Receptor for Advanced Glycation End Products and its Inflammatory Ligands are Upregulated in Amyotrophic Lateral Sclerosis
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Title
Receptor for Advanced Glycation End Products and its Inflammatory Ligands are Upregulated in Amyotrophic Lateral Sclerosis
Authors
Keywords
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Journal
Frontiers in Cellular Neuroscience
Volume 9, Issue -, Pages -
Publisher
Frontiers Media SA
Online
2015-12-22
DOI
10.3389/fncel.2015.00485
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Note: Only part of the references are listed.- Receptor for advanced glycation end-products in neurodegenerative diseases
- (2015) Judyta Juranek et al. REVIEWS IN THE NEUROSCIENCES
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- (2014) Dora Brites et al. Frontiers in Cellular Neuroscience
- Impaired slow axonal transport in diabetic peripheral nerve is independent of RAGE
- (2013) Judyta K. Juranek et al. EUROPEAN JOURNAL OF NEUROSCIENCE
- Receptor for advanced glycation end-products (RAGE) activates divergent signaling pathways to augment neurite outgrowth of adult sensory neurons
- (2013) Ali Saleh et al. EXPERIMENTAL NEUROLOGY
- Radical Roles for RAGE in the Pathogenesis of Oxidative Stress in Cardiovascular Diseases and Beyond
- (2013) Gurdip Daffu et al. INTERNATIONAL JOURNAL OF MOLECULAR SCIENCES
- Increased expression of the receptor for advanced glycation end-products in human peripheral neuropathies
- (2013) Judyta K. Juranek et al. Brain and Behavior
- S100B is increased in Parkinson’s disease and ablation protects against MPTP-induced toxicity through the RAGE and TNF-α pathway
- (2012) Kinnari Sathe et al. BRAIN
- Decreased plasma levels of soluble low density lipoprotein receptor-related protein-1 (sLRP) and the soluble form of the receptor for advanced glycation end products (sRAGE) in the clinical diagnosis of Alzheimer’s disease
- (2012) Furu Liang et al. JOURNAL OF CLINICAL NEUROSCIENCE
- Insights into the regulation of protein abundance from proteomic and transcriptomic analyses
- (2012) Christine Vogel et al. NATURE REVIEWS GENETICS
- Receptor for advanced glycation endproducts (RAGE) deficiency protects against MPTP toxicity
- (2012) Peter Teismann et al. NEUROBIOLOGY OF AGING
- Immunohistochemical localization of receptor for advanced glycation end (RAGE) products in the R6/2 mouse model of Huntington's disease
- (2011) Serenella Anzilotti et al. BRAIN RESEARCH BULLETIN
- High-mobility group box-1 impairs memory in mice through both toll-like receptor 4 and Receptor for Advanced Glycation End Products
- (2011) Andréy Mazarati et al. EXPERIMENTAL NEUROLOGY
- S100B Protein Stimulates Microglia Migration via RAGE-dependent Up-regulation of Chemokine Expression and Release
- (2011) Roberta Bianchi et al. JOURNAL OF BIOLOGICAL CHEMISTRY
- Image Analysis Tools for Evaluation of Microscopic Views of Immunohistochemically Stained Specimen in Medical Research–a Review
- (2011) Keerthana Prasad et al. JOURNAL OF MEDICAL SYSTEMS
- HMGB1 Acts on Microglia Mac1 to Mediate Chronic Neuroinflammation That Drives Progressive Neurodegeneration
- (2011) H.-M. Gao et al. JOURNAL OF NEUROSCIENCE
- The design and delivery of a thermally responsive peptide to inhibit S100B-mediated neurodegeneration
- (2011) S.M. Hearst et al. NEUROSCIENCE
- Toll-like receptor signaling in amyotrophic lateral sclerosis spinal cord tissue
- (2011) M. Casula et al. NEUROSCIENCE
- High-Mobility Group Box 1, Oxidative Stress, and Disease
- (2010) Daolin Tang et al. ANTIOXIDANTS & REDOX SIGNALING
- Association of the RAGE G82S polymorphism with Alzheimer’s disease
- (2010) Jonny Daborg et al. JOURNAL OF NEURAL TRANSMISSION
- CSF glial markers correlate with survival in amyotrophic lateral sclerosis
- (2010) S. D. Sussmuth et al. NEUROLOGY
- Exposure to CSF from sporadic amyotrophic lateral sclerosis patients induces morphological transformation of astroglia and enhances GFAP and S100β expression
- (2010) K. Shobha et al. NEUROSCIENCE LETTERS
- Receptor for advanced glycation end products is upregulated in optic neuropathy of Alzheimer’s disease
- (2009) Michelle Y. Wang et al. ACTA NEUROPATHOLOGICA
- Tempering the wrath of RAGE: An emerging therapeutic strategy against diabetic complications, neurodegeneration, and inflammation
- (2009) Shi Fang Yan et al. ANNALS OF MEDICINE
- RAGE regulates BACE1 and Aβ generation via NFAT1 activation in Alzheimer’s disease animal model
- (2009) H. J. Cho et al. FASEB JOURNAL
- RAGE-dependent signaling in microglia contributes to neuroinflammation, Aβ accumulation, and impaired learning/memory in a mouse model of Alzheimer’s disease
- (2009) Fang Fang et al. FASEB JOURNAL
- Association between the RAGE G82S polymorphism and Alzheimer’s disease
- (2009) Keshen Li et al. JOURNAL OF NEURAL TRANSMISSION
- Immunohistochemical analysis of human brain suggests pathological synergism of Alzheimer's disease and diabetes mellitus
- (2009) Tony Valente et al. NEUROBIOLOGY OF DISEASE
- Serum-soluble receptor for advanced glycation end product levels in patients with amyotrophic lateral sclerosis
- (2008) J. Iłżecka ACTA NEUROLOGICA SCANDINAVICA
- Pivotal Advance: HMGB1 expression in active lesions of human and experimental multiple sclerosis
- (2008) Åsa Andersson et al. JOURNAL OF LEUKOCYTE BIOLOGY
- S100B/RAGE-dependent activation of microglia via NF-κB and AP-1
- (2008) Roberta Bianchi et al. NEUROBIOLOGY OF AGING
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