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10.1182/blood-2016-11-753202 http://scihub22266oqcxt.onion/10.1182/blood-2016-11-753202 C5418637!5418637 !28242605     free     free     free Warning: file_get_contents(https://eutils.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&id=28242605 &cmd=llinks): Failed to open stream: HTTP request failed! 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Depletion of coagulation factor XII ameliorates brain pathology and cognitive impairment in Alzheimer disease mice |pdf=|usr=}}{{28242605 }} gab.com Text Depletion of coagulation factor XII ameliorates brain pathology and cognitive impairment in Alzheimer disease mice JO: Blood http://www.kidney.de/pget.php?&tw=1&pmid=28242605 #FOAvip Vascular abnormalities and inflammation are found in many Alzheimer disease (AD) patients, but whether these changes play a causative role in AD is not clear. The factor XII (FXII) -initiated contact system can trigger both vascular pathology and inflammation and is activated in AD patients and AD mice. We have investigated the role of the contact system in AD pathogenesis. Cleavage of high-molecular-weight kininogen (HK), a marker for activation of the inflammatory arm of the contact system, is increased in a mouse model of AD, and this cleavage is temporally correlated with the onset of brain inflammation. Depletion of FXII in AD mice inhibited HK cleavage in plasma and reduced neuroinflammation, fibrinogen deposition, and neurodegeneration in the brain. Moreover, FXII-depleted AD mice showed better cognitive function than untreated AD mice. These results indicate that FXII-mediated contact system activation contributes to AD pathogenesis, and therefore this system may offer novel targets for AD treatment. Twit Text FOAVip Depletion of coagulation factor XII ameliorates brain pathology and cognitive impairment in Alzheimer disease mice ????Blood http://www.kidney.de/pget.php?&tw=1&pmid=28242605 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=28242605 #FOAvip English Wikipedia <ref>{{Cite pmid|28242605 }}</ref> Depletion of coagulation factor XII ameliorates brain pathology and cognitive impairment in Alzheimer disease mice #MMPMID28242605 Chen ZL ; Revenko AS ; Singh P ; MacLeod AR ; Norris EH ; Strickland S Blood 2017[May]; 129 (18 ): 2547-2556 PMID28242605 show ga Vascular abnormalities and inflammation are found in many Alzheimer disease (AD) patients, but whether these changes play a causative role in AD is not clear. The factor XII (FXII) -initiated contact system can trigger both vascular pathology and inflammation and is activated in AD patients and AD mice. We have investigated the role of the contact system in AD pathogenesis. Cleavage of high-molecular-weight kininogen (HK), a marker for activation of the inflammatory arm of the contact system, is increased in a mouse model of AD, and this cleavage is temporally correlated with the onset of brain inflammation. Depletion of FXII in AD mice inhibited HK cleavage in plasma and reduced neuroinflammation, fibrinogen deposition, and neurodegeneration in the brain. Moreover, FXII-depleted AD mice showed better cognitive function than untreated AD mice. These results indicate that FXII-mediated contact system activation contributes to AD pathogenesis, and therefore this system may offer novel targets for AD treatment. |*Alzheimer Disease/blood/genetics/pathology/physiopathology [MESH] |*Brain/blood supply/metabolism/pathology/physiopathology [MESH] |*Cognitive Dysfunction/blood/genetics/pathology/physiopathology [MESH] |*Vascular Diseases/blood/genetics/pathology/physiopathology [MESH] |Animals [MESH] |Factor XII/*metabolism [MESH] |Kininogen, High-Molecular-Weight/blood [MESH] |Mice [MESH]Depletion of coagulation factor XII ameliorates brain pathology and co(epmc).pdf DeepDyve Pubget Overpricing