Exogenous α-Synuclein Fibrils Induce Lewy Body Pathology Leading to Synaptic Dysfunction and Neuron Death

[1]  V. Lee,et al.  Seeding of Normal Tau by Pathological Tau Conformers Drives Pathogenesis of Alzheimer-like Tangles* , 2011, The Journal of Biological Chemistry.

[2]  Fred H. Gage,et al.  In vivo demonstration that α-synuclein oligomers are toxic , 2011, Proceedings of the National Academy of Sciences.

[3]  P. Brundin,et al.  α-Synuclein propagates from mouse brain to grafted dopaminergic neurons and seeds aggregation in cultured human cells. , 2011, The Journal of clinical investigation.

[4]  S. Chandra,et al.  αβγ-Synuclein triple knockout mice reveal age-dependent neuronal dysfunction , 2010, Proceedings of the National Academy of Sciences.

[5]  T. Südhof,et al.  α-Synuclein Promotes SNARE-Complex Assembly in Vivo and in Vitro , 2010, Science.

[6]  R. Nicoll,et al.  Increased Expression of α-Synuclein Reduces Neurotransmitter Release by Inhibiting Synaptic Vesicle Reclustering after Endocytosis , 2010, Neuron.

[7]  Lawrence Rajendran,et al.  The Transcellular Spread of Cytosolic Amyloids, Prions, and Prionoids , 2009, Neuron.

[8]  J. Trojanowski,et al.  Exogenous α-synuclein fibrils seed the formation of Lewy body-like intracellular inclusions in cultured cells , 2009, Proceedings of the National Academy of Sciences.

[9]  Brian Spencer,et al.  Inclusion formation and neuronal cell death through neuron-to-neuron transmission of α-synuclein , 2009, Proceedings of the National Academy of Sciences.

[10]  E. Waxman,et al.  Molecular mechanisms of alpha-synuclein neurodegeneration. , 2009, Biochimica et biophysica acta.

[11]  Martin Beibel,et al.  Transmission and spreading of tauopathy in transgenic mouse brain , 2009, Nature Cell Biology.

[12]  M. Diamond,et al.  Propagation of Tau Misfolding from the Outside to the Inside of a Cell* , 2009, Journal of Biological Chemistry.

[13]  R. Hauser,et al.  Transplanted dopaminergic neurons develop PD pathologic changes: A second case report , 2008, Movement disorders : official journal of the Movement Disorder Society.

[14]  T. Tlusty,et al.  Development of input connections in neural cultures , 2008, Proceedings of the National Academy of Sciences.

[15]  E. Waxman,et al.  Specificity and Regulation of Casein Kinase-Mediated Phosphorylation of &agr;-Synuclein , 2008, Journal of neuropathology and experimental neurology.

[16]  R. Hauser,et al.  Lewy body–like pathology in long-term embryonic nigral transplants in Parkinson's disease , 2008, Nature Medicine.

[17]  Elisabet Englund,et al.  Lewy bodies in grafted neurons in subjects with Parkinson's disease suggest host-to-graft disease propagation , 2008, Nature Medicine.

[18]  J. Kordower,et al.  Age-associated increases of α-synuclein in monkeys and humans are associated with nigrostriatal dopamine depletion: Is this the target for Parkinson's disease? , 2007, Neurobiology of Disease.

[19]  Jordi Soriano,et al.  Percolation in living neural networks. , 2006, Physical review letters.

[20]  Thomas C. Südhof,et al.  α-Synuclein Cooperates with CSPα in Preventing Neurodegeneration , 2005, Cell.

[21]  C. Cotman,et al.  A microfluidic culture platform for CNS axonal injury, regeneration and transport , 2005, Nature Methods.

[22]  Olga Pletnikova,et al.  Aggregation promoting C-terminal truncation of alpha-synuclein is a normal cellular process and is enhanced by the familial Parkinson's disease-linked mutations. , 2005, Proceedings of the National Academy of Sciences of the United States of America.

[23]  T. Südhof,et al.  Alpha-synuclein cooperates with CSPalpha in preventing neurodegeneration. , 2005, Cell.

[24]  H. Braak,et al.  Neuropathological stageing of Alzheimer-related changes , 2004, Acta Neuropathologica.

[25]  Janel O. Johnson,et al.  α-Synuclein Locus Triplication Causes Parkinson's Disease , 2003, Science.

[26]  John Q. Trojanowski,et al.  Ubiquitination of α-Synuclein Is Not Required for Formation of Pathological Inclusions in α-Synucleinopathies , 2003 .

