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10.3390/ijms160510281 http://scihub22266oqcxt.onion/10.3390/ijms160510281 C4463646!4463646 !25955648     free     free     free Warning: file_get_contents(https://eutils.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&id=25955648 &cmd=llinks): Failed to open stream: HTTP request failed! 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Anti-NR2A/B Antibodies and Other Major Molecular Mechanisms in the Pathogenesis of Cognitive Dysfunction in Systemic Lupus Erythematosus |pdf=|usr=}}{{25955648 }} gab.com Text Anti-NR2A/B Antibodies and Other Major Molecular Mechanisms in the Pathogenesis of Cognitive Dysfunction in Systemic Lupus Erythematosus JO: Int J Mol Sci http://www.kidney.de/pget.php?&tw=1&pmid=25955648 #FOAvip Systemic lupus erythematosus (SLE) is an autoimmune disease that affects approximately 1-45.3 per 100,000 people worldwide. Although deaths as a result of active and renal diseases have been substantially declining amongst SLE patients, disease involving the central nervous system (CNS), collectively termed neuropsychiatric systemic lupus erythematosus (NPSLE), remains one of the important causes of death in these patients. Cognitive dysfunction is one of the most common manifestations of NPSLE, which comprises deficits in information-processing speed, attention and executive function, in conjunction with preservation of speech. Albeit a prevalent manifestation of NPSLE, the pathogenetic mechanisms of cognitive dysfunction remain unclear. Recent advances in genetic studies, molecular techniques, neuropathology, neuroimaging and cognitive science have gleaned valuable insights into the pathophysiology of lupus-related cognitive dysfunction. In recent years, a role for autoantibodies, molecular and cellular mechanisms in cognitive dysfunction, has been emerging, challenging our previous concept of the brain as an immune privileged site. This review will focus on the potential pathogenic factors involved in NPSLE, including anti-N-methyl-d-aspartate receptor subunit NR2A/B (anti-NR2A/B) antibodies, matrix metalloproteinase-9, neutrophil extracellular traps and pro-inflammatory mediators. Better understanding of these mechanistic processes will enhance identification of new therapeutic modalities to halt the progression of cognitive decline in SLE patients. Twit Text FOAVip Anti-NR2A/B Antibodies and Other Major Molecular Mechanisms in the Pathogenesis of Cognitive Dysfunction in Systemic Lupus Erythematosus ????Int J Mol Sci http://www.kidney.de/pget.php?&tw=1&pmid=25955648 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=25955648 #FOAvip English Wikipedia <ref>{{Cite pmid|25955648 }}</ref> Anti-NR2A/B Antibodies and Other Major Molecular Mechanisms in the Pathogenesis of Cognitive Dysfunction in Systemic Lupus Erythematosus #MMPMID25955648 Tay SH ; Mak A Int J Mol Sci 2015[May]; 16 (5 ): 10281-300 PMID25955648 show ga Systemic lupus erythematosus (SLE) is an autoimmune disease that affects approximately 1-45.3 per 100,000 people worldwide. Although deaths as a result of active and renal diseases have been substantially declining amongst SLE patients, disease involving the central nervous system (CNS), collectively termed neuropsychiatric systemic lupus erythematosus (NPSLE), remains one of the important causes of death in these patients. Cognitive dysfunction is one of the most common manifestations of NPSLE, which comprises deficits in information-processing speed, attention and executive function, in conjunction with preservation of speech. Albeit a prevalent manifestation of NPSLE, the pathogenetic mechanisms of cognitive dysfunction remain unclear. Recent advances in genetic studies, molecular techniques, neuropathology, neuroimaging and cognitive science have gleaned valuable insights into the pathophysiology of lupus-related cognitive dysfunction. In recent years, a role for autoantibodies, molecular and cellular mechanisms in cognitive dysfunction, has been emerging, challenging our previous concept of the brain as an immune privileged site. This review will focus on the potential pathogenic factors involved in NPSLE, including anti-N-methyl-d-aspartate receptor subunit NR2A/B (anti-NR2A/B) antibodies, matrix metalloproteinase-9, neutrophil extracellular traps and pro-inflammatory mediators. Better understanding of these mechanistic processes will enhance identification of new therapeutic modalities to halt the progression of cognitive decline in SLE patients. |Animals [MESH] |Autoantibodies/*immunology [MESH] |Cognition Disorders/etiology/*metabolism [MESH] |Extracellular Traps/metabolism [MESH] |Humans [MESH] |Inflammation Mediators/metabolism [MESH] |Lupus Erythematosus, Systemic/etiology/*metabolism/physiopathology [MESH] |Matrix Metalloproteinase 9/metabolism [MESH] |Neutrophils/metabolism [MESH]Anti-NR2A/B Antibodies and Other Major Molecular Mechanisms in the Pat(epmc).pdf DeepDyve Pubget Overpricing