Long-Term Accumulation of Amyloid-β, β-Secretase, Presenilin-1, and Caspase-3 in Damaged Axons Following Brain Trauma
暂无分享,去创建一个
[1] E. A. Shores,et al. Traumatic Brain Injury as a Risk Factor for Alzheimer's Disease: A Review , 2004, Neuropsychology Review.
[2] F. Sherriff,et al. Early detection of axonal injury after human head trauma using immunocytochemistry for β-amyloid precursor protein , 2004, Acta Neuropathologica.
[3] D. Graham,et al. Amyloid β accumulation in axons after traumatic brain injury in humans , 2003 .
[4] Douglas H. Smith,et al. Long‐Term Accumulation of Amyloid‐β in Axons Following Brain Trauma Without Persistent Upregulation of Amyloid Precursor Protein Genes , 2002, Journal of neuropathology and experimental neurology.
[5] Phil M E Waite,et al. Axonal injury in children after motor vehicle crashes: extent, distribution, and size of axonal swellings using beta-APP immunohistochemistry. , 2002, Journal of neurotrauma.
[6] D. Bredesen,et al. Caspase cleavage of members of the amyloid precursor family of proteins , 2002, Journal of neurochemistry.
[7] Dae-Yeop Hwang,et al. Alterations in behavior, amyloid p‐42, caspase‐3, and Cox‐2 in mutant PS2 transgenic mouse model of Alzheimer's disease , 2002, FASEB journal : official publication of the Federation of American Societies for Experimental Biology.
[8] D. Okonkwo,et al. Caspase-3-mediated cleavage of amyloid precursor protein and formation of amyloid Beta peptide in traumatic axonal injury. , 2002, Journal of neurotrauma.
[9] Tatsuo Yamada,et al. A pH-dependent conformational transition of Abeta peptide and physicochemical properties of the conformers in the glial cell. , 2002, The Biochemical journal.
[10] T. Hara,et al. Cell death induced by a caspase-cleaved transmembrane fragment of the Alzheimer amyloid precursor protein , 2002, Cell Death and Differentiation.
[11] J. Shioi,et al. Presenilin-1 is expressed in neural progenitor cells in the hippocampus of adult mice , 2002, Neuroscience Letters.
[12] J. Busciglio,et al. Fast axonal transport misregulation and Alzheimer’s Disease , 2002, NeuroMolecular Medicine.
[13] J. Trojanowski,et al. Tau and axonopathy in neurodegenerative disorders , 2002, NeuroMolecular Medicine.
[14] S. Brady,et al. Regulation of Kinesin: Implications for Neuronal Development , 2001, Developmental Neuroscience.
[15] L. Goldstein,et al. Kinesin-mediated axonal transport of a membrane compartment containing β-secretase and presenilin-1 requires APP , 2001, Nature.
[16] S. Al-Sarraj,et al. Specificity and sensitivity of betaAPP in head injury. , 2001, Clinical neuropathology.
[17] K. Jellinger,et al. Effects of closed traumatic brain injury and genetic factors on the development of Alzheimer’s disease , 2001, European journal of neurology.
[18] M. Wolfe,et al. A Portrait of Alzheimer Secretases--New Features and Familiar Faces , 2001, Science.
[19] S. Chandra,et al. The Amyloidogenic Pathway of Amyloid Precursor Protein (APP) Is Independent of Its Cleavage by Caspases* , 2001, The Journal of Biological Chemistry.
[20] David J. Cummins,et al. Peripheral anti-Aβ antibody alters CNS and plasma Aβ clearance and decreases brain Aβ burden in a mouse model of Alzheimer's disease , 2001, Proceedings of the National Academy of Sciences of the United States of America.
[21] D. Meaney,et al. Axonal Damage in Traumatic Brain Injury , 2000 .
[22] L. Goldstein,et al. Axonal Transport of Amyloid Precursor Protein Is Mediated by Direct Binding to the Kinesin Light Chain Subunit of Kinesin-I , 2000, Neuron.
[23] J. Guralnik,et al. Documented head injury in early adulthood and risk of Alzheimer’s disease and other dementias , 2000, Neurology.
[24] D. Small,et al. Regulation of APP cleavage by α‐, β‐ and γ‐secretases , 2000 .
[25] Lye Tc,et al. Traumatic brain injury as a risk factor for Alzheimer's disease: a review. , 2000 .
[26] D. Selkoe,et al. In search of γ-secretase: Presenilin at the cutting edge , 2000 .
[27] P. Mehta,et al. Traumatic Brain Injury Elevates the Alzheimer's Amyloid Peptide Aβ42 in Human CSF: A Possible Role for Nerve Cell Injury , 2000, Annals of the New York Academy of Sciences.
[28] G. Cole,et al. β‐Amyloid (Aβ)42(43), Aβ42, Aβ40 and apoE immunostaining of plaques in fatal head injury , 2000, Neuropathology and applied neurobiology.
