Early start of progressive motor deficits in Line 61 α-synuclein transgenic mice

[1]  B. Hutter-Paier,et al.  Quantitative evaluation of orofacial motor function in mice: The pasta gnawing test, a voluntary and stress-free behavior test , 2016, Journal of Neuroscience Methods.

[2]  T. Heurtaux,et al.  Alpha-Synuclein Proteins Promote Pro-Inflammatory Cascades in Microglia: Stronger Effects of the A53T Mutant , 2016, PloS one.

[3]  E. Masliah,et al.  Lenalidomide reduces microglial activation and behavioral deficits in a transgenic model of Parkinson’s disease , 2015, Journal of Neuroinflammation.

[4]  F. Gage,et al.  Accumulation of oligomer-prone α-synuclein exacerbates synaptic and neuronal degeneration in vivo. , 2014, Brain : a journal of neurology.

[5]  M. Tansey,et al.  Neuroimmunological processes in Parkinson's disease and their relation to α-synuclein: microglia as the referee between neuronal processes and peripheral immunity , 2013, ASN neuro.

[6]  M. Chesselet,et al.  A Progressive Mouse Model of Parkinson’s Disease: The Thy1-aSyn (“Line 61”) Mice , 2012, Neurotherapeutics.

[7]  M. Chesselet,et al.  Analysis of striatal transcriptome in mice overexpressing human wild-type alpha-synuclein supports synaptic dysfunction and suggests mechanisms of neuroprotection for striatal neurons , 2011, Molecular Neurodegeneration.

[8]  Lawrence K Cormack,et al.  Assessing the role of dopamine in limb and cranial-oromotor control in a rat model of Parkinson's disease. , 2011, Journal of communication disorders.

[9]  M. Chesselet,et al.  Elevated tonic extracellular dopamine concentration and altered dopamine modulation of synaptic activity precede dopamine loss in the striatum of mice overexpressing human α‐synuclein , 2011, Journal of neuroscience research.

[10]  A. Sidhu,et al.  Tauopathic Changes in the Striatum of A53T α-Synuclein Mutant Mouse Model of Parkinson's Disease , 2011, PloS one.

[11]  E. Masliah,et al.  Oral N-Acetyl-Cysteine Attenuates Loss of Dopaminergic Terminals in α-Synuclein Overexpressing Mice , 2010, PloS one.

[12]  G. Miller,et al.  Behavioral phenotyping of mouse models of Parkinson's disease , 2010, Behavioural Brain Research.

[13]  M. Didriksen,et al.  Nest building performance following MPTP toxicity in mice , 2010, Behavioural Brain Research.

[14]  C. Cepeda,et al.  Alpha‐synuclein overexpression in mice alters synaptic communication in the corticostriatal pathway , 2009, Journal of neuroscience research.

[15]  M. Chesselet,et al.  Olfactory deficits in mice overexpressing human wildtype α‐synuclein , 2008, The European journal of neuroscience.

[16]  M. Chesselet,et al.  Abnormal colonic motility in mice overexpressing human wild-type &agr;-synuclein , 2008, Neuroreport.

[17]  M. Chesselet,et al.  Behavioral and histopathological consequences of paraquat intoxication in mice: Effects of α‐synuclein over‐expression , 2007, Synapse.

[18]  M. Chesselet,et al.  Behavioral effects of dopaminergic agonists in transgenic mice overexpressing human wildtype α-synuclein , 2006, Neuroscience.

[19]  R. Deacon.  Assessing nest building in mice , 2006, Nature Protocols.

[20]  K. Chaudhuri,et al.  Non-motor symptoms of Parkinson's disease: diagnosis and management , 2006, The Lancet Neurology.

[21]  Makoto Hashimoto,et al.  Neurological and Neurodegenerative Alterations in a Transgenic Mouse Model Expressing Human α-Synuclein under Oligodendrocyte Promoter: Implications for Multiple System Atrophy , 2005, The Journal of Neuroscience.

[22]  Jonathan Salcedo,et al.  Early and Progressive Sensorimotor Anomalies in Mice Overexpressing Wild-Type Human α-Synuclein , 2004, The Journal of Neuroscience.

[23]  Philippe Amouyel,et al.  α-synuclein locus duplication as a cause of familial Parkinson's disease , 2004, The Lancet.

[24]  A Dürr,et al.  Causal relation between α-synuclein locus duplication as a cause of familial Parkinson's disease , 2004, The Lancet.

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

[26]  Makoto Hashimoto,et al.  Transgenic Models of α‐Synuclein Pathology , 2003 .

[27]  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.

[28]  M. Bernardi,et al.  Effects of dopamine receptor antagonists on ongoing maternal behavior in rats , 2001, Pharmacology Biochemistry and Behavior.

[29]  L. Mucke,et al.  Dopaminergic loss and inclusion body formation in alpha-synuclein mice: implications for neurodegenerative disorders. , 2000, Science.

[30]  Robert L. Nussbaum,et al.  Mutation in the α-Synuclein Gene Identified in Families with Parkinson's Disease , 1997 .

[31]  N W DUNHAM,et al.  A note on a simple apparatus for detecting neurological deficit in rats and mice. , 1957, Journal of the American Pharmaceutical Association. American Pharmaceutical Association.

[32]  U Inserm,et al.  Causal relation between α synuclein gene duplication and familial Parkinson’s disease , 2005 .

[33]  M. Chesselet,et al.  Early and progressive sensorimotor anomalies in mice overexpressing wild-type human alpha-synuclein. , 2004, The Journal of neuroscience : the official journal of the Society for Neuroscience.

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

[35]  Makoto Hashimoto,et al.  Transgenic models of alpha-synuclein pathology: past, present, and future. , 2003, Annals of the New York Academy of Sciences.

[36]  R. Krüger,et al.  Ala30Pro mutation in the gene encoding alpha-synuclein in Parkinson's disease. , 1998, Nature genetics.

[37]  M G Spillantini,et al.  Alpha-synuclein in Lewy bodies. , 1997, Nature.

[38]  S E Ide,et al.  Mutation in the alpha-synuclein gene identified in families with Parkinson's disease. , 1997, Science.

[39]  R. Morris.  Thy-1 in developing nervous tissue. , 1985, Developmental neuroscience.

[40]  R. Morris.  Thy-1 in Developing Nervous Tissue (Part 1 of 2) , 1985 .