A genome-wide gene-expression analysis and database in transgenic mice during development of amyloid or tau pathology.
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F. Edwards | J. Hardy | Sebastian Guelfi | J. Richardson | M. Matarin | D. Salih | Marina V. Yasvoina | D. Cummings | Wenfei Liu | M. A. Nahaboo Solim | T. Moens | Rocío Moreno Paublete | Shabinah S. Ali | M. Perona | R. Desai | Kenneth J. Smith | J. Latcham | M. Fulleylove | S. Guelfi | M. N. Nahaboo Solim | J. Hardy | J. Richardson
[1] J. DeFelipe,et al. The influence of phospho-tau on dendritic spines of cortical pyramidal neurons in patients with Alzheimer’s disease , 2013, Brain : a journal of neurology.
[2] E. Hol,et al. Cortical beta amyloid protein triggers an immune response, but no synaptic changes in the APPswe/PS1dE9 Alzheimer's disease mouse model , 2013, Neurobiology of Aging.
[3] A. Singleton,et al. TREM2 variants in Alzheimer's disease. , 2013, The New England journal of medicine.
[4] A. Hofman,et al. Variant of TREM2 associated with the risk of Alzheimer's disease. , 2013, The New England journal of medicine.
[5] C. Dalgard,et al. Controlled Cortical Impact and Craniotomy Induce Strikingly Similar Profiles of Inflammatory Gene Expression, but with Distinct Kinetics , 2012, Front. Neur..
[6] L. Ferrucci,et al. Correspondence between in vivo 11C-PiB-PET amyloid imaging and postmortem, region-matched assessment of plaques , 2012, Acta Neuropathologica.
[7] Stefan Platzer,et al. Small-Animal PET Imaging of Amyloid-Beta Plaques with [11C]PiB and Its Multi-Modal Validation in an APP/PS1 Mouse Model of Alzheimer's Disease , 2012, PloS one.
[8] A. Ramasamy,et al. Quality control parameters on a large dataset of regionally dissected human control brains for whole genome expression studies , 2011, Journal of neurochemistry.
[9] Daniel R. Salomon,et al. Strategies for aggregating gene expression data: The collapseRows R function , 2011, BMC Bioinformatics.
[10] J. Hardy,et al. Alzheimer's disease genetics: lessons to improve disease modelling. , 2011, Biochemical Society transactions.
[11] J. Richardson,et al. The pathology of APP transgenic mice: a model of Alzheimer's disease or simply overexpression of APP? , 2009, Histology and histopathology.
[12] I. Bechmann,et al. TREM2 is upregulated in amyloid plaque‐associated microglia in aged APP23 transgenic mice , 2008, Glia.
[13] Ajit Varki,et al. Human uniqueness: genome interactions with environment, behaviour and culture , 2008, Nature Reviews Genetics.
[14] Bin Zhang,et al. Defining clusters from a hierarchical cluster tree: the Dynamic Tree Cut package for R , 2008, Bioinform..
[15] J. Richardson,et al. Abeta deposition and related pathology in an APP x PS1 transgenic mouse model of Alzheimer's disease. , 2008, Histology and histopathology.
[16] M. Gadjeva,et al. C1q and its growing family. , 2007, Immunobiology.
[17] Andy M. Yip,et al. Gene network interconnectedness and the generalized topological overlap measure , 2007, BMC Bioinformatics.
[18] S. Horvath,et al. Conservation and evolution of gene coexpression networks in human and chimpanzee brains , 2006, Proceedings of the National Academy of Sciences.
[19] S. Horvath,et al. Analysis of oncogenic signaling networks in glioblastoma identifies ASPM as a molecular target , 2006, Proceedings of the National Academy of Sciences.
[20] D. Bozyczko‐Coyne,et al. Comparative analysis of cortical gene expression in mouse models of Alzheimer's disease , 2006, Neurobiology of Aging.
[21] Pablo Tamayo,et al. Gene set enrichment analysis: A knowledge-based approach for interpreting genome-wide expression profiles , 2005, Proceedings of the National Academy of Sciences of the United States of America.
[22] S. Horvath,et al. Statistical Applications in Genetics and Molecular Biology , 2011 .
[23] J. Quinn,et al. Gene expression profiles of transcripts in amyloid precursor protein transgenic mice: up-regulation of mitochondrial metabolism and apoptotic genes is an early cellular change in Alzheimer's disease. , 2004, Human molecular genetics.
[24] Dietmar Rudolf Thal,et al. Neurodegeneration in normal brain aging and disease. , 2004, Science of aging knowledge environment : SAGE KE.
[25] A. Barabasi,et al. Network biology: understanding the cell's functional organization , 2004, Nature Reviews Genetics.
[26] J. Barnes,et al. Ultrastructural and behavioural changes precede amyloid deposition in a transgenic model of Alzheimer’s disease , 2003, Neuroscience.
[27] J. Loring,et al. Selectively Reduced Expression of Synaptic Plasticity-Related Genes in Amyloid Precursor Protein + Presenilin-1 Transgenic Mice , 2003, The Journal of Neuroscience.
[28] Jeffrey A. Johnson,et al. Lack of Neurodegeneration in Transgenic Mice Overexpressing Mutant Amyloid Precursor Protein Is Associated with Increased Levels of Transthyretin and the Activation of Cell Survival Pathways , 2002, The Journal of Neuroscience.
[29] F. Speleman,et al. Accurate normalization of real-time quantitative RT-PCR data by geometric averaging of multiple internal control genes , 2002, Genome Biology.
[30] B. Strooper,et al. Presenilin-1 deficiency leads to loss of Cajal–Retzius neurons and cortical dysplasia similar to human type 2 lissencephaly , 1999, Current Biology.
[31] Ronald C. Petersen,et al. Association of missense and 5′-splice-site mutations in tau with the inherited dementia FTDP-17 , 1998, Nature.
[32] B. Hyman,et al. Microglial response to amyloid plaques in APPsw transgenic mice. , 1998, The American journal of pathology.
[33] B. Winblad,et al. A pathogenic mutation for probable Alzheimer's disease in the APP gene at the N–terminus of β–amyloid , 1992, Nature Genetics.