Systemic proteasome inhibition triggers neurodegeneration in a transgenic mouse model expressing human α-synuclein under oligodendrocyte promoter: implications for multiple system atrophy
暂无分享,去创建一个
[1] G. Wenning,et al. Animal models of multiple system atrophy , 2005, Clinical Autonomic Research.
[2] P. Remy,et al. Chronic systemic treatment with a high-dose proteasome inhibitor in mice produces akinesia unrelated to nigrostriatal degeneration , 2011, Neurobiology of Aging.
[3] B. Hyman,et al. Distinct Roles In Vivo for the Ubiquitin–Proteasome System and the Autophagy–Lysosomal Pathway in the Degradation of α-Synuclein , 2011, The Journal of Neuroscience.
[4] K. Jellinger,et al. Glial dysfunction in the pathogenesis of α-synucleinopathies: emerging concepts , 2011, Acta Neuropathologica.
[5] S. Waxman,et al. Slowly Progressive Axonal Degeneration in a Rat Model of Chronic, Nonimmune-Mediated Demyelination , 2010, Journal of neuropathology and experimental neurology.
[6] W. Poewe,et al. Targeted overexpression of human α-synuclein in oligodendroglia induces lesions linked to MSA -like progressive autonomic failure , 2010, Experimental Neurology.
[7] B. Trapp,et al. Demyelination Increases Axonal Stationary Mitochondrial Size and the Speed of Axonal Mitochondrial Transport , 2010, The Journal of Neuroscience.
[8] P. Jenner,et al. A comparison of changes in proteasomal subunit expression in the substantia nigra in Parkinson's disease, multiple system atrophy and progressive supranuclear palsy , 2010, Brain Research.
[9] K. Jellinger,et al. Papp–Lantos inclusions and the pathogenesis of multiple system atrophy: an update , 2010, Acta Neuropathologica.
[10] R. Seth,et al. Proteasome inhibitors prevent cisplatin-induced mitochondrial release of apoptosis-inducing factor and markedly ameliorate cisplatin nephrotoxicity. , 2010, Biochemical pharmacology.
[11] W. Möbius,et al. Electron microscopy of the mouse central nervous system. , 2010, Methods in cell biology.
[12] Ubiquitin enzymes, ubiquitin and proteasome activity in blood mononuclear cells of MCI, Alzheimer and Parkinson patients. , 2010, Current Alzheimer research.
[13] G. Wenning,et al. Multiple system atrophy: an update , 2009, The Lancet Neurology.
[14] J. Middeldorp,et al. Intermediate filament transcription in astrocytes is repressed by proteasome inhibition , 2009, FASEB journal : official publication of the Federation of American Societies for Experimental Biology.
[15] Sonja W. Scholz,et al. SNCA variants are associated with increased risk for multiple system atrophy , 2009, Annals of neurology.
[16] K. Jellinger,et al. Multiple system atrophy: A primary oligodendrogliopathy , 2008, Annals of neurology.
[17] Klaus-Armin Nave,et al. Axon-glial signaling and the glial support of axon function. , 2008, Annual review of neuroscience.
[18] M. Umeda,et al. Proteasome Inhibitor Does Not Enhance MPTP Neurotoxicity in Mice , 2008, Cellular and Molecular Neurobiology.
[19] W. Poewe,et al. Microglial activation mediates neurodegeneration related to oligodendroglial α‐synucleinopathy: Implications for multiple system atrophy , 2007, Movement disorders : official journal of the Movement Disorder Society.
[20] C. Ide,et al. Gene expression changes in postmortem tissue from the rostral pons of multiple system atrophy patients , 2007, Movement disorders : official journal of the Movement Disorder Society.
[21] A. Landau,et al. Proteasome inhibitor model of Parkinson's disease in mice is confounded by neurotoxicity of the ethanol vehicle , 2007, Movement disorders : official journal of the Movement Disorder Society.
[22] P. Jenner,et al. Reproducible nigral cell loss after systemic proteasomal inhibitor administration to rats , 2006, Annals of neurology.
[23] J. Cooper,et al. Proteasomal inhibition causes loss of nigral tyrosine hydroxylase neurons , 2006, Annals of neurology.
