Modelling α-Synuclein Aggregation and Neurodegeneration with Fibril Seeds in Primary Cultures of Mouse Dopaminergic Neurons
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J. Prehn | S. Hunot | P. Michel | O. Corti | R. Melki | Aurore Tourville | David Akbar
[1] L. Stefanis,et al. Endogenous Levels of Alpha-Synuclein Modulate Seeding and Aggregation in Cultured Cells , 2021, Molecular Neurobiology.
[2] J. Trojanowski,et al. Alpha-synuclein from patient Lewy bodies exhibits distinct pathological activity that can be propagated in vitro , 2021, Acta neuropathologica communications.
[3] D. Surmeier,et al. Disruption of mitochondrial complex I induces progressive parkinsonism , 2021, Nature.
[4] P. Michel,et al. The Chemically-Modified Tetracycline COL-3 and Its Parent Compound Doxycycline Prevent Microglial Inflammatory Responses by Reducing Glucose-Mediated Oxidative Stress , 2021, Cells.
[5] R. Fischer,et al. Phenotypic manifestation of α-synuclein strains derived from Parkinson’s disease and multiple system atrophy in human dopaminergic neurons , 2021, Nature Communications.
[6] C. Dobson,et al. The release of toxic oligomers from α-synuclein fibrils induces dysfunction in neuronal cells , 2021, Nature Communications.
[7] Gabriel Dias de Abreu,et al. Contributive Role of TNF-α to L-DOPA-Induced Dyskinesia in a Unilateral 6-OHDA Lesion Model of Parkinson’s Disease , 2021, Frontiers in Pharmacology.
[8] D. Surmeier,et al. Determinants of seeding and spreading of α-synuclein pathology in the brain , 2020, Science Advances.
[9] P. Gracia,et al. Multiplicity of α-Synuclein Aggregated Species and Their Possible Roles in Disease , 2020, International journal of molecular sciences.
[10] C. Follmer,et al. In Vitro Protective Action of Monomeric and Fibrillar α-Synuclein on Neuronal Cells Exposed to the Dopaminergic Toxins Salsolinol and DOPAL. , 2020, ACS chemical neuroscience.
[11] R. Moratalla,et al. Modeling Parkinson’s Disease With the Alpha-Synuclein Protein , 2020, Frontiers in Pharmacology.
[12] C. Sandi,et al. Pronounced α-Synuclein Pathology in a Seeding-Based Mouse Model Is Not Sufficient to Induce Mitochondrial Respiration Deficits in the Striatum and Amygdala , 2020, bioRxiv.
[13] J. Peyrin,et al. The expression level of alpha-synuclein in different neuronal populations is the primary determinant of its prion-like seeding , 2020, Scientific Reports.
[14] G. Knott,et al. The process of Lewy body formation, rather than simply α-synuclein fibrillization, is one of the major drivers of neurodegeneration , 2020, Proceedings of the National Academy of Sciences.
[15] A. Triller,et al. Differential Membrane Binding and Seeding of Distinct α-Synuclein Fibrillar Polymorphs , 2020, Biophysical journal.
[16] P. McLean,et al. Alpha-synuclein-induced mitochondrial dysfunction is mediated via a sirtuin 3-dependent pathway , 2020, Molecular Neurodegeneration.
[17] A. Raj,et al. Neural connectivity predicts spreading of alpha-synuclein pathology in fibril-injected mouse models: Involvement of retrograde and anterograde axonal propagation , 2019, Neurobiology of Disease.
[18] Joseph R. Patterson,et al. Time course and magnitude of alpha-synuclein inclusion formation and nigrostriatal degeneration in the rat model of synucleinopathy triggered by intrastriatal α-synuclein preformed fibrils , 2019, Neurobiology of Disease.
[19] K. Luk,et al. GDNF/RET signaling pathway activation eliminates Lewy Body pathology in midbrain dopamine neurons , 2019, bioRxiv.
[20] J. Kordower,et al. Spreading of alpha‐synuclein – relevant or epiphenomenon? , 2019, Journal of neurochemistry.
[21] P. Alam,et al. α‐synuclein oligomers and fibrils: a spectrum of species, a spectrum of toxicities , 2019, Journal of neurochemistry.
[22] D. Sulzer,et al. The physiological role of α‐synuclein and its relationship to Parkinson’s Disease , 2019, Journal of neurochemistry.
[23] W. V. van IJcken,et al. Lewy pathology in Parkinson’s disease consists of crowded organelles and lipid membranes , 2019, Nature Neuroscience.
[24] A. Perrier,et al. Propagation of α-Synuclein Strains within Human Reconstructed Neuronal Network , 2019, Stem cell reports.
[25] A. West,et al. Sensitivity and specificity of phospho‐Ser129 α‐synuclein monoclonal antibodies , 2018, The Journal of comparative neurology.
[26] L. Trudeau,et al. On Cell Loss and Selective Vulnerability of Neuronal Populations in Parkinson's Disease , 2018, Front. Neurol..
