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10.1098/rsob.170216 http://scihub22266oqcxt.onion/10.1098/rsob.170216 C5830535!5830535 !29445033     free     free     free Warning: file_get_contents(https://eutils.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&id=29445033 &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 Warning: imagejpeg(C:\Inetpub\vhosts\kidney.de\httpdocs\phplern\29445033 .jpg): Failed to open stream: No such file or directory in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 117       Open+Biol 2018 ; 8 (2 ): ä Nephropedia Template TP {{tp|p=29445033 |t=2018. Rett syndrome: a neurological disorder with metabolic components |pdf=|usr=}}{{29445033 }} gab.com Text Rett syndrome: a neurological disorder with metabolic components JO: Open Biol http://www.kidney.de/pget.php?&tw=1&pmid=29445033 #FOAvip Rett syndrome (RTT) is a neurological disorder caused by mutations in the X-linked gene methyl-CpG-binding protein 2 (MECP2), a ubiquitously expressed transcriptional regulator. Despite remarkable scientific progress since its discovery, the mechanism by which MECP2 mutations cause RTT symptoms is largely unknown. Consequently, treatment options for patients are currently limited and centred on symptom relief. Thought to be an entirely neurological disorder, RTT research has focused on the role of MECP2 in the central nervous system. However, the variety of phenotypes identified in Mecp2 mutant mouse models and RTT patients implicate important roles for MeCP2 in peripheral systems. Here, we review the history of RTT, highlighting breakthroughs in the field that have led us to present day. We explore the current evidence supporting metabolic dysfunction as a component of RTT, presenting recent studies that have revealed perturbed lipid metabolism in the brain and peripheral tissues of mouse models and patients. Such findings may have an impact on the quality of life of RTT patients as both dietary and drug intervention can alter lipid metabolism. Ultimately, we conclude that a thorough knowledge of MeCP2's varied functional targets in the brain and body will be required to treat this complex syndrome. Twit Text FOAVip Rett syndrome: a neurological disorder with metabolic components ????Open Biol http://www.kidney.de/pget.php?&tw=1&pmid=29445033 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=29445033 #FOAvip English Wikipedia <ref>{{Cite pmid|29445033 }}</ref> Rett syndrome: a neurological disorder with metabolic components #MMPMID29445033 Kyle SM ; Vashi N ; Justice MJ Open Biol 2018[Feb]; 8 (2 ): ä PMID29445033 show ga Rett syndrome (RTT) is a neurological disorder caused by mutations in the X-linked gene methyl-CpG-binding protein 2 (MECP2), a ubiquitously expressed transcriptional regulator. Despite remarkable scientific progress since its discovery, the mechanism by which MECP2 mutations cause RTT symptoms is largely unknown. Consequently, treatment options for patients are currently limited and centred on symptom relief. Thought to be an entirely neurological disorder, RTT research has focused on the role of MECP2 in the central nervous system. However, the variety of phenotypes identified in Mecp2 mutant mouse models and RTT patients implicate important roles for MeCP2 in peripheral systems. Here, we review the history of RTT, highlighting breakthroughs in the field that have led us to present day. We explore the current evidence supporting metabolic dysfunction as a component of RTT, presenting recent studies that have revealed perturbed lipid metabolism in the brain and peripheral tissues of mouse models and patients. Such findings may have an impact on the quality of life of RTT patients as both dietary and drug intervention can alter lipid metabolism. Ultimately, we conclude that a thorough knowledge of MeCP2's varied functional targets in the brain and body will be required to treat this complex syndrome. |*Lipid Metabolism/drug effects [MESH] |Animals [MESH] |Brain/*metabolism [MESH] |Disease Models, Animal [MESH] |Disease Progression [MESH] |Drug Repositioning [MESH] |Female [MESH] |History, 20th Century [MESH] |Humans [MESH] |Lovastatin/pharmacology/therapeutic use [MESH] |Methyl-CpG-Binding Protein 2/*genetics [MESH] |Mice [MESH] |Mutation [MESH] |Quality of Life [MESH]Rett syndrome: a neurological disorder with metabolic components (epmc).pdf DeepDyve Pubget Overpricing