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10.1038/jcbfm.2015.131 http://scihub22266oqcxt.onion/10.1038/jcbfm.2015.131 C4640326!4640326!26104292     free     free     free Deprecated: Implicit conversion from float 235.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 235.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 235.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 235.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534       J+Cereb+Blood+Flow+Metab 2015 ; 35 (9): 1406-10 Nephropedia Template TP {{tp|p=26104292|t=2015. Cerebral hypoperfusion: a new pathophysiologic concept in multiple sclerosis?|pdf=|usr=}}{{26104292}} gab.com Text Cerebral hypoperfusion: a new pathophysiologic concept in multiple sclerosis JO: J Cereb Blood Flow Metab http://www.kidney.de/pget.php?&tw=1&pmid=26104292 #FOAvip The exact pathogenesis of multiple sclerosis (MS) is incompletely understood. Although auto-immune responses have an important role in the development of hallmark focal demyelinating lesions, the underlying mechanism of axonal degeneration, the other key player in MS pathology and main determinant of long-term disability, remains unclear and corresponds poorly with inflammatory disease activity. Perfusion-weighted imaging studies have demonstrated that there is a widespread cerebral hypoperfusion in patients with MS, which is present from the early beginning to more advanced disease stages. This reduced cerebral blood flow (CBF) does not seems to be secondary to loss of axonal integrity with decreased metabolic demands but appears to be mediated by elevated levels of the potent vasospastic peptide endothelin-1 in the cerebral circulation. Evidence is evolving that cerebral hypoperfusion in MS is associated with chronic hypoxia, focal lesion formation, diffuse axonal degeneration, cognitive dysfunction, and fatigue. Restoring CBF may therefore emerge as a new therapeutic target in MS. Twit Text FOAVip Cerebral hypoperfusion: a new pathophysiologic concept in multiple sclerosis ????J Cereb Blood Flow Metab http://www.kidney.de/pget.php?&tw=1&pmid=26104292 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=26104292 #FOAvip English Wikipedia <ref>{{Cite pmid|26104292}}</ref> Cerebral hypoperfusion: a new pathophysiologic concept in multiple sclerosis? #MMPMID26104292 D'haeseleer M; Hostenbach S; Peeters I; Sankari SE; Nagels G; De Keyser J; D'hooghe MB J Cereb Blood Flow Metab 2015[Sep]; 35 (9): 1406-10 PMID26104292show ga The exact pathogenesis of multiple sclerosis (MS) is incompletely understood. Although auto-immune responses have an important role in the development of hallmark focal demyelinating lesions, the underlying mechanism of axonal degeneration, the other key player in MS pathology and main determinant of long-term disability, remains unclear and corresponds poorly with inflammatory disease activity. Perfusion-weighted imaging studies have demonstrated that there is a widespread cerebral hypoperfusion in patients with MS, which is present from the early beginning to more advanced disease stages. This reduced cerebral blood flow (CBF) does not seems to be secondary to loss of axonal integrity with decreased metabolic demands but appears to be mediated by elevated levels of the potent vasospastic peptide endothelin-1 in the cerebral circulation. Evidence is evolving that cerebral hypoperfusion in MS is associated with chronic hypoxia, focal lesion formation, diffuse axonal degeneration, cognitive dysfunction, and fatigue. Restoring CBF may therefore emerge as a new therapeutic target in MS. äCerebral hypoperfusion: a new pathophysiologic concept in multiple scl(epmc).pdf DeepDyve Pubget Overpricing