[24] J. Langston,et al. Lack of nigrostriatal pathology in a rat model of proteasome inhibition , 2006, Annals of neurology.
[25] J. Kordower,et al. Failure of proteasome inhibitor administration to provide a model of Parkinson's disease in rats and monkeys , 2006, Annals of neurology.
[26] Jeffrey H Kordower,et al. Proteasome inhibition and Parkinson's disease modeling , 2006, Annals of neurology.
[27] O. Ottersen,et al. Immunolocalization of BK channels in hippocampal pyramidal neurons , 2006, The European journal of neuroscience.
[28] A. Brusco,et al. Morphometric study on cytoskeletal components of neuronal and astroglial cells after chronic CB1 agonist treatment. , 2006, Methods in molecular medicine.
[29] I. Amende,et al. Journal of Neuroengineering and Rehabilitation Open Access Gait Dynamics in Mouse Models of Parkinson's Disease and Huntington's Disease Gait Variabilitygaitmouse Modelsneurodegenerationmovement Disordersamyotrophic Lateral Sclerosissod1 , 2022 .
[30] T. Tanaka,et al. α-Synuclein-positive structures induced in leupeptin-infused rats , 2005, Brain Research.
[31] 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.
[32] D. Perl,et al. Systemic exposure to proteasome inhibitors causes a progressive model of Parkinson's disease , 2004, Annals of neurology.
[33] Carmen Birchmeier,et al. Axonal Neuregulin-1 Regulates Myelin Sheath Thickness , 2004, Science.
[34] J. Culvenor,et al. α-synuclein fibrils constitute the central core of oligodendroglial inclusion filaments in multiple system atrophy , 2003, Experimental Neurology.
[35] P. Elliott,et al. Proteasome inhibition: a new anti-inflammatory strategy , 2003, Journal of Molecular Medicine.
[36] K. Nave,et al. Disruption of Cnp1 uncouples oligodendroglial functions in axonal support and myelination , 2003, Nature Genetics.
[37] J. Culvenor,et al. alpha-Synuclein fibrils constitute the central core of oligodendroglial inclusion filaments in multiple system atrophy. , 2003, Experimental neurology.
[38] Hideo Fujiwara,et al. Misfolded proteinase K-resistant hyperphosphorylated alpha-synuclein in aged transgenic mice with locomotor deterioration and in human alpha-synucleinopathies. , 2002, The Journal of clinical investigation.
[39] Hideo Fujiwara,et al. Hyperphosphorylation and insolubility of α‐synuclein in transgenic mouse oligodendrocytes , 2002 .
[40] W. Spooren,et al. Hyperphosphorylation and insolubility of alpha-synuclein in transgenic mouse oligodendrocytes. , 2002, EMBO reports.
[41] J. Trojanowski,et al. Misfolded proteinase K-resistant hyperphosphorylated alpha-synuclein in aged transgenic mice with locomotor deterioration and in human alpha-synucleinopathies. , 2002, The Journal of clinical investigation.
[42] J. Trojanowski,et al. Selective Insolubility of α-Synuclein in Human Lewy Body Diseases Is Recapitulated in a Transgenic Mouse Model , 2001 .
[43] D. German,et al. Degeneration of neurons and glia in the Niemann–Pick C mouse is unrelated to the low-density lipoprotein receptor , 2001, Neuroscience.
[44] J. Trojanowski,et al. Selective insolubility of alpha-synuclein in human Lewy body diseases is recapitulated in a transgenic mouse model. , 2001, The American journal of pathology.
[45] H. Hinterhuber,et al. Synaptic loss reflected by secretoneurin‐like immunoreactivity in the human hippocampus in Alzheimer's disease , 1998, The European journal of neuroscience.
[46] M. Clayton,et al. The temporal progression of the myelination defect in the taiep rat , 1997, Journal of neurocytology.
[47] T M Mayhew,et al. If you assume, you can make an ass out of u and me': a decade of the disector for stereological counting of particles in 3D space. , 1996, Journal of anatomy.
[48] W. Stoffel,et al. Adhesive properties of proteolipid protein are responsible for the compaction of CNS myelin sheaths , 1995, The Journal of neuroscience : the official journal of the Society for Neuroscience.