Neuropathology and biochemistry of Aβ and its aggregates in Alzheimer’s disease
暂无分享,去创建一个
M. Fändrich | D. Thal | J. Walter | T. Saido
[1] H. Soininen,et al. Alzheimer’s disease-related plaques in nondemented subjects , 2014, Alzheimer's & Dementia.
[2] S. Prusiner,et al. Serial propagation of distinct strains of Aβ prions from Alzheimer’s disease patients , 2014, Proceedings of the National Academy of Sciences.
[3] S. Prusiner,et al. Distinct synthetic Aβ prion strains producing different amyloid deposits in bigenic mice , 2014, Proceedings of the National Academy of Sciences.
[4] E. Mandelkow,et al. Stages and Conformations of the Tau Repeat Domain during Aggregation and Its Effect on Neuronal Toxicity* , 2014, The Journal of Biological Chemistry.
[5] Oliver Wirths,et al. Focusing the amyloid cascade hypothesis on N-truncated Abeta peptides as drug targets against Alzheimer’s disease , 2014, Acta Neuropathologica.
[6] Martin Hallbeck,et al. Spreading of amyloid-β peptides via neuritic cell-to-cell transfer is dependent on insufficient cellular clearance , 2014, Neurobiology of Disease.
[7] S. Becker,et al. Turn plasticity distinguishes different modes of amyloid-β aggregation. , 2014, Journal of the American Chemical Society.
[8] C. V. von Arnim,et al. Biochemical stages of amyloid-β peptide aggregation and accumulation in the human brain and their association with symptomatic and pathologically preclinical Alzheimer's disease. , 2014, Brain : a journal of neurology.
[9] M. Staufenbiel,et al. The type of Aβ-related neuronal degeneration differs between amyloid precursor protein (APP23) and amyloid β-peptide (APP48) transgenic mice , 2013, Acta neuropathologica communications.
[10] K. Nilsson,et al. Seeded strain‐like transmission of β‐amyloid morphotypes in APP transgenic mice , 2013, EMBO reports.
[11] J. Walter,et al. Cross-talk of membrane lipids and Alzheimer-related proteins , 2013, Molecular Neurodegeneration.
[12] R O Weller,et al. Review: Cerebral amyloid angiopathy, prion angiopathy, CADASIL and the spectrum of protein elimination failure angiopathies (PEFA) in neurodegenerative disease with a focus on therapy , 2013, Neuropathology and applied neurobiology.
[13] A. Fagan,et al. Preclinical Alzheimer's disease and its outcome: a longitudinal cohort study , 2013, The Lancet Neurology.
[14] J. Attems,et al. Pathology of clinical and preclinical Alzheimer’s disease , 2013, European Archives of Psychiatry and Clinical Neuroscience.
[15] F. Heppner,et al. Microglia actions in Alzheimer’s disease , 2013, Acta Neuropathologica.
[16] Charles D. Schwieters,et al. Molecular Structure of β-Amyloid Fibrils in Alzheimer’s Disease Brain Tissue , 2013, Cell.
[17] F. Heppner,et al. Microglia as Dynamic and Essential Components of the Amyloid Hypothesis , 2013, Neuron.
[18] David A Bennett,et al. Brain amyloid-β oligomers in ageing and Alzheimer's disease. , 2013, Brain : a journal of neurology.
[19] T. Bayer,et al. Early intraneuronal accumulation and increased aggregation of phosphorylated Abeta in a mouse model of Alzheimer’s disease , 2013, Acta Neuropathologica.
[20] Francis Eustache,et al. Amyloid imaging in cognitively normal individuals, at-risk populations and preclinical Alzheimer's disease , 2013, NeuroImage: Clinical.
[21] M. Staufenbiel,et al. Dispersible amyloid β-protein oligomers, protofibrils, and fibrils represent diffusible but not soluble aggregates: their role in neurodegeneration in amyloid precursor protein (APP) transgenic mice , 2012, Neurobiology of Aging.
[22] R. Tanzi. The genetics of Alzheimer disease. , 2012, Cold Spring Harbor perspectives in medicine.
[23] M. Fändrich,et al. Oligomeric intermediates in amyloid formation: structure determination and mechanisms of toxicity. , 2012, Journal of molecular biology.
