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10.1186/s40478-017-0429-5 http://scihub22266oqcxt.onion/10.1186/s40478-017-0429-5 C5379578!5379578 !28376923     free     free     free Deprecated: Implicit conversion from float 233.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 233.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 233.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 233.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 233.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 233.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 233.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 233.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 267.2 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 267.2 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 267.2 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 267.2 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Warning: imagejpeg(C:\Inetpub\vhosts\kidney.de\httpdocs\phplern\28376923 .jpg): Failed to open stream: No such file or directory in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 117       Acta+Neuropathol+Commun 2017 ; 5 (1 ): 26 Nephropedia Template TP {{tp|p=28376923 |t=2017. Taxifolin inhibits amyloid-? oligomer formation and fully restores vascular integrity and memory in cerebral amyloid angiopathy |pdf=|usr=}}{{28376923 }} gab.com Text Taxifolin inhibits amyloid- oligomer formation and fully restores vascular integrity and memory in cerebral amyloid angiopathy JO: Acta Neuropathol Commun http://www.kidney.de/pget.php?&tw=1&pmid=28376923 #FOAvip Cerebral amyloid angiopathy (CAA) induces various forms of cerebral infarcts and hemorrhages from vascular amyloid-? accumulation, resulting in acceleration of cognitive impairment, which is currently untreatable. Soluble amyloid-? protein likely impairs cerebrovascular integrity as well as cognitive function in early stage Alzheimer's disease. Taxifolin, a flavonol with strong anti-oxidative and anti-glycation activities, has been reported to disassemble amyloid-? in vitro but the in vivo relevance remains unknown. Here, we investigated whether taxifolin has therapeutic potential in attenuating CAA, hypothesizing that inhibiting amyloid-? assembly may facilitate its clearance through several elimination pathways. Vehicle- or taxifolin-treated Tg-SwDI mice (commonly used to model CAA) were used in this investigation. Cognitive and cerebrovascular function, as well as the solubility and oligomerization of brain amyloid-? proteins, were investigated. Spatial reference memory was assessed by water maze test. Cerebral blood flow was measured with laser speckle flowmetry and cerebrovascular reactivity evaluated by monitoring cerebral blood flow changes in response to hypercapnia. Significantly reduced cerebrovascular pan-amyloid-? and amyloid-?(1-40) accumulation was found in taxifolin-treated Tg-SwDI mice compared to vehicle-treated counterparts (n?=?5). Spatial reference memory was severely impaired in vehicle-treated Tg-SwDI mice but normalized after taxifolin treatment, with scoring similar to wild type mice (n?=?10-17). Furthermore, taxifolin completely restored decreased cerebral blood flow and cerebrovascular reactivity in Tg-SwDI mice (n?=?4-6). An in vitro thioflavin-T assay showed taxifolin treatment resulted in efficient inhibition of amyloid-?(1-40) assembly. In addition, a filter trap assay and ELISA showed Tg-SwDI mouse brain homogenates exhibited significantly reduced levels of amyloid-? oligomers in vivo after taxifolin treatment (n?=?4-5), suggesting the effects of taxifolin on CAA are attributable to the inhibition of amyloid-? oligomer formation. In conclusion, taxifolin prevents amyloid-? oligomer assembly and fully sustains cognitive and cerebrovascular function in a CAA model mice. Taxifolin thus appears a promising therapeutic approach for CAA. Twit Text FOAVip Taxifolin inhibits amyloid- oligomer formation and fully restores vascular integrity and memory in cerebral amyloid angiopathy ????Acta Neuropathol Commun http://www.kidney.de/pget.php?&tw=1&pmid=28376923 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=28376923 #FOAvip English Wikipedia <ref>{{Cite pmid|28376923 }}</ref> Taxifolin inhibits amyloid-? oligomer formation and fully restores vascular integrity and memory in cerebral amyloid angiopathy #MMPMID28376923 Saito S ; Yamamoto Y ; Maki T ; Hattori Y ; Ito H ; Mizuno K ; Harada-Shiba M ; Kalaria RN ; Fukushima M ; Takahashi R ; Ihara M Acta Neuropathol Commun 2017[Apr]; 5 (1 ): 26 PMID28376923 show ga Cerebral amyloid angiopathy (CAA) induces various forms of cerebral infarcts and hemorrhages from vascular amyloid-? accumulation, resulting in acceleration of cognitive impairment, which is currently untreatable. Soluble amyloid-? protein likely impairs cerebrovascular integrity as well as cognitive function in early stage Alzheimer's disease. Taxifolin, a flavonol with strong anti-oxidative and anti-glycation activities, has been reported to disassemble amyloid-? in vitro but the in vivo relevance remains unknown. Here, we investigated whether taxifolin has therapeutic potential in attenuating CAA, hypothesizing that inhibiting amyloid-? assembly may facilitate its clearance through several elimination pathways. Vehicle- or taxifolin-treated Tg-SwDI mice (commonly used to model CAA) were used in this investigation. Cognitive and cerebrovascular function, as well as the solubility and oligomerization of brain amyloid-? proteins, were investigated. Spatial reference memory was assessed by water maze test. Cerebral blood flow was measured with laser speckle flowmetry and cerebrovascular reactivity evaluated by monitoring cerebral blood flow changes in response to hypercapnia. Significantly reduced cerebrovascular pan-amyloid-? and amyloid-?(1-40) accumulation was found in taxifolin-treated Tg-SwDI mice compared to vehicle-treated counterparts (n?=?5). Spatial reference memory was severely impaired in vehicle-treated Tg-SwDI mice but normalized after taxifolin treatment, with scoring similar to wild type mice (n?=?10-17). Furthermore, taxifolin completely restored decreased cerebral blood flow and cerebrovascular reactivity in Tg-SwDI mice (n?=?4-6). An in vitro thioflavin-T assay showed taxifolin treatment resulted in efficient inhibition of amyloid-?(1-40) assembly. In addition, a filter trap assay and ELISA showed Tg-SwDI mouse brain homogenates exhibited significantly reduced levels of amyloid-? oligomers in vivo after taxifolin treatment (n?=?4-5), suggesting the effects of taxifolin on CAA are attributable to the inhibition of amyloid-? oligomer formation. In conclusion, taxifolin prevents amyloid-? oligomer assembly and fully sustains cognitive and cerebrovascular function in a CAA model mice. Taxifolin thus appears a promising therapeutic approach for CAA. |Amyloid beta-Peptides/antagonists & inhibitors/genetics/*metabolism [MESH] |Animals [MESH] |Cerebral Amyloid Angiopathy/*drug therapy/*metabolism/pathology/psychology [MESH] |Cerebrovascular Circulation/drug effects/physiology [MESH] |Disease Models, Animal [MESH] |Humans [MESH] |Male [MESH] |Memory Disorders/drug therapy/metabolism/pathology [MESH] |Mice, Inbred C57BL [MESH] |Mice, Transgenic [MESH] |Neuroprotective Agents/pharmacokinetics/*pharmacology [MESH] |Nootropic Agents/pharmacology [MESH] |Protein Aggregation, Pathological/drug therapy/metabolism/pathology/psychology [MESH] |Quercetin/*analogs & derivatives/pharmacokinetics/pharmacology [MESH] |Random Allocation [MESH] |Receptor for Advanced Glycation End Products/metabolism [MESH]Taxifolin inhibits amyloid-? oligomer formation and fully restores vas(epmc).pdf DeepDyve Pubget Overpricing