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10.1093/jnen/nlv028 http://scihub22266oqcxt.onion/10.1093/jnen/nlv028 C4934612!4934612!26888304     free     free     free Deprecated: Implicit conversion from float 231.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 231.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 231.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 231.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 231.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 231.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 231.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 265.2 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534       J+Neuropathol+Exp+Neurol 2016 ; 75 (3): 284-90 Nephropedia Template TP {{tp|p=26888304|t=2016. Neuropathology of Autosomal Dominant Alzheimer Disease in the National Alzheimer Coordinating Center Database |pdf=|usr=}}{{26888304}} gab.com Text Neuropathology of Autosomal Dominant Alzheimer Disease in the National Alzheimer Coordinating Center Database JO: J Neuropathol Exp Neurol http://www.kidney.de/pget.php?&tw=1&pmid=26888304 #FOAvip Alzheimer disease (AD) represents a genetically heterogeneous entity. To elucidate neuropathologic features of autosomal dominant AD ([ADAD] due to PSEN1, APP, or PSEN2 mutations), we compared hallmark AD pathologic findings in 60 cases of ADAD and 120 cases of sporadic AD matched for sex, race, ethnicity, and disease duration. Greater degrees of neuritic plaque and neurofibrillary tangle formation and cerebral amyloid angiopathy (CAA) were found in ADAD (p values < 0.01). Moderate to severe CAA was more prevalent in ADAD (63.3% vs. 39.2%, p?=?0.003), and persons with PSEN1 mutations beyond codon 200 had higher average Braak scores and severity and prevalence of CAA than those with mutations before codon 200. Lewy body pathology was less extensive in ADAD but was present in 27.1% of cases. We also describe a novel pathogenic PSEN1 mutation (P267A). The finding of more severe neurofibrillary pathology and CAA in ADAD, particularly in carriers of PSEN1 mutations beyond codon 200, warrants consideration when designing trials to treat or prevent ADAD. The finding of Lewy body pathology in a substantial minority of ADAD cases supports the assertion that development of Lewy bodies may be in part driven by abnormal ?-amyloid protein precursor processing. Twit Text FOAVip Neuropathology of Autosomal Dominant Alzheimer Disease in the National Alzheimer Coordinating Center Database ????J Neuropathol Exp Neurol http://www.kidney.de/pget.php?&tw=1&pmid=26888304 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=26888304 #FOAvip English Wikipedia <ref>{{Cite pmid|26888304}}</ref> Neuropathology of Autosomal Dominant Alzheimer Disease in the National Alzheimer Coordinating Center Database #MMPMID26888304 Ringman JM; Monsell S; Ng DW; Zhou Y; Nguyen A; Coppola G; Van Berlo V; Mendez MF; Tung S; Weintraub S; Mesulam MM; Bigio EH; Gitelman DR; Fisher-Hubbard AO; Albin RL; Vinters HV J Neuropathol Exp Neurol 2016[Mar]; 75 (3): 284-90 PMID26888304show ga Alzheimer disease (AD) represents a genetically heterogeneous entity. To elucidate neuropathologic features of autosomal dominant AD ([ADAD] due to PSEN1, APP, or PSEN2 mutations), we compared hallmark AD pathologic findings in 60 cases of ADAD and 120 cases of sporadic AD matched for sex, race, ethnicity, and disease duration. Greater degrees of neuritic plaque and neurofibrillary tangle formation and cerebral amyloid angiopathy (CAA) were found in ADAD (p values < 0.01). Moderate to severe CAA was more prevalent in ADAD (63.3% vs. 39.2%, p?=?0.003), and persons with PSEN1 mutations beyond codon 200 had higher average Braak scores and severity and prevalence of CAA than those with mutations before codon 200. Lewy body pathology was less extensive in ADAD but was present in 27.1% of cases. We also describe a novel pathogenic PSEN1 mutation (P267A). The finding of more severe neurofibrillary pathology and CAA in ADAD, particularly in carriers of PSEN1 mutations beyond codon 200, warrants consideration when designing trials to treat or prevent ADAD. The finding of Lewy body pathology in a substantial minority of ADAD cases supports the assertion that development of Lewy bodies may be in part driven by abnormal ?-amyloid protein precursor processing. äNeuropathology of Autosomal Dominant Alzheimer Disease in the National(epmc).pdf DeepDyve Pubget Overpricing