[24] Ole A. Andreassen,et al. A mutation in APP protects against Alzheimer’s disease and age-related cognitive decline , 2012, Nature.
[25] C. Haass,et al. Trafficking and proteolytic processing of APP. , 2012, Cold Spring Harbor perspectives in medicine.
[26] David Eisenberg,et al. Atomic View of a Toxic Amyloid Small Oligomer , 2012, Science.
[27] K. Reymann,et al. Structural basis of β-amyloid-dependent synaptic dysfunctions. , 2012, Angewandte Chemie.
[28] M. Fändrich,et al. High-molecular weight Aβ oligomers and protofibrils are the predominant Aβ species in the native soluble protein fraction of the AD brain , 2012, Journal of cellular and molecular medicine.
[29] M. Siepmann,et al. Phosphorylation of Amyloid-β Peptide at Serine 8 Attenuates Its Clearance via Insulin-degrading and Angiotensin-converting Enzymes* , 2012, The Journal of Biological Chemistry.
[30] J. Schneider,et al. National Institute on Aging–Alzheimer's Association guidelines for the neuropathologic assessment of Alzheimer's disease , 2012, Alzheimer's & Dementia.
[31] M. Fändrich,et al. Assembly of Alzheimer's Aβ peptide into nanostructured amyloid fibrils , 2011 .
[32] E. Capetillo-Zarate,et al. High-resolution 3D reconstruction reveals intra-synaptic amyloid fibrils. , 2011, The American journal of pathology.
[33] Dietmar R. Thal,et al. Stages of the Pathologic Process in Alzheimer Disease: Age Categories From 1 to 100 Years , 2011, Journal of neuropathology and experimental neurology.
[34] F. Jessen,et al. Nitration of Tyrosine 10 Critically Enhances Amyloid β Aggregation and Plaque Formation , 2011, Neuron.
[35] 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.
[36] M. Hoch,et al. Extracellular phosphorylation of the amyloid β‐peptide promotes formation of toxic aggregates during the pathogenesis of Alzheimer's disease , 2011, The EMBO journal.
[37] Nikolaus Grigorieff,et al. Recent progress in understanding Alzheimer's β-amyloid structures. , 2011, Trends in biochemical sciences.
[38] J. Morris,et al. The diagnosis of dementia due to Alzheimer’s disease: Recommendations from the National Institute on Aging-Alzheimer’s Association workgroups on diagnostic guidelines for Alzheimer's disease , 2011, Alzheimer's & Dementia.
[39] Denise C. Park,et al. Toward defining the preclinical stages of Alzheimer’s disease: Recommendations from the National Institute on Aging-Alzheimer's Association workgroups on diagnostic guidelines for Alzheimer's disease , 2011, Alzheimer's & Dementia.
[40] E. Giralt,et al. Aβ40 and Aβ42 amyloid fibrils exhibit distinct molecular recycling properties. , 2011, Journal of the American Chemical Society.
[41] 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.
[42] Shinichiro Nakamura,et al. Two Distinct Amyloid β-Protein (Aβ) Assembly Pathways Leading to Oligomers and Fibrils Identified by Combined Fluorescence Correlation Spectroscopy, Morphology, and Toxicity Analyses* , 2011, The Journal of Biological Chemistry.
[43] C. Haass,et al. Amyloid-β protein modulates the perivascular clearance of neuronal apolipoprotein E in mouse models of Alzheimer’s disease , 2011, Journal of Neural Transmission.
[44] H. Kretzschmar,et al. Multiple Events Lead to Dendritic Spine Loss in Triple Transgenic Alzheimer's Disease Mice , 2010, PloS one.
[45] Frank Baumann,et al. Peripherally Applied Aβ-Containing Inoculates Induce Cerebral β-Amyloidosis , 2010, Science.
[46] A. Caflisch,et al. Micelle-like architecture of the monomer ensemble of Alzheimer's amyloid-β peptide in aqueous solution and its implications for Aβ aggregation. , 2010, Journal of molecular biology.
[47] A. Bush,et al. Biological metals and Alzheimer's disease: Implications for therapeutics and diagnostics , 2010, Progress in Neurobiology.
[48] E. Salmon,et al. 18F‐flutemetamol amyloid imaging in Alzheimer disease and mild cognitive impairment: A phase 2 trial , 2010, Annals of neurology.