[29] J. Lambert,et al. Kinesin and kinectin can associate with the melanosomal surface and form a link with microtubules in normal human melanocytes. , 2000, The Journal of investigative dermatology.
[30] D. Selkoe. In search of X-secretase : Presenilins at the cutting edge , 2000 .
[31] David G. Tew,et al. Identification of a Novel Aspartic Protease (Asp 2) as β-Secretase , 1999, Molecular and Cellular Neuroscience.
[32] J. Wolf,et al. Prolonged Activation of NF-?B Following Traumatic Brain Injury in Rats , 1999 .
[33] J. Treanor,et al. Beta-secretase cleavage of Alzheimer's amyloid precursor protein by the transmembrane aspartic protease BACE. , 1999, Science.
[34] J Q Trojanowski,et al. Accumulation of amyloid beta and tau and the formation of neurofilament inclusions following diffuse brain injury in the pig. , 1999, Journal of neuropathology and experimental neurology.
[35] J. Wolf,et al. Evolution of neurofilament subtype accumulation in axons following diffuse brain injury in the pig. , 1999, Journal of neuropathology and experimental neurology.
[36] S. Gauthier,et al. β-Amyloid precursor protein is detectable on monocytes and is increased in Alzheimer’s disease , 1999, Neurobiology of Aging.
[37] J. Marcilloux,et al. Stereotaxic atlas of the pig brain , 1999, Brain Research Bulletin.
[38] David Smith,et al. Involvement of Caspases in Proteolytic Cleavage of Alzheimer’s Amyloid-β Precursor Protein and Amyloidogenic Aβ Peptide Formation , 1999, Cell.
[39] H. Akiyama,et al. Immunohistochemical localization of amyloid β-protein with amino-terminal aspartate in the cerebral cortex of patients with Alzheimer's disease , 1999, Brain Research.
[40] K Paliga,et al. Proteolytic Processing of the Alzheimer’s Disease Amyloid Precursor Protein within Its Cytoplasmic Domain by Caspase-like Proteases* , 1999, The Journal of Biological Chemistry.
[41] E. Kokmen,et al. Traumatic brain injury and time to onset of Alzheimer's disease: a population-based study. , 1999, American journal of epidemiology.
[42] P. Mehta,et al. Traumatic Brain Injury Increases β‐Amyloid Peptide 1‐42 in Cerebrospinal Fluid , 1998 .
[43] M. Balass,et al. N-terminal EFRH sequence of Alzheimer's β-amyloid peptide represents the epitope of its anti-aggregating antibodies , 1998, Journal of Neuroimmunology.
[44] R. Oppenheim,et al. Increased Production of Amyloid Precursor Protein Provides a Substrate for Caspase-3 in Dying Motoneurons , 1998, The Journal of Neuroscience.
[45] J. Trojanowski,et al. Enduring cognitive, neurobehavioral and histopathological changes persist for up to one year following severe experimental brain injury in rats , 1998, Neuroscience.
[46] J. Miguel-Hidalgo,et al. β-Amyloid(1–40)-induced neurodegeneration in the rat hippocampal neurons of the CA1 subfield , 1998, Acta Neuropathologica.
[47] Hugo Vanderstichele,et al. Deficiency of presenilin-1 inhibits the normal cleavage of amyloid precursor protein , 1998, Nature.
[48] E. J. Green,et al. Temporal and Regional Patterns of Axonal Damage following Traumatic Brain Injury: A Beta‐amyloid Precursor Protein Immunocytochemical Study in Rats , 1997, Journal of neuropathology and experimental neurology.
[49] J Q Trojanowski,et al. Progressive atrophy and neuron death for one year following brain trauma in the rat. , 1997, Journal of neurotrauma.
[50] Jinhe Li,et al. Alzheimer Presenilins in the Nuclear Membrane, Interphase Kinetochores, and Centrosomes Suggest a Role in Chromosome Segregation , 1997, Cell.
[51] T A Gennarelli,et al. Characterization of diffuse axonal pathology and selective hippocampal damage following inertial brain trauma in the pig. , 1997, Journal of neuropathology and experimental neurology.
[52] K. Marder,et al. Alzheimer's disease after remote head injury: an incidence study. , 1997, Journal of neurology, neurosurgery, and psychiatry.
[53] B. Greenberg,et al. Enhanced Amyloidogenic Processing of the β-Amyloid Precursor Protein in Gene-targeted Mice Bearing the Swedish Familial Alzheimer's Disease Mutations and a “Humanized” Aβ Sequence* , 1996, The Journal of Biological Chemistry.
[54] S. Srinivasula,et al. In vitro activation of CPP32 and Mch3 by Mch4, a novel human apoptotic cysteine protease containing two FADD-like domains. , 1996, Proceedings of the National Academy of Sciences of the United States of America.
