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10.1007/s11011-015-9667-z http://scihub22266oqcxt.onion/10.1007/s11011-015-9667-z C4800977!4800977!25862550     free     free     free Warning: file_get_contents(https://eutils.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&id=25862550&cmd=llinks): Failed to open stream: HTTP request failed! HTTP/1.1 429 Too Many Requests in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 215 Deprecated: Implicit conversion from float 209.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 209.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 209.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534       Metab+Brain+Dis 2015 ; 30 (5): 1275-8 Nephropedia Template TP {{tp|p=25862550|t=2015. Alterations in mitochondrial number and function in Alzheimer?s disease fibroblasts |pdf=|usr=}}{{25862550}} gab.com Text Alterations in mitochondrial number and function in Alzheimer s disease fibroblasts JO: Metab Brain Dis http://www.kidney.de/pget.php?&tw=1&pmid=25862550 #FOAvip Introduction: Mitochondrial dysfunction is observed in brains of Alzheimer?s Disease patients as well as many rodent model systems including those modeling mutations in preseinilin 1 (PSEN1). The aim of our study was to characterize mitochondrial function and number in fibroblasts from AD patients with PSEN1 mutations. Methods: We used biochemical assays, metabolic profiling and fluorescent labeling to assess mitochondrial number and function in fibroblasts from three AD patients compared to fibroblasts form three controls. Results: The mutant AD fibroblasts showed increased AB42 relative to controls. Reductions in ATP as well as basal and maximal mitochondrial respiration were also observed in these fibroblasts as was impaired spare mitochondrial respiratory capacity. Fluorescent staining and expression of genes encoding electron transport chain enzymes showed diminished mitochondrial content in the AD fibroblasts. Conclusions: This study demonstrates that mitochondrial dysfunction is observable in AD fibroblasts and provides evidence that this model system could be useful as a tool to screen disease-modifying compounds. Twit Text FOAVip Alterations in mitochondrial number and function in Alzheimer s disease fibroblasts ????Metab Brain Dis http://www.kidney.de/pget.php?&tw=1&pmid=25862550 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=25862550 #FOAvip English Wikipedia <ref>{{Cite pmid|25862550}}</ref> Alterations in mitochondrial number and function in Alzheimer?s disease fibroblasts #MMPMID25862550 Gray NE; Quinn JF Metab Brain Dis 2015[Oct]; 30 (5): 1275-8 PMID25862550show ga Introduction: Mitochondrial dysfunction is observed in brains of Alzheimer?s Disease patients as well as many rodent model systems including those modeling mutations in preseinilin 1 (PSEN1). The aim of our study was to characterize mitochondrial function and number in fibroblasts from AD patients with PSEN1 mutations. Methods: We used biochemical assays, metabolic profiling and fluorescent labeling to assess mitochondrial number and function in fibroblasts from three AD patients compared to fibroblasts form three controls. Results: The mutant AD fibroblasts showed increased AB42 relative to controls. Reductions in ATP as well as basal and maximal mitochondrial respiration were also observed in these fibroblasts as was impaired spare mitochondrial respiratory capacity. Fluorescent staining and expression of genes encoding electron transport chain enzymes showed diminished mitochondrial content in the AD fibroblasts. Conclusions: This study demonstrates that mitochondrial dysfunction is observable in AD fibroblasts and provides evidence that this model system could be useful as a tool to screen disease-modifying compounds. äAlterations in mitochondrial number and function in Alzheimer?s diseas(epmc).pdf DeepDyve Pubget Overpricing