[49] Michael T. Lin,et al. Co-occurrence of Alzheimer's disease β-amyloid and tau pathologies at synapses , 2010, Neurobiology of Aging.
[50] D. Selkoe,et al. The presence of sodium dodecyl sulphate-stable Abeta dimers is strongly associated with Alzheimer-type dementia. , 2010, Brain : a journal of neurology.
[51] Judianne Davis,et al. Structural conversion of neurotoxic amyloid-β(1–42) oligomers to fibrils , 2010, Nature Structural &Molecular Biology.
[52] E. Capetillo-Zarate,et al. Intraneuronal β-amyloid accumulation and synapse pathology in Alzheimer’s disease , 2010, Acta Neuropathologica.
[53] K. Reymann,et al. Mechanism of amyloid plaque formation suggests an intracellular basis of Aβ pathogenicity , 2010, Proceedings of the National Academy of Sciences.
[54] N. Grigorieff,et al. Nanoscale Flexibility Parameters of Alzheimer Amyloid Fibrils Determined by Electron Cryo-Microscopy** , 2010, Angewandte Chemie.
[55] Tuomas P. J. Knowles,et al. An Analytical Solution to the Kinetics of Breakable Filament Assembly , 2009, Science.
[56] N. Grigorieff,et al. Comparison of Alzheimer Aβ(1–40) and Aβ(1–42) amyloid fibrils reveals similar protofilament structures , 2009, Proceedings of the National Academy of Sciences.
[57] F. Heppner,et al. Formation and maintenance of Alzheimer's disease β-amyloid plaques in the absence of microglia , 2009, Nature Neuroscience.
[58] Hans-Ulrich Demuth,et al. Pyroglutamate formation influences solubility and amyloidogenicity of amyloid peptides. , 2009, Biochemistry.
[59] T. Bayer,et al. Intraneuronal pyroglutamate-Abeta 3–42 triggers neurodegeneration and lethal neurological deficits in a transgenic mouse model , 2009, Acta Neuropathologica.
[60] N. Grigorieff,et al. Structural polymorphism of Alzheimer Aβ and other amyloid fibrils , 2009, Prion.
[61] D. Holtzman,et al. Microglia Mediate the Clearance of Soluble Aβ through Fluid Phase Macropinocytosis , 2009, The Journal of Neuroscience.
[62] N. Grigorieff,et al. Abeta(1-40) fibril polymorphism implies diverse interaction patterns in amyloid fibrils. , 2009, Journal of molecular biology.
[63] Scott A. Small,et al. Linking Aβ and Tau in Late-Onset Alzheimer's Disease: A Dual Pathway Hypothesis , 2008, Neuron.
[64] C. Masters,et al. Amyloid-β Peptide (Aβ) Neurotoxicity Is Modulated by the Rate of Peptide Aggregation: Aβ Dimers and Trimers Correlate with Neurotoxicity , 2008, The Journal of Neuroscience.
[65] C. Glabe,et al. Structural Classification of Toxic Amyloid Oligomers* , 2008, Journal of Biological Chemistry.
[66] Hans-Ulrich Demuth,et al. Glutaminyl cyclase inhibition attenuates pyroglutamate Aβ and Alzheimer's disease–like pathology , 2008, Nature Medicine.
[67] Shaomin Li,et al. Amyloid-β protein dimers isolated directly from Alzheimer's brains impair synaptic plasticity and memory , 2008, Nature Medicine.
[68] N. Grigorieff,et al. Paired β-sheet structure of an Aβ(1-40) amyloid fibril revealed by electron microscopy , 2008, Proceedings of the National Academy of Sciences.
[69] S. Barghorn,et al. Aβ-globulomers are formed independently of the fibril pathway , 2008, Neurobiology of Disease.
[70] C. Rowe,et al. Aβ deposits in older non-demented individuals with cognitive decline are indicative of preclinical Alzheimer's disease , 2008, Neuropsychologia.
[71] R O Weller,et al. Solutes, but not cells, drain from the brain parenchyma along basement membranes of capillaries and arteries: significance for cerebral amyloid angiopathy and neuroimmunology , 2008, Neuropathology and applied neurobiology.
