[79]  T. Iwatsubo,et al.  Visualization of Aβ42(43) and Aβ40 in senile plaques with end-specific Aβ monoclonals: Evidence that an initially deposited species is Aβ42(43) , 1994, Neuron.

[80]  J Carter,et al.  Molecular Pathology of Alzheimer's Disease , 2013 .

[81]  M. Tabaton,et al.  Soluble amyloid beta-protein is a marker of Alzheimer amyloid in brain but not in cerebrospinal fluid. , 1994, Biochemical and biophysical research communications.

[82]  T. Iwatsubo,et al.  Visualization of A beta 42(43) and A beta 40 in senile plaques with end-specific A beta monoclonals: evidence that an initially deposited species is A beta 42(43). , 1994, Neuron.

[83]  M J Ball,et al.  beta-Amyloid-(1-42) is a major component of cerebrovascular amyloid deposits: implications for the pathology of Alzheimer disease. , 1993, Proceedings of the National Academy of Sciences of the United States of America.

[84]  Khadija Iqbal,et al.  Peptide compositions of the cerebrovascular and senile plaque core amyloid deposits of Alzheimer's disease. , 1993, Archives of biochemistry and biophysics.

[85]  D. Selkoe,et al.  Mass spectrometry of purified amyloid beta protein in Alzheimer's disease. , 1992, The Journal of biological chemistry.

[86]  B. Winblad,et al.  A pathogenic mutation for probable Alzheimer's disease in the APP gene at the N–terminus of β–amyloid , 1992, Nature Genetics.

[87]  J. Hardy,et al.  Alzheimer's disease: the amyloid cascade hypothesis. , 1992, Science.

[88]  C. Barrow,et al.  Solution structures of beta peptide and its constituent fragments: relation to amyloid deposition. , 1991, Science.

[89]  J. Hardy,et al.  Amyloid deposition as the central event in the aetiology of Alzheimer's disease. , 1991, Trends in pharmacological sciences.

[90]  G. Glenner,et al.  Differences Between Vascular and Plaque Core Amyloid in Alzheimer's Disease , 1988, Journal of neurochemistry.

[91]  K. Grzeschik,et al.  The precursor of Alzheimer??s disease amyloid A4 protein resembles a cell-surface receptor , 1987 .

[92]  R. Martins,et al.  Neuronal origin of a cerebral amyloid: neurofibrillary tangles of Alzheimer's disease contain the same protein as the amyloid of plaque cores and blood vessels. , 1985, The EMBO journal.

[93]  C. Masters,et al.  Amyloid plaque core protein in Alzheimer disease and Down syndrome. , 1985, Proceedings of the National Academy of Sciences of the United States of America.

[94]  G. Glenner,et al.  Alzheimer's disease: initial report of the purification and characterization of a novel cerebrovascular amyloid protein. , 1984, Biochemical and biophysical research communications.