Neurological and Neurodegenerative Alterations in a Transgenic Mouse Model Expressing Human α-Synuclein under Oligodendrocyte Promoter: Implications for Multiple System Atrophy
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Makoto Hashimoto | Takeshi Iwatsubo | E. Masliah | T. Iwatsubo | G. Larrea | E. Rockenstein | L. Crews | A. Adame | C. Shults | M. Hashimoto | M. Mante | Eliezer Masliah | Clifford W Shults | Edward Rockenstein | David Song | Leslie Crews | Anthony Adame | Michael Mante | Gabriel Larrea | Kyoko Tsuboi | K. Tsuboi | David Song
[1] A. Makrigiannakis,et al. Endometrial Pinopodes and Uterine Receptivity , 2003, Annals of the New York Academy of Sciences.
[2] K. Wakabayashi,et al. An autopsy case of early (“minimal change”) olivopontocerebellar atrophy (multiple system atrophy-cerebellar) , 2005, Acta Neuropathologica.
[3] Janel O. Johnson,et al. α-Synuclein Locus Triplication Causes Parkinson's Disease , 2003, Science.
[4] Nancy A. Jenkins,et al. Human α-synuclein-harboring familial Parkinson's disease-linked Ala-53 → Thr mutation causes neurodegenerative disease with α-synuclein aggregation in transgenic mice , 2002, Proceedings of the National Academy of Sciences of the United States of America.
[5] J. Trojanowski,et al. Synucleins Are Developmentally Expressed, and α-Synuclein Regulates the Size of the Presynaptic Vesicular Pool in Primary Hippocampal Neurons , 2000, The Journal of Neuroscience.
[6] D. Oppenheimer,et al. Orthostatic hypotension and nicotine sensitivity in a case of multiple system atrophy. , 1969, Journal of neurology, neurosurgery, and psychiatry.
[7] Akihiko Iwai,et al. The precursor protein of non-Aβ component of Alzheimer's disease amyloid is a presynaptic protein of the central nervous system , 1995, Neuron.
[8] P. Lantos,et al. Cellular pathology of multiple system atrophy: a review. , 1994, Journal of neurology, neurosurgery, and psychiatry.
[9] Werner Poewe,et al. Oxidative stress in transgenic mice with oligodendroglial alpha-synuclein overexpression replicates the characteristic neuropathology of multiple system atrophy. , 2005, The American journal of pathology.
[10] M. Beal. Mitochondria, Oxidative Damage, and Inflammation in Parkinson's Disease , 2003, Annals of the New York Academy of Sciences.
[11] E. Masliah,et al. Neurofibrillary Pathology in Transgenic Mice Overexpressing V717F β‐Amyloid Precursor Protein , 2001, Journal of neuropathology and experimental neurology.
[12] David F. Clayton,et al. The synucleins: a family of proteins involved in synaptic function, plasticity, neurodegeneration and disease , 1998, Trends in Neurosciences.
[13] J. Trojanowski,et al. Selective Insolubility of α-Synuclein in Human Lewy Body Diseases Is Recapitulated in a Transgenic Mouse Model , 2001 .
[14] L. Mucke,et al. Central nervous system damage produced by expression of the HIV-1 coat protein gpl20 in transgenic mice , 1994, Nature.
[15] Carlo Colosimo,et al. Multiple system atrophy , 2004, The Lancet Neurology.
[16] W. Honer,et al. Abnormal accumulation of NACP/alpha-synuclein in neurodegenerative disorders. , 1998, The American journal of pathology.
[17] F. Doricchi,et al. Attentional functions in multiple system atrophy and Parkinson's disease. , 1996, Journal of neurology, neurosurgery, and psychiatry.
[18] E. Masliah,et al. Reduced Neuritic Outgrowth and Cell Adhesion in Neuronal Cells Transfected with Human α-Synuclein , 2001, Molecular and Cellular Neuroscience.
[19] P. Gonzalez-Cabrera,et al. Mice expressing the α1B‐adrenergic receptor induces a synucleinopathy with excessive tyrosine nitration but decreased phosphorylation , 2002, Journal of neurochemistry.
[20] M. L. Schmidt,et al. α-Synuclein in Lewy bodies , 1997, Nature.
[21] P. Lansbury,et al. Is there a cause-and-effect relationship between α-synuclein fibrillization and Parkinson’s disease? , 2000, Nature Cell Biology.
[22] Takeshi Iwatsubo,et al. Fatal attractions: abnormal protein aggregation and neuron death in Parkinson's disease and Lewy body dementia , 1998, Cell Death and Differentiation.
[23] C. Masters,et al. Oligodendrocytes from neural stem cells express &agr;-synuclein: increased numbers from presenilin 1 deficient mice , 2002, Neuroreport.