[72] F. LaFerla,et al. Modeling behavioral and neuronal symptoms of Alzheimer's disease in mice: A role for intraneuronal amyloid , 2007, Neuroscience & Biobehavioral Reviews.
[73] 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.
[74] Walter Richter,et al. Effect of different salt ions on the propensity of aggregation and on the structure of Alzheimer's abeta(1-40) amyloid fibrils. , 2007, Journal of molecular biology.
[75] J. Cladera,et al. Conversion of non-fibrillar beta-sheet oligomers into amyloid fibrils in Alzheimer's disease amyloid peptide aggregation. , 2007, Biochemical and biophysical research communications.
[76] P. Scheltens,et al. Research criteria for the diagnosis of Alzheimer's disease: revising the NINCDS–ADRDA criteria , 2007, The Lancet Neurology.
[77] A. Aguzzi,et al. Insights into prion strains and neurotoxicity , 2007, Nature Reviews Molecular Cell Biology.
[78] D. Selkoe,et al. Aβ Oligomers – a decade of discovery , 2007, Journal of neurochemistry.
[79] R. Kayed,et al. Small Molecule Inhibitors of Aggregation Indicate That Amyloid β Oligomerization and Fibrillization Pathways Are Independent and Distinct* , 2007, Journal of Biological Chemistry.
[80] Bernardo L Sabatini,et al. Natural Oligomers of the Alzheimer Amyloid-β Protein Induce Reversible Synapse Loss by Modulating an NMDA-Type Glutamate Receptor-Dependent Signaling Pathway , 2007, The Journal of Neuroscience.
[81] D. Selkoe,et al. Soluble protein oligomers in neurodegeneration: lessons from the Alzheimer's amyloid β-peptide , 2007, Nature Reviews Molecular Cell Biology.
[82] D. Walsh,et al. Exogenous Induction of Cerebral ß-Amyloidogenesis Is Governed by Agent and Host , 2006, Science.
[83] Hans-Ulrich Demuth,et al. On the seeding and oligomerization of pGlu-amyloid peptides (in vitro). , 2006, Biochemistry.
[84] N. Grigorieff,et al. Quaternary structure of a mature amyloid fibril from Alzheimer's Abeta(1-40) peptide. , 2006, Journal of molecular biology.
[85] P. Verkade,et al. Alzheimer's disease beta-amyloid peptides are released in association with exosomes. , 2006, Proceedings of the National Academy of Sciences of the United States of America.
[86] M. Gallagher,et al. A specific amyloid-β protein assembly in the brain impairs memory , 2006, Nature.
[87] S. Hébert,et al. The amyloid‐β precursor protein: integrating structure with biological function , 2005 .
[88] P. Keller,et al. Globular amyloid β‐peptide1−42 oligomer − a homogenous and stable neuropathological protein in Alzheimer's disease , 2005 .
[89] P. T. Nguyen,et al. Dendritic Spine Abnormalities in Amyloid Precursor Protein Transgenic Mice Demonstrated by Gene Transfer and Intravital Multiphoton Microscopy , 2005, The Journal of Neuroscience.
[90] M. Fändrich,et al. The aggregation kinetics of Alzheimer's β‐amyloid peptide is controlled by stochastic nucleation , 2005, Protein science : a publication of the Protein Society.
[91] Jaime Grutzendler,et al. Fibrillar amyloid deposition leads to local synaptic abnormalities and breakage of neuronal branches , 2004, Nature Neuroscience.
[92] D. Selkoe,et al. A Seed for Alzheimer Amyloid in the Brain , 2004, The Journal of Neuroscience.
[93] P. Lansbury,et al. Protofibrils, pores, fibrils, and neurodegeneration: separating the responsible protein aggregates from the innocent bystanders. , 2003, Annual review of neuroscience.
[94] Richard Mayeux,et al. The Genetics of Adult-Onset Neuropsychiatric Disease: Complexities and Conundra? , 2003, Science.
[95] M. Staufenbiel,et al. Extracellular amyloid formation and associated pathology in neural grafts , 2003, Nature Neuroscience.
[96] P. Fraser,et al. Alternate Aggregation Pathways of the Alzheimer β-Amyloid Peptide: Aβ Association Kinetics at Endosomal pH , 2003 .
