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10.1002/jnr.23753 http://scihub22266oqcxt.onion/10.1002/jnr.23753 C5027974!5027974!27638588     free     free     free Warning: file_get_contents(https://eutils.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&id=27638588&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 Warning: imagejpeg(C:\Inetpub\vhosts\kidney.de\httpdocs\phplern\27638588.jpg): Failed to open stream: No such file or directory in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 117       J+Neurosci+Res 2016 ; 94 (11): 1031-6 Nephropedia Template TP {{tp|p=27638588|t=2016. SYNAPTIC FAILURE: THE ACHILLES TENDON OF SPHINGOLIPIDOSES |pdf=|usr=}}{{27638588}} gab.com Text SYNAPTIC FAILURE: THE ACHILLES TENDON OF SPHINGOLIPIDOSES JO: J Neurosci Res http://www.kidney.de/pget.php?&tw=1&pmid=27638588 #FOAvip The presence of life-threatening neurological symptoms in more than two thirds of lysosomal storage disease (LSDs) underlines how vulnerable the nervous system is to lysosomal failure. Neurological dysfunction in LSDs has historically been attributed to the disruption of neuronal and glial homeostasis due to the progressive jamming of the endosomal/lysosomal pathway. In neurons, a dysfunctional endosomal-lysosomal system can elicit dire consequences. Considering that neurons are largely postmitotic after birth, one can clearly understand that the inability of these cells to proliferate obliterates any possibility of diluting stored lysosomal material by means of cellular division. At its most advanced stage, this situation constitutes a terminal factor in neuronal life, resulting in cell death. However, synaptic deficits in the absence of classical neuronal cell death appear to be a common feature during the early stages in many LSDs, particularly sphingolipidoses. In essence, failure of synapses to convey their messages, even without major structural damage of the neuronal bodies, is a form of physiological death. This concept of dying back neuropathology is not only highly relevant for understanding the dynamics of the neurological decline in these diseases, but more importantly, it may constitute an important target for molecular therapies to protect perhaps the ?Achilles? point in the entire physiological architecture of brain and avoid an irreversible journey to neuronal demise. Twit Text FOAVip SYNAPTIC FAILURE: THE ACHILLES TENDON OF SPHINGOLIPIDOSES ????J Neurosci Res http://www.kidney.de/pget.php?&tw=1&pmid=27638588 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=27638588 #FOAvip English Wikipedia <ref>{{Cite pmid|27638588}}</ref> SYNAPTIC FAILURE: THE ACHILLES TENDON OF SPHINGOLIPIDOSES #MMPMID27638588 Cantuti-Castelvetri L; Bongarzone ER J Neurosci Res 2016[Nov]; 94 (11): 1031-6 PMID27638588show ga The presence of life-threatening neurological symptoms in more than two thirds of lysosomal storage disease (LSDs) underlines how vulnerable the nervous system is to lysosomal failure. Neurological dysfunction in LSDs has historically been attributed to the disruption of neuronal and glial homeostasis due to the progressive jamming of the endosomal/lysosomal pathway. In neurons, a dysfunctional endosomal-lysosomal system can elicit dire consequences. Considering that neurons are largely postmitotic after birth, one can clearly understand that the inability of these cells to proliferate obliterates any possibility of diluting stored lysosomal material by means of cellular division. At its most advanced stage, this situation constitutes a terminal factor in neuronal life, resulting in cell death. However, synaptic deficits in the absence of classical neuronal cell death appear to be a common feature during the early stages in many LSDs, particularly sphingolipidoses. In essence, failure of synapses to convey their messages, even without major structural damage of the neuronal bodies, is a form of physiological death. This concept of dying back neuropathology is not only highly relevant for understanding the dynamics of the neurological decline in these diseases, but more importantly, it may constitute an important target for molecular therapies to protect perhaps the ?Achilles? point in the entire physiological architecture of brain and avoid an irreversible journey to neuronal demise. äSYNAPTIC FAILURE: THE ACHILLES TENDON OF SPHINGOLIPIDOSES (epmc).pdf DeepDyve Pubget Overpricing