[55] N. Thornberry,et al. Apopain/CPP32 cleaves proteins that are essential for cellular repair: a fundamental principle of apoptotic death , 1996, The Journal of experimental medicine.
[56] J. Trojanowski,et al. Immunohistochemical characterization of alterations in the distribution of amyloid precursor proteins and beta-amyloid peptide after experimental brain injury in the rat , 1996, The Journal of neuroscience : the official journal of the Society for Neuroscience.
[57] B. Solomon,et al. Monoclonal antibodies inhibit in vitro fibrillar aggregation of the Alzheimer beta-amyloid peptide. , 1996, Proceedings of the National Academy of Sciences of the United States of America.
[58] D. Graham,et al. Is beta-APP a marker of axonal damage in short-surviving head injury? , 1996, Acta neuropathologica.
[59] D. Smith,et al. Inflammatory leukocytic recruitment and diffuse neuronal degeneration are separate pathological processes resulting from traumatic brain injury , 1995, The Journal of neuroscience : the official journal of the Society for Neuroscience.
[60] T A Gennarelli,et al. Biomechanical analysis of experimental diffuse axonal injury. , 1995, Journal of neurotrauma.
[61] B. Greenberg,et al. Mutant and native human β-amyloid precursor proteins in transgenic mouse brain , 1995, Neurobiology of Aging.
[62] A. Odaka,et al. Amyloid β protein 1–42/43 (Aβ 1–42/43) in cerebellar diffuse plaques: enzyme-linked immunosorbent assay and immunocytochemical study , 1995, Brain Research.
[63] M. Folstein,et al. Head injury as a risk factor in Alzheimer's disease. , 1995, Brain injury.
[64] S. Gentleman,et al. Distribution of β‐amyloid protein in the brain following severe head injury , 1995 .
[65] G. L. Li,et al. Traumatic brain injury in rat produces changes of beta-amyloid precursor protein immunoreactivity. , 1995, Neuroreport.
[66] B. Greenberg,et al. Elevated Aβ levels in Alzheimer's disease brain are associated with selective accumulation of Aβ42 in parenchymal amyloid plaques and both Aβ40 and Aβ42 in cerebrovascular deposits , 1995 .
[67] H. Vinters,et al. Monoclonal antibody to the C‐terminus of β‐amyloid , 1994 .
[68] 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.
[69] L. Forno,et al. Development of a monoclonal antibody specific for the COOH-terminal of beta-amyloid 1-42 and its immunohistochemical reactivity in Alzheimer's disease and related disorders. , 1994, The American journal of pathology.
[70] D. Selkoe,et al. Cell biology of the amyloid beta-protein precursor and the mechanism of Alzheimer's disease. , 1994, Annual review of cell biology.
[71] K. Beyreuther,et al. Amyloid-like properties of peptides flanking the epitope of amyloid precursor protein-specific monoclonal antibody 22C11. , 1993, The Journal of biological chemistry.
[72] D. Graham,et al. β-Amyloid precursor protein (βAPP) as a marker for axonal injury after head injury , 1993, Neuroscience Letters.
[73] B T Hyman,et al. Kunitz Protease Inhibitor‐Containing Amyloid β Protein Precursor Immunoreactivity in Alzheimer's Disease , 1992, Journal of neuropathology and experimental neurology.
[74] D. Graham,et al. βA4 amyloid protein deposition in brain after head trauma , 1991, The Lancet.
[75] G. Shaw,et al. A molecular dissection of the carboxyterminal tails of the major neurofilament subunits NF‐M and NF‐H , 1991, Journal of neuroscience research.
[76] R. Neve,et al. The primary structure and analysis of the squid kinesin heavy chain. , 1990, The Journal of biological chemistry.
[77] J. Adams,et al. Diffuse axonal injury in head injury: Definition, diagnosis and grading , 1989, Histopathology.
[78] B. Greenberg,et al. A new A4 amyloid mRNA contains a domain homologous to serine proteinase inhibitors , 1988, Nature.
[79] K. Grzeschik,et al. The precursor of Alzheimer??s disease amyloid A4 protein resembles a cell-surface receptor , 1987 .
[80] G. Shaw,et al. Reactivity of a panel of neurofilament antibodies on phosphorylated and dephosphorylated neurofilaments. , 1986, European journal of cell biology.
[81] J. Povlishock,et al. Fate of reactive axonal swellings induced by head injury. , 1988, Laboratory investigation; a journal of technical methods and pathology.
[82] Povlishock Jt,et al. Fate of reactive axonal swellings induced by head injury. , 1985 .
[83] L M Schuman,et al. Head injury as a risk factor for Alzheimer's disease , 1985, Neurology.
[84] J. Adams,et al. Diffuse axonal injury in non-missile head injury. , 1982, Injury.
[85] H. Schmidt,et al. Release of immunoreactive-dynorphin from the isolated guinea-pig small intestine is reduced during peristaltic activity , 1981, Neuroscience Letters.