[97] Shigeo Murayama,et al. Isoaspartate formation at position 23 of amyloid beta peptide enhanced fibril formation and deposited onto senile plaques and vascular amyloids in Alzheimer's disease , 2002, Journal of neuroscience research.
[98] T. Miyakawa. Vascular Pathology in Alzheimer's Disease , 2002, Annals of the New York Academy of Sciences.
[99] Jia-Jia Liu,et al. Microtubule-associated protein 1B , 2002, The Journal of cell biology.
[100] H. Braak,et al. Phases of Aβ-deposition in the human brain and its relevance for the development of AD , 2002, Neurology.
[101] 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.
[102] Oliver Wirths,et al. Intraneuronal Aβ accumulation precedes plaque formation in β-amyloid precursor protein and presenilin-1 double-transgenic mice , 2001, Neuroscience Letters.
[103] R. Terry. Cell death or synaptic loss in Alzheimer disease. , 2000, Journal of neuropathology and experimental neurology.
[104] H. Braak,et al. Sequence of Aβ‐Protein Deposition in the Human Medial Temporal Lobe , 2000 .
[105] S. Müller,et al. Studies on the in Vitro Assembly of Aβ 1–40: Implications for the Search for Aβ Fibril Formation Inhibitors , 2000 .
[106] A. Roher,et al. Evidence for Seeding of β-Amyloid by Intracerebral Infusion of Alzheimer Brain Extracts in β-Amyloid Precursor Protein-Transgenic Mice , 2000, The Journal of Neuroscience.
[107] B. Sommer,et al. Neuronal overexpression of mutant amyloid precursor protein results in prominent deposition of cerebrovascular amyloid. , 1999, Proceedings of the National Academy of Sciences of the United States of America.
[108] M. Frotscher,et al. Cerebral Amyloid Induces Aberrant Axonal Sprouting and Ectopic Terminal Formation in Amyloid Precursor Protein Transgenic Mice , 1999, The Journal of Neuroscience.
[109] T. Arendt,et al. Progression of neurofibrillary changes and PHF-τ in end-stage Alzheimer’s disease is different from plaque and cortical microglial pathology , 1998, Neurobiology of Aging.
[110] Yu-Min Kuo,et al. Cerebral amyloid angiopathy: amyloid beta accumulates in putative interstitial fluid drainage pathways in Alzheimer's disease. , 1998, The American journal of pathology.
[111] T. Morgan,et al. Diffusible, nonfibrillar ligands derived from Abeta1-42 are potent central nervous system neurotoxins. , 1998, Proceedings of the National Academy of Sciences of the United States of America.
[112] Y. Ihara,et al. Astrocytes containing amyloid beta-protein (Abeta)-positive granules are associated with Abeta40-positive diffuse plaques in the aged human brain. , 1998, The American journal of pathology.
[113] Y. Ihara,et al. Diffuse plaques associated with astroglial amyloid β protein, possibly showing a disappearing stage of senile plaques , 1998, Acta Neuropathologica.
[114] Dietmar R. Thal,et al. Brain tissue damage and regeneration monitored by β‐amyloid precursor protein in experimental laser‐induced interstitial thermotherapy , 1998 .
[115] J. Seelig,et al. Interaction of Alzheimer beta-amyloid peptide(1-40) with lipid membranes. , 1997, Biochemistry.
[116] D. Dickson,et al. The Pathogenesis of Senile Plaques , 1997, Journal of neuropathology and experimental neurology.
[117] J. Trojanowski,et al. Full-length amyloid-beta (1-42(43)) and amino-terminally modified and truncated amyloid-beta 42(43) deposit in diffuse plaques. , 1996, The American journal of pathology.
[118] D. Graham,et al. Is β-APP a marker of axonal damage in short-surviving head injury? , 1996, Acta Neuropathologica.
[119] T. Iwatsubo,et al. Amino- and carboxyl-terminal heterogeneity of β-amyloid peptides deposited in human brain , 1996, Neuroscience Letters.
[120] P. Mcgeer,et al. Granules in glial cells of patients with Alzheimer's disease are immunopositive for C-terminal sequences of β-amyloid protein , 1996, Neuroscience Letters.
[121] D. Selkoe,et al. Sequence of Deposition of Heterogeneous Amyloid β-Peptides and APO E in Down Syndrome: Implications for Initial Events in Amyloid Plaque Formation , 1996, Neurobiology of Disease.