[27]  P. Axelsen,et al.  Role of α-Synuclein Carboxy-Terminus on Fibril Formation in Vitro† , 2003 .

[28]  H. Braak,et al.  Staging of brain pathology related to sporadic Parkinson’s disease , 2003, Neurobiology of Aging.

[29]  P. Lansbury,et al.  The N-Terminal Repeat Domain of α-Synuclein Inhibits β-Sheet and Amyloid Fibril Formation† , 2003 .

[30]  J. Trojanowski,et al.  Ubiquitination of alpha-synuclein is not required for formation of pathological inclusions in alpha-synucleinopathies. , 2003, The American journal of pathology.

[31]  A. Singleton,et al.  alpha-Synuclein locus triplication causes Parkinson's disease. , 2003, Science.

[32]  P. Lansbury,et al.  The N-terminal repeat domain of alpha-synuclein inhibits beta-sheet and amyloid fibril formation. , 2003, Biochemistry.

[33]  J. Trojanowski,et al.  Role of alpha-synuclein carboxy-terminus on fibril formation in vitro. , 2003, Biochemistry.

[34]  E. Masliah,et al.  α-Synuclein is phosphorylated in synucleinopathy lesions , 2002, Nature Cell Biology.

[35]  E. Masliah,et al.  alpha-Synuclein is phosphorylated in synucleinopathy lesions. , 2002, Nature cell biology.

[36]  V. Uversky,et al.  Evidence for a Partially Folded Intermediate in α-Synuclein Fibril Formation* , 2001, The Journal of Biological Chemistry.

[37]  J Q Trojanowski,et al.  A Hydrophobic Stretch of 12 Amino Acid Residues in the Middle of α-Synuclein Is Essential for Filament Assembly* , 2001, The Journal of Biological Chemistry.

[38]  A. Dehejia,et al.  Human and mouse alpha-synuclein genes: comparative genomic sequence analysis and identification of a novel gene regulatory element. , 2001, Genome research.

[39]  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.

[40]  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.

[41]  L. Serpell,et al.  Fiber diffraction of synthetic alpha-synuclein filaments shows amyloid-like cross-beta conformation. , 2000, Proceedings of the National Academy of Sciences of the United States of America.

[42]  J. Trojanowski,et al.  A panel of epitope‐specific antibodies detects protein domains distributed throughout human α‐synuclein in lewy bodies of Parkinson's disease , 2000, Journal of neuroscience research.

[43]  Heidi Phillips,et al.  Mice Lacking α-Synuclein Display Functional Deficits in the Nigrostriatal Dopamine System , 2000, Neuron.

[44]  P. Lansbury,et al.  Acceleration of oligomerization, not fibrillization, is a shared property of both alpha-synuclein mutations linked to early-onset Parkinson's disease: implications for pathogenesis and therapy. , 2000, Proceedings of the National Academy of Sciences of the United States of America.

[45]  D. Sulzer,et al.  Mice lacking alpha-synuclein display functional deficits in the nigrostriatal dopamine system. , 2000, Neuron.

[46]  M. Citron,et al.  alpha-synuclein fibrillogenesis is nucleation-dependent. Implications for the pathogenesis of Parkinson's disease. , 1999, The Journal of biological chemistry.

[47]  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.

[48]  J Q Trojanowski,et al.  Aggregation of alpha-synuclein in Lewy bodies of sporadic Parkinson's disease and dementia with Lewy bodies. , 1998, The American journal of pathology.

[49]  A. Kastin,et al.  Adsorptive endocytosis mediates the passage of HIV-1 across the blood-brain barrier: evidence for a post-internalization coreceptor. , 1998, Journal of cell science.

[50]  R A Crowther,et al.  Filamentous alpha-synuclein inclusions link multiple system atrophy with Parkinson's disease and dementia with Lewy bodies. , 1998, Neuroscience letters.

[51]  P. Lansbury,et al.  The core Alzheimer's peptide NAC forms amyloid fibrils which seed and are seeded by beta-amyloid: is NAC a common trigger or target in neurodegenerative disease? , 1995, Chemistry & biology.

[52]  M. Salcman,et al.  Transcytotic pathway for blood-borne protein through the blood-brain barrier. , 1988, Proceedings of the National Academy of Sciences of the United States of America.

[53]  S. Avrameas,et al.  DETECTION OF PLASMA MEMBRANE CARBOHYDRATES WITH LECTIN PEROXIDASE CONJUGATES , 1973, The Journal of cell biology.