[24] J. Trojanowski,et al. Neurodegeneration with Brain Iron Accumulation, Type 1 Is Characterized by α-, β-, and γ-Synuclein Neuropathology , 2000 .
[25] A. Dürr,et al. Genetics of movement disorders , 1996, Current opinion in neurology.
[26] Bradley T. Hyman,et al. Patterns of protein nitration in dementia with Lewy bodies and striatonigral degeneration , 2002, Acta Neuropathologica.
[27] W. Bender,et al. A Drosophila model of Parkinson's disease , 2000, Nature.
[28] P. Lansbury. Evolution of amyloid: what normal protein folding may tell us about fibrillogenesis and disease. , 1999, Proceedings of the National Academy of Sciences of the United States of America.
[29] K. Mizukawa,et al. MPTP-induced parkinsonian model in mice: biochemistry, pharmacology and behavior. , 1987, European neurology.
[30] M. Jaber,et al. Motor behaviour deficits and their histopathological and functional correlates in the nigrostriatal system of dopamine transporter knockout mice , 2003, Neuroscience.
[31] Nigel J. Cairns,et al. Filamentous α-synuclein inclusions link multiple system atrophy with Parkinson's disease and dementia with Lewy bodies , 1998, Neuroscience Letters.
[32] Hitoshi Takahashi,et al. NACP, a presynaptic protein, immunoreactivity in Lewy bodies in Parkinson's disease , 1997, Neuroscience Letters.
[33] J. Hoenicka,et al. The new mutation, E46K, of α‐synuclein causes parkinson and Lewy body dementia , 2004, Annals of neurology.
[34] J. Trojanowski,et al. Mouse Model of Multiple System Atrophy α-Synuclein Expression in Oligodendrocytes Causes Glial and Neuronal Degeneration , 2005, Neuron.
[35] Olaf Riess,et al. AlaSOPro mutation in the gene encoding α-synuclein in Parkinson's disease , 1998, Nature Genetics.
[36] Makoto Hashimoto,et al. Differential neuropathological alterations in transgenic mice expressing α‐synuclein from the platelet‐derived growth factor and Thy‐1 promoters , 2002, Journal of neuroscience research.
[37] Hitoshi Takahashi,et al. Accumulation of α-synuclein/NACP is a cytopathological feature common to Lewy body disease and multiple system atrophy , 1998, Acta Neuropathologica.
[38] D. Dickson,et al. Multiple System Atrophy: A Sporadic Synucleinopathy , 1999, Brain pathology.
[39] E. Masliah,et al. Molecular cloning of cDNA encoding an unrecognized component of amyloid in Alzheimer disease. , 1993, Proceedings of the National Academy of Sciences of the United States of America.
[40] J. Trojanowski,et al. α‐synuclein is developmentally expressed in cultured rat brain oligodendrocytes , 2000, Journal of neuroscience research.
[41] Todd B. Sherer,et al. Chronic systemic pesticide exposure reproduces features of Parkinson's disease , 2000, Nature Neuroscience.
[42] A. Brice,et al. Alpha-synuclein and Parkinson's disease , 2000, Cellular and Molecular Life Sciences CMLS.
[43] J. Trojanowski,et al. Neuronal α-Synucleinopathy with Severe Movement Disorder in Mice Expressing A53T Human α-Synuclein , 2002, Neuron.
[44] L. Mucke,et al. Levels and Alternative Splicing of Amyloid β Protein Precursor (APP) Transcripts in Brains of APP Transgenic Mice and Humans with Alzheimer's Disease (*) , 1995, The Journal of Biological Chemistry.
[45] I Litvan,et al. Consensus statement on the diagnosis of multiple system atrophy , 1998, Journal of the Neurological Sciences.
[46] N. Ogawa,et al. A simple quantitative bradykinesia test in MPTP-treated mice. , 1985, Research communications in chemical pathology and pharmacology.
[47] D. Dickson,et al. Alpha-synuclein and the Lewy body disorders. , 2001, Current opinion in neurology.
[48] Makoto Hashimoto,et al. Human recombinant NACP/α-synuclein is aggregated and fibrillated in vitro: Relevance for Lewy body disease , 1998, Brain Research.
[49] E. Masliah,et al. Alpha-synuclein overexpression in oligodendrocytic cells results in impaired adhesion to fibronectin and cell death , 2005, Molecular and Cellular Neuroscience.
[50] H. Ischiropoulos,et al. Oxidative stress and nitration in neurodegeneration: cause, effect, or association? , 2003, The Journal of clinical investigation.
[51] Robert L. Nussbaum,et al. Mutation in the α-Synuclein Gene Identified in Families with Parkinson's Disease , 1997 .
[52] Pico Caroni,et al. Neuropathology in Mice Expressing Human α-Synuclein , 2000, The Journal of Neuroscience.