[122] T A Gennarelli,et al. The Nature, Distribution and Causes of Traumatic Brain Injury , 1995, Brain pathology.
[123] D. Munoz,et al. Qualitative and Quantitative Differences in Senile Plaque Dystrophie Neurites of Alzheimer's Disease and Normal Aged Brain , 1995, Journal of neuropathology and experimental neurology.
[124] R. Mrak,et al. Interleukin‐1 Expression in Different Plaque Types in Alzheimer's Disease: Significance in Plaque Evalution , 1995, Journal of neuropathology and experimental neurology.
[125] D. Mann,et al. Dominant and differential deposition of distinct β-amyloid peptide species, Aβ N3(pE), in senile plaques , 1995, Neuron.
[126] 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.
[127] 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.
[128] M J Ball,et al. Structural alterations in the peptide backbone of beta-amyloid core protein may account for its deposition and stability in Alzheimer's disease. , 1993, The Journal of biological chemistry.
[129] R. Kalaria,et al. Accumulation of the beta amyloid precursor protein at sites of ischemic injury in rat brain. , 1993, Neuroreport.
[130] Bradley T. Hyman,et al. Distribution of Alzheimer‐type pathologic changes in nondemented elderly individuals matches the pattern in Alzheimer's disease , 1992, Neurology.
[131] D. Selkoe,et al. Mass spectrometry of purified amyloid beta protein in Alzheimer's disease. , 1992, The Journal of biological chemistry.
[132] Bradley T. Hyman,et al. Neurofibrillary tangles but not senile plaques parallel duration and severity of Alzheimer's disease , 1992, Neurology.
[133] J. Vonsattel,et al. Cerebral amyloid angiopathy without and with cerebral hemorrhages: A comparative histological study , 1991, Annals of neurology.
[134] J. Price,et al. The distribution of tangles, plaques and related immunohistochemical markers in healthy aging and Alzheimer's disease , 1991, Neurobiology of Aging.
[135] S. M. Sumi,et al. The Consortium to Establish a Registry for Alzheimer's Disease (CERAD) , 1991, Neurology.
[136] S. DeKosky,et al. Synapse loss in frontal cortex biopsies in Alzheimer's disease: Correlation with cognitive severity , 1990, Annals of neurology.
[137] W. Griffin,et al. Brain interleukin 1 and S-100 immunoreactivity are elevated in Down syndrome and Alzheimer disease. , 1989, Proceedings of the National Academy of Sciences of the United States of America.
[138] D. Dickson,et al. Alzheimer's disease. A double-labeling immunohistochemical study of senile plaques. , 1988, The American journal of pathology.
[139] S. Mirra,et al. Neuritic Plaque Amyloid in Alzheimer's Disease Is Highly Racemized , 1988, Journal of neurochemistry.
[140] H. Wiśniewski,et al. Microtubule-associated protein tau. A component of Alzheimer paired helical filaments. , 1986, The Journal of biological chemistry.
[141] 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.
[142] G. Glenner,et al. Alzheimer's disease: Initial report of the purification and characterization of a novel cerebrovascular amyloid protein , 1984 .
[143] Michael Ewers,et al. Spreading of amyloid, tau, and microvascular pathology in Alzheimer's disease: findings from neuropathological and neuroimaging studies. , 2014, Journal of Alzheimer's disease : JAD.
[144] C. Schwieters,et al. Molecular Structure of beta-Amyloid Fibrils in Alzheimer's Disease Brain Tissue. , 2013 .
[145] Charles Duyckaerts,et al. National Institute on Aging–Alzheimer’s Association guidelines for the neuropathologic assessment of Alzheimer’s disease: a practical approach , 2011, Acta Neuropathologica.
[146] F. Heppner,et al. Formation and maintenance of Alzheimer’s disease beta-amyloid plaques in the absence of microglia , 2010 .
[147] J. Hardy,et al. The Amyloid Hypothesis of Alzheimer ’ s Disease : Progress and Problems on the Road to Therapeutics , 2009 .
[148] Michela Gallagher,et al. A specific amyloid-beta protein assembly in the brain impairs memory. , 2006, Nature.
[149] P. Keller,et al. Globular amyloid beta-peptide oligomer - a homogenous and stable neuropathological protein in Alzheimer's disease. , 2005, Journal of neurochemistry.
