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10.1002/jnr.23751 http://scihub22266oqcxt.onion/10.1002/jnr.23751 C5027968!5027968!27638614     free     free     free Warning: file_get_contents(https://eutils.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&id=27638614&cmd=llinks): Failed to open stream: HTTP request failed! 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Beyond Krabbe?s disease: the potential contribution of GALC deficiency to neuronal vulnerability in late onset synucleinopathies |pdf=|usr=}}{{27638614}} gab.com Text Beyond Krabbe s disease: the potential contribution of GALC deficiency to neuronal vulnerability in late onset synucleinopathies JO: J Neurosci Res http://www.kidney.de/pget.php?&tw=1&pmid=27638614 #FOAvip New insights into the pathophysiological mechanisms behind late onset neurodegenerative diseases have come from unexpected sources in recent years. Specifically, the group of inherited metabolic disorders known as lysosomal storage diseases that most commonly affect infants has been found to have surprising similarities with adult neurodegenerative disorders. Most notable has been the identification of Gaucher?s disease as a co-morbidity for Parkinson?s disease. Prompted by the recent identification of neuronal aggregates of ?-synuclein within another lysosomal storage disease, Krabbe?s disease, we propose the idea that a similar connection exists between adult synucleionopathies and Krabbe. Similarities between the two diseases, including the pattern of ?-synuclein aggregation in the brain of the Twitcher mouse (the authentic murine model of Krabbe?s disease), changes to lipid membrane dynamics, and possible dysfunction in synaptic function and macroautophagy underline a link between Krabbe?s disease and late onset synucleinopathies. Silent GALC mutations may even constitute a risk factor for the development of Parkinson?s in certain patients. More research is required to definitively identify any link and the validity of this hypothesis, but such connection would prove invaluable for developing novel therapeutic targets for Parkinson?s based on our current understanding of Krabbe?s disease and establishing new biomarkers for the identification of at-risk patients. Twit Text FOAVip Beyond Krabbe s disease: the potential contribution of GALC deficiency to neuronal vulnerability in late onset synucleinopathies ????J Neurosci Res http://www.kidney.de/pget.php?&tw=1&pmid=27638614 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=27638614 #FOAvip English Wikipedia <ref>{{Cite pmid|27638614}}</ref> Beyond Krabbe?s disease: the potential contribution of GALC deficiency to neuronal vulnerability in late onset synucleinopathies #MMPMID27638614 Marshall MS; Bongarzone ER J Neurosci Res 2016[Nov]; 94 (11): 1328-32 PMID27638614show ga New insights into the pathophysiological mechanisms behind late onset neurodegenerative diseases have come from unexpected sources in recent years. Specifically, the group of inherited metabolic disorders known as lysosomal storage diseases that most commonly affect infants has been found to have surprising similarities with adult neurodegenerative disorders. Most notable has been the identification of Gaucher?s disease as a co-morbidity for Parkinson?s disease. Prompted by the recent identification of neuronal aggregates of ?-synuclein within another lysosomal storage disease, Krabbe?s disease, we propose the idea that a similar connection exists between adult synucleionopathies and Krabbe. Similarities between the two diseases, including the pattern of ?-synuclein aggregation in the brain of the Twitcher mouse (the authentic murine model of Krabbe?s disease), changes to lipid membrane dynamics, and possible dysfunction in synaptic function and macroautophagy underline a link between Krabbe?s disease and late onset synucleinopathies. Silent GALC mutations may even constitute a risk factor for the development of Parkinson?s in certain patients. More research is required to definitively identify any link and the validity of this hypothesis, but such connection would prove invaluable for developing novel therapeutic targets for Parkinson?s based on our current understanding of Krabbe?s disease and establishing new biomarkers for the identification of at-risk patients. äBeyond Krabbe?s disease: the potential contribution of GALC deficiency(epmc).pdf DeepDyve Pubget Overpricing