[53] M. Mallory,et al. Early formation of mature amyloid‐β protein deposits in a mutant APP transgenic model depends on levels of Aβ1–42 , 2001, Journal of neuroscience research.
[54] E. Masliah,et al. Alpha‐synuclein in Lewy Body Disease and Alzheimer's Disease , 1999, Brain pathology.
[55] M. Ikeda,et al. Constant involvement of the Betz cells and pyramidal tract in multiple system atrophy: a clinicopathological study of seven autopsy cases , 2000, Acta Neuropathologica.
[56] P. Lantos,et al. The definition of multiple system atrophy: a review of recent developments. , 1998, Journal of neuropathology and experimental neurology.
[57] Joseph P Huston,et al. Behavioral phenotyping of the MPTP mouse model of Parkinson's disease , 2001, Behavioural Brain Research.
[58] C. Marsden,et al. Cognitive performance in multiple system atrophy. , 1992, Brain : a journal of neurology.
[59] E. Masliah,et al. α-Synuclein is phosphorylated in synucleinopathy lesions , 2002, Nature Cell Biology.
[60] Hideo Fujiwara,et al. Hyperphosphorylation and insolubility of α‐synuclein in transgenic mouse oligodendrocytes , 2002 .
[61] K. Jellinger,et al. The role of α-synuclein in the pathogenesis of multiple system atrophy , 2005, Acta Neuropathologica.
[62] T. Montine,et al. Immunohistochemical and Biochemical Studies Demonstrate a Distinct Profile of α‐Synuclein Permutations in Multiple System Atrophy , 2000, Journal of neuropathology and experimental neurology.
[63] V. Uversky,et al. The Herbicide Paraquat Causes Up-regulation and Aggregation of α-Synuclein in Mice , 2002, The Journal of Biological Chemistry.
[64] Michel Goedert,et al. Alpha-synuclein and neurodegenerative diseases , 2001, Nature Reviews Neuroscience.
[65] E. Masliah,et al. Oxidative stress induces amyloid-like aggregate formation of NACP/α-synuclein in vitro , 1999 .
[66] E. Masliah,et al. Enhanced substantia nigra mitochondrial pathology in human α-synuclein transgenic mice after treatment with MPTP 1 1 1-Methyl-4-phenyl-1,2,3,6-tetrahydropyridine. , 2004, Experimental Neurology.
[67] Makoto Hashimoto,et al. β-Amyloid peptides enhance α-synuclein accumulation and neuronal deficits in a transgenic mouse model linking Alzheimer's disease and Parkinson's disease , 2001, Proceedings of the National Academy of Sciences of the United States of America.
[68] T. Sherer,et al. Animal models of Parkinson's disease. , 2002, BioEssays : news and reviews in molecular, cellular and developmental biology.
[69] Jonathan Salcedo,et al. Early and Progressive Sensorimotor Anomalies in Mice Overexpressing Wild-Type Human α-Synuclein , 2004, The Journal of Neuroscience.
[70] D. Burn,et al. Multiple system atrophy: cellular and molecular pathology , 2001, Molecular pathology : MP.
[71] W. Poewe,et al. Glial cell death induced by overexpression of α‐synuclein , 2001 .
[72] A. Iwai. Properties of NACP/α-synuclein and its role in Alzheimer’s disease , 2000 .
[73] Hitoshi Takahashi,et al. α-Synuclein immunoreactivity in glial cytoplasmic inclusions in multiple system atrophy , 1998, Neuroscience Letters.
[74] J. Culvenor,et al. α‐Synuclein Immunoisolation of Glial Inclusions from Multiple System Atrophy Brain Tissue Reveals Multiprotein Components , 1999, Journal of neurochemistry.
[75] E. Masliah,et al. Altered presynaptic protein NACP is associated with plaque formation and neurodegeneration in Alzheimer's disease. , 1996, The American journal of pathology.
[76] N. Ogawa,et al. Pole test is a useful method for evaluating the mouse movement disorder caused by striatal dopamine depletion , 1997, Journal of Neuroscience Methods.
[77] L. Mucke,et al. Dopaminergic loss and inclusion body formation in alpha-synuclein mice: implications for neurodegenerative disorders. , 2000, Science.
[78] S. Speciale,et al. MPTP: insights into parkinsonian neurodegeneration. , 2002, Neurotoxicology and teratology.
[79] K. Schmid,et al. Cell Death Mechanisms in Multiple System Atrophy , 1998, Journal of neuropathology and experimental neurology.
[80] V. Friedrich,et al. Myelin basic protein gene contains separate enhancers for oligodendrocyte and Schwann cell expression , 1992, The Journal of cell biology.
[81] E. Masliah,et al. An antiaggregation gene therapy strategy for Lewy body disease utilizing β-synuclein lentivirus in a transgenic model , 2004, Gene Therapy.