[27] Michael J. Devine,et al. α-synuclein oligomers interact with ATP synthase and open the permeability transition pore in Parkinson’s disease , 2018, Nature Communications.
[28] A. Brice,et al. Parkin deficiency modulates NLRP3 inflammasome activation by attenuating an A20‐dependent negative feedback loop , 2018, Glia.
[29] S. Xie,et al. Differential α-synuclein expression contributes to selective vulnerability of hippocampal neuron subpopulations to fibril-induced toxicity , 2018, Acta Neuropathologica.
[30] M. Feany,et al. α-synuclein Induces Mitochondrial Dysfunction through Spectrin and the Actin Cytoskeleton , 2018, Neuron.
[31] M. Goedert,et al. Neurodegeneration and the ordered assembly of α-synuclein , 2017, Cell and Tissue Research.
[32] Xiaomin Su,et al. Alpha-Synuclein mRNA Is Not Increased in Sporadic PD and Alpha-Synuclein Accumulation Does Not Block GDNF Signaling in Parkinson's Disease and Disease Models. , 2017, Molecular therapy : the journal of the American Society of Gene Therapy.
[33] J. Kordower,et al. Endocytic vesicle rupture is a conserved mechanism of cellular invasion by amyloid proteins , 2017, Acta Neuropathologica.
[34] J. Kordower,et al. Aging and Parkinson’s Disease: Different Sides of the Same Coin? , 2017, Movement disorders : official journal of the Movement Disorder Society.
[35] E. Hirsch,et al. The noble gas xenon provides protection and trophic stimulation to midbrain dopamine neurons , 2017, Journal of neurochemistry.
[36] S. Przedborski. The two-century journey of Parkinson disease research , 2017, Nature Reviews Neuroscience.
[37] V. Torre,et al. An improved method for growing neurons: Comparison with standard protocols , 2017, Journal of Neuroscience Methods.
[38] K. Thorn,et al. α-Synuclein Promotes Dilation of the Exocytotic Fusion Pore , 2017, Nature Neuroscience.
[39] A. Makky,et al. Nanomechanical properties of distinct fibrillar polymorphs of the protein α-synuclein , 2016, Scientific Reports.
[40] P. Michel,et al. A simplified approach for efficient isolation of functional microglial cells: Application for modeling neuroinflammatory responses in vitro , 2016, Glia.
[41] E. Hirsch,et al. Understanding Dopaminergic Cell Death Pathways in Parkinson Disease , 2016, Neuron.
[42] R. Melki,et al. Structural and functional properties of prefibrillar α-synuclein oligomers , 2016, Scientific Reports.
[43] D. Dickson,et al. Proaggregant nuclear factor(s) trigger rapid formation of α-synuclein aggregates in apoptotic neurons , 2016, Acta Neuropathologica.
[44] Philipp Selenko,et al. Structural disorder of monomeric α-synuclein persists in mammalian cells , 2016, Nature.
[45] B. Liss,et al. GDNF–Ret signaling in midbrain dopaminergic neurons and its implication for Parkinson disease , 2015, FEBS letters.
[46] M. Emborg,et al. α-Synuclein and nonhuman primate models of Parkinson's disease , 2015, Journal of Neuroscience Methods.
[47] H. Qing,et al. The phosphorylation of α‐synuclein: development and implication for the mechanism and therapy of the Parkinson's disease , 2015, Journal of neurochemistry.
[48] Stephanie M. Williams,et al. Toxic Oligomeric Alpha-Synuclein Variants Present in Human Parkinson’s Disease Brains Are Differentially Generated in Mammalian Cell Models , 2015, Biomolecules.
[49] D. Klenerman,et al. Aggregated α-synuclein and complex I deficiency: exploration of their relationship in differentiated neurons , 2015, Cell Death and Disease.
[50] V. Baekelandt,et al. Nigral overexpression of alpha-synuclein in the absence of parkin enhances alpha-synuclein phosphorylation but does not modulate dopaminergic neurodegeneration , 2015, Molecular Neurodegeneration.
[51] K. Gamble,et al. Formation of α-synuclein Lewy neurite–like aggregates in axons impedes the transport of distinct endosomes , 2014, Molecular biology of the cell.
[52] P. Greengard,et al. Molecular determinants of selective dopaminergic vulnerability in Parkinson’s disease: an update , 2014, Front. Neuroanat..
[53] A. Schapira,et al. Targeting mitochondria for neuroprotection in Parkinson disease. , 2014, JAMA neurology.
[54] E. Hirsch,et al. The Iron-Binding Protein Lactoferrin Protects Vulnerable Dopamine Neurons from Degeneration by Preserving Mitochondrial Calcium Homeostasis , 2013, Molecular Pharmacology.
[55] Richard Wade-Martins,et al. Deficits in dopaminergic transmission precede neuron loss and dysfunction in a new Parkinson model , 2013, Proceedings of the National Academy of Sciences.