[150] S. Hébert,et al. The amyloid-beta precursor protein: integrating structure with biological function. , 2005, The EMBO journal.
[151] J. Zimmer,et al. Microglial and astroglial reactions to anterograde axonal degeneration: a histochemical and immunocytochemical study of the adult rat fascia dentata after entorhinal perforant path lesions , 2004, Experimental Brain Research.
[152] K. Solly,et al. Migration of xenogenic astrocytes in myelinated tracts: a novel probe for immune responses in white matter , 2004, Acta Neuropathologica.
[153] P. Fraser,et al. Alternate aggregation pathways of the Alzheimer beta-amyloid peptide: Abeta association kinetics at endosomal pH. , 2003, Journal of molecular biology.
[154] T. Wyss-Coray,et al. Adult mouse astrocytes degrade amyloid-beta in vitro and in situ. , 2003, Nature medicine.
[155] N. Milton. Phosphorylation of amyloid-beta at the serine 26 residue by human cdc2 kinase. , 2001, Neuroreport.
[156] T. Bayer,et al. Intraneuronal Abeta accumulation precedes plaque formation in beta-amyloid precursor protein and presenilin-1 double-transgenic mice. , 2001, Neuroscience letters.
[157] A. Roher,et al. Evidence for seeding of beta -amyloid by intracerebral infusion of Alzheimer brain extracts in beta -amyloid precursor protein-transgenic mice. , 2000, The Journal of neuroscience : the official journal of the Society for Neuroscience.
[158] P. Greengard,et al. Intraneuronal Abeta42 accumulation in human brain. , 2000, The American journal of pathology.
[159] S. Müller,et al. Studies on the in vitro assembly of a beta 1-40: implications for the search for a beta fibril formation inhibitors. , 2000, Journal of structural biology.
[160] H. Braak,et al. Sequence of Abeta-protein deposition in the human medial temporal lobe. , 2000, Journal of neuropathology and experimental neurology.
[161] P. Greengard,et al. Intraneuronal Aβ42 Accumulation in Human Brain , 2000 .
[162] R O Weller,et al. Cerebral amyloid angiopathy: amyloid beta accumulates in putative interstitial fluid drainage pathways in Alzheimer's disease. , 1998, The American journal of pathology.
[163] D. Thal,et al. Stage-correlated distribution of type 1 and 2 dystrophic neurites in cortical and hippocampal plaques in Alzheimer's disease. , 1998, Journal fur Hirnforschung.
[164] Charles M. Lieber,et al. Observation of metastable Abeta amyloid protofibrils by atomic force microscopy. , 1997, Chemistry & biology.
[165] D. Thal,et al. Differential pattern of β-amyloid, amyloid precursor protein and apolipoprotein E expression in cortical senile plaques , 1997, Acta Neuropathologica.
[166] P. Lansbury,et al. Models of amyloid seeding in Alzheimer's disease and scrapie: mechanistic truths and physiological consequences of the time-dependent solubility of amyloid proteins. , 1997, Annual review of biochemistry.
[167] Peter T. Lansbury,et al. Observation of metastable Aβ amyloid protofibrils by atomic force microscopy , 1997 .
[168] D. Graham,et al. Is beta-APP a marker of axonal damage in short-surviving head injury? , 1996, Acta neuropathologica.
[169] D. Mann,et al. Dominant and differential deposition of distinct beta-amyloid peptide species, A beta N3(pE), in senile plaques. , 1995, Neuron.
[170] 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.
[171] K. Grzeschik,et al. The precursor of Alzheimer??s disease amyloid A4 protein resembles a cell-surface receptor , 1987 .
[172] 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.
[173] H. M. Zimmerman. Progress in neuropathology , 1971 .
[174] A. Alzheimer. Uber eine eigenartige Erkrankung der Hirnrinde , 1907 .
[175] D. Wilcock,et al. Sanders-brown Center on Aging Faculty Publications Aging Transition from an M1 to a Mixed Neuroinflammatory Phenotype Increases Amyloid Deposition in App/ps1 Transgenic Mice Repository Citation Transition from an M1 to a Mixed Neuroinflammatory Phenotype Increases Amyloid Deposition in App/ps1 Trans , 2022 .