Use my Search Websuite to scan PubMed, PMCentral, Journal Hosts and Journal Archives, FullText. Kick-your-searchterm to multiple Engines kick-your-query now !>

A dictionary by aggregated review articles of nephrology, medicine and the life sciences Your one-stop-run pathway from word to the immediate pdf of peer-reviewed on-topic knowledge.

10.1002/jnr.23753 http://scihub22266oqcxt.onion/10.1002/jnr.23753 C5027974!5027974 !27638588     free     free     free 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\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 diseases (LSDs) underscores 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 resulting from the progressive jamming of the endosomal/lysosomal pathway. In neurons, a dysfunctional endosomal-lysosomal system can elicit dire consequences. Given 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 common features during the early stages in many LSDs, particularly sphingolipidoses. In essence, failure of synapses to convey their messages, even without major structural damage to the neuronal bodies, is a form of physiological death. This concept of dying-back neuropathology is highly relevant not only for understanding the dynamics of the neurological decline in these diseases, but, more importantly; it might also constitute an important target for molecular therapies to protect perhaps the "Achilles" point in the entire physiological architecture of the brain, thus avoiding an irreversible journey to neuronal demise. © 2016 Wiley Periodicals, Inc. 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 PMID27638588 show ga The presence of life-threatening neurological symptoms in more than two-thirds of lysosomal storage diseases (LSDs) underscores 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 resulting from the progressive jamming of the endosomal/lysosomal pathway. In neurons, a dysfunctional endosomal-lysosomal system can elicit dire consequences. Given 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 common features during the early stages in many LSDs, particularly sphingolipidoses. In essence, failure of synapses to convey their messages, even without major structural damage to the neuronal bodies, is a form of physiological death. This concept of dying-back neuropathology is highly relevant not only for understanding the dynamics of the neurological decline in these diseases, but, more importantly; it might also constitute an important target for molecular therapies to protect perhaps the "Achilles" point in the entire physiological architecture of the brain, thus avoiding an irreversible journey to neuronal demise. © 2016 Wiley Periodicals, Inc. |Animals [MESH] |Humans [MESH] |Models, Neurological [MESH] |Nervous System/*pathology [MESH] |Neurons/*pathology [MESH] |Sphingolipidoses/*pathology [MESH]Synaptic failure: The achilles tendon of sphingolipidoses (epmc).pdf DeepDyve Pubget Overpricing