[56] P. Baas,et al. Mitotic Motors Coregulate Microtubule Patterns in Axons and Dendrites , 2012, The Journal of Neuroscience.
[57] K. Kirkegaard,et al. Neuron‐to‐neuron transmission of α‐synuclein fibrils through axonal transport , 2012, Annals of neurology.
[58] Johannes E. Schindelin,et al. Fiji: an open-source platform for biological-image analysis , 2012, Nature Methods.
[59] R. R. Reijo Pera,et al. Modeling Parkinson’s Disease Using Induced Pluripotent Stem Cells , 2012, Current Neurology and Neuroscience Reports.
[60] Tanja Waldmann,et al. Rapid, complete and large‐scale generation of post‐mitotic neurons from the human LUHMES cell line , 2011, Journal of neurochemistry.
[61] A. Brice,et al. What genetics tells us about the causes and mechanisms of Parkinson's disease. , 2011, Physiological reviews.
[62] Yusuke Nakamura,et al. Genome-wide association study identifies common variants at four loci as genetic risk factors for Parkinson's disease , 2009, Nature Genetics.
[63] 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.
[64] Uwe Walter,et al. No Lewy pathology in monkeys with over 10 years of severe MPTP Parkinsonism , 2009, Movement disorders : official journal of the Movement Disorder Society.
[65] Kostas Vekrellis,et al. Inducible over‐expression of wild type α‐synuclein in human neuronal cells leads to caspase‐dependent non‐apoptotic death , 2009, Journal of neurochemistry.
[66] E. Hirsch,et al. Paraxanthine, the Primary Metabolite of Caffeine, Provides Protection against Dopaminergic Cell Death via Stimulation of Ryanodine Receptor Channels , 2008, Molecular Pharmacology.
[67] Hitoshi Takahashi,et al. The Lewy body in Parkinson's disease: Molecules implicated in the formation and degradation of α‐synuclein aggregates , 2007, Neuropathology : official journal of the Japanese Society of Neuropathology.
[68] J. Mallet,et al. PA700, the regulatory complex of the 26S proteasome, interferes with α‐synuclein assembly , 2005 .
[69] A. R. Vancha,et al. Use of polyethyleneimine polymer in cell culture as attachment factor and lipofection enhancer , 2004, BMC biotechnology.
[70] D. Perl,et al. Lewy-body formation is an aggresome-related process: a hypothesis , 2004, The Lancet Neurology.
[71] J. Joseph,et al. α-Synuclein Up-regulation and Aggregation during MPP+-induced Apoptosis in Neuroblastoma Cells , 2004, Journal of Biological Chemistry.
[72] A. Lees,et al. Alteration in α‐synuclein mRNA expression in Parkinson's disease , 2004 .
[73] H. Braak,et al. Staging of brain pathology related to sporadic Parkinson’s disease , 2003, Neurobiology of Aging.
[74] D. Sulzer,et al. Methamphetamine-Induced Degeneration of Dopaminergic Neurons Involves Autophagy and Upregulation of Dopamine Synthesis , 2002, The Journal of Neuroscience.
[75] S. Shin,et al. Formation and Removal of α-Synuclein Aggregates in Cells Exposed to Mitochondrial Inhibitors* , 2002, The Journal of Biological Chemistry.
[76] E. Masliah,et al. α-Synuclein is phosphorylated in synucleinopathy lesions , 2002, Nature Cell Biology.
[77] R. Burke,et al. α‐Synuclein expression in substantia nigra and cortex in Parkinson's disease , 1999 .
[78] R. Crowther,et al. α-Synuclein in filamentous inclusions of Lewy bodies from Parkinson’s disease and dementia with Lewy bodies , 1998 .
[79] S. Minoshima,et al. Mutations in the parkin gene cause autosomal recessive juvenile parkinsonism , 1998, Nature.
[80] Y. Agid,et al. Rescue of Mesencephalic Dopamine Neurons by Anticancer Drug Cytosine Arabinoside , 1997, Journal of neurochemistry.
[81] J. Lile,et al. GDNF: a glial cell line-derived neurotrophic factor for midbrain dopaminergic neurons. , 1993, Science.
[82] F. Hefti,et al. Toxicity of 1‐Methyl‐4‐Phenylpyridinium for Rat Dopaminergic Neurons in Culture: Selectivity and Irreversibility , 1990, Journal of neurochemistry.
[83] P. Danias,et al. Mesencephalic Dopamine Neurons Become Less Sensitive to 1 ‐Methyl‐4‐Phenyl‐l,2,3,6‐Tetrahydropyridine Toxicity During Development In Vitro , 1989, Journal of neurochemistry.
[84] G. Banker. Trophic interactions between astroglial cells and hippocampal neurons in culture. , 1980, Science.
[85] Y Agid,et al. Relationship of aging to Parkinson's disease. , 1987, Advances in neurology.