Title Progranulin Deficiency Promotes Circuit-Specific Synaptic Pruning by Microglia via Complement Activation Permalink

[1]  Shaomin Li,et al.  Complement C3-Deficient Mice Fail to Display Age-Related Hippocampal Decline , 2015, The Journal of Neuroscience.

[2]  Ying Sun,et al.  Prosaposin facilitates sortilin-independent lysosomal trafficking of progranulin , 2015, The Journal of cell biology.

[3]  T. Maniatis,et al.  An RNA-Sequencing Transcriptome and Splicing Database of Glia, Neurons, and Vascular Cells of the Cerebral Cortex , 2014, The Journal of Neuroscience.

[4]  G. Feng,et al.  Striatal circuits, habits, and implications for obsessive–compulsive disorder , 2014, Current Opinion in Neurobiology.

[5]  E. Kremmer,et al.  Common pathobiochemical hallmarks of progranulin-associated frontotemporal lobar degeneration and neuronal ceroid lipofuscinosis , 2014, Acta Neuropathologica.

[6]  J. Yates,et al.  Microglia Promote Learning-Dependent Synapse Formation through Brain-Derived Neurotrophic Factor , 2013, Cell.

[7]  T. Reinheckel,et al.  Intracellular Complement Activation Sustains T Cell Homeostasis and Mediates Effector Differentiation , 2013, Immunity.

[8]  E. Huang,et al.  A Dramatic Increase of C1q Protein in the CNS during Normal Aging , 2013, The Journal of Neuroscience.

[9]  K. Sims,et al.  Neuronal Ceroid Lipofuscinosis: Impact of Recent Genetic Advances and Expansion of the Clinicopathologic Spectrum , 2013, Current Neurology and Neuroscience Reports.

[10]  A. Aguzzi,et al.  Microglia: Scapegoat, Saboteur, or Something Else? , 2013, Science.

[11]  Thomas J. Davidson,et al.  Closed-loop optogenetic control of thalamus as a new tool to interrupt seizures after cortical injury , 2012, Nature Neuroscience.

[12]  Steven Finkbeiner,et al.  Progranulin deficiency promotes neuroinflammation and neuron loss following toxin-induced injury. , 2012, The Journal of clinical investigation.

[13]  Katherine R. Smith,et al.  Strikingly different clinicopathological phenotypes determined by progranulin-mutation dosage. , 2012, American journal of human genetics.

[14]  I. Komuro,et al.  Complement C1q Activates Canonical Wnt Signaling and Promotes Aging-Related Phenotypes , 2012, Cell.

[15]  Ben A. Barres,et al.  Microglia Sculpt Postnatal Neural Circuits in an Activity and Complement-Dependent Manner , 2012, Neuron.

[16]  Robert V Farese,et al.  Functional Genomic Analyses Identify Pathways Dysregulated by Progranulin Deficiency, Implicating Wnt Signaling , 2011, Neuron.

[17]  M. Giustetto,et al.  Synaptic Pruning by Microglia Is Necessary for Normal Brain Development , 2011, Science.

[18]  Kate Dimond Fitzgerald,et al.  Developmental alterations of frontal-striatal-thalamic connectivity in obsessive-compulsive disorder. , 2011, Journal of the American Academy of Child and Adolescent Psychiatry.

[19]  Nick C Fox,et al.  Sensitivity of revised diagnostic criteria for the behavioural variant of frontotemporal dementia. , 2011, Brain : a journal of neurology.

[20]  Karl Deisseroth,et al.  A new mode of corticothalamic transmission revealed in the Gria4−/− model of absence epilepsy , 2011, Nature Neuroscience.

[21]  D. di Bernardo,et al.  Transcriptional gene network inference from a massive dataset elucidates transcriptome organization and gene function , 2011, Nucleic acids research.

[22]  Robert V Farese,et al.  A neurodegenerative disease mutation that accelerates the clearance of apoptotic cells , 2011, Proceedings of the National Academy of Sciences of the United States of America.

[23]  C. Iadecola,et al.  Exaggerated inflammation, impaired host defense, and neuropathology in progranulin-deficient mice , 2010, The Journal of experimental medicine.

[24]  K. Sleegers,et al.  Serum biomarker for progranulin‐associated frontotemporal lobar degeneration , 2009, Annals of neurology.

[25]  V. Perry,et al.  Microglial physiology: unique stimuli, specialized responses. , 2009, Annual review of immunology.

[26]  R. Petersen,et al.  Plasma progranulin levels predict progranulin mutation status in frontotemporal dementia patients and asymptomatic family members , 2009, Brain : a journal of neurology.

[27]  Steve Horvath,et al.  WGCNA: an R package for weighted correlation network analysis , 2008, BMC Bioinformatics.

[28]  G. Binetti,et al.  Low plasma progranulin levels predict progranulin mutations in frontotemporal lobar degeneration , 2008, Neurology.

[29]  J. Cooper,et al.  Immune system irregularities in lysosomal storage disorders , 2008, Acta Neuropathologica.

[30]  John D. Lambris,et al.  The Classical Complement Cascade Mediates CNS Synapse Elimination , 2007, Cell.

[31]  C. Petersen.  The Functional Organization of the Barrel Cortex , 2007, Neuron.

[32]  C. Duijn,et al.  Null mutations in progranulin cause ubiquitin-positive frontotemporal dementia linked to chromosome 17q21 , 2006, Nature.

[33]  S. Melquist,et al.  Mutations in progranulin cause tau-negative frontotemporal dementia linked to chromosome 17 , 2006, Nature.

[34]  S. Horvath,et al.  Statistical Applications in Genetics and Molecular Biology , 2011 .

[35]  J R Hodges,et al.  The prevalence of frontotemporal dementia , 2002, Neurology.

[36]  M. Walport.  Complement. First of two parts. , 2001, The New England journal of medicine.

[37]  C. Cotman,et al.  Decreased levels of C1q in cerebrospinal fluid of living Alzheimer patients correlate with disease state , 1994, Neurobiology of Aging.

[38]  Y. Moriyama,et al.  Bafilomycin A1, a specific inhibitor of vacuolar-type H(+)-ATPase, inhibits acidification and protein degradation in lysosomes of cultured cells. , 1991, The Journal of biological chemistry.

[39]  P Siekevitz,et al.  Isolation and characterization of postsynaptic densities from various brain regions: enrichment of different types of postsynaptic densities , 1980, The Journal of cell biology.

[40]  M. Colombo,et al.  Assays to assess autophagy induction and fusion of autophagic vacuoles with a degradative compartment, using monodansylcadaverine (MDC) and DQ-BSA. , 2009, Methods in enzymology.