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10.3390/ijms18020469 http://scihub22266oqcxt.onion/10.3390/ijms18020469 C5344001!5344001 !28241427     free     free     free Deprecated: Implicit conversion from float 211.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 211.6 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\28241427 .jpg): Failed to open stream: No such file or directory in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 117       Int+J+Mol+Sci 2017 ; 18 (2 ): ä Nephropedia Template TP {{tp|p=28241427 |t=2017. Potential Modes of Intercellular ?-Synuclein Transmission |pdf=|usr=}}{{28241427 }} gab.com Text Potential Modes of Intercellular -Synuclein Transmission JO: Int J Mol Sci http://www.kidney.de/pget.php?&tw=1&pmid=28241427 #FOAvip Intracellular aggregates of the ?-synuclein protein result in cell loss and dysfunction in Parkinson's disease and atypical Parkinsonism, such as multiple system atrophy and dementia with Lewy bodies. Each of these neurodegenerative conditions, known collectively as ?-synucleinopathies, may be characterized by a different suite of molecular triggers that initiate pathogenesis. The mechanisms whereby ?-synuclein aggregates mediate cytotoxicity also remain to be fully elucidated. However, recent studies have implicated the cell-to-cell spread of ?-synuclein as the major mode of disease propagation between brain regions during disease progression. Here, we review the current evidence for different modes of ?-synuclein cellular release, movement and uptake, including exocytosis, exosomes, tunneling nanotubes, glymphatic flow and endocytosis. A more detailed understanding of the major modes by which ?-synuclein pathology spreads throughout the brain may provide new targets for therapies that halt the progression of disease. Twit Text FOAVip Potential Modes of Intercellular -Synuclein Transmission ????Int J Mol Sci http://www.kidney.de/pget.php?&tw=1&pmid=28241427 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=28241427 #FOAvip English Wikipedia <ref>{{Cite pmid|28241427 }}</ref> Potential Modes of Intercellular ?-Synuclein Transmission #MMPMID28241427 Valdinocci D ; Radford RA ; Siow SM ; Chung RS ; Pountney DL Int J Mol Sci 2017[Feb]; 18 (2 ): ä PMID28241427 show ga Intracellular aggregates of the ?-synuclein protein result in cell loss and dysfunction in Parkinson's disease and atypical Parkinsonism, such as multiple system atrophy and dementia with Lewy bodies. Each of these neurodegenerative conditions, known collectively as ?-synucleinopathies, may be characterized by a different suite of molecular triggers that initiate pathogenesis. The mechanisms whereby ?-synuclein aggregates mediate cytotoxicity also remain to be fully elucidated. However, recent studies have implicated the cell-to-cell spread of ?-synuclein as the major mode of disease propagation between brain regions during disease progression. Here, we review the current evidence for different modes of ?-synuclein cellular release, movement and uptake, including exocytosis, exosomes, tunneling nanotubes, glymphatic flow and endocytosis. A more detailed understanding of the major modes by which ?-synuclein pathology spreads throughout the brain may provide new targets for therapies that halt the progression of disease. |*Models, Biological [MESH] |Animals [MESH] |Astrocytes/metabolism [MESH] |Cell Communication [MESH] |Exosomes/metabolism [MESH] |Extracellular Space/metabolism [MESH] |Humans [MESH] |Intracellular Space/*metabolism [MESH] |Lewy Bodies/metabolism [MESH] |Lewy Body Disease/metabolism/pathology [MESH] |Microglia/metabolism [MESH] |Multiple System Atrophy/metabolism/pathology [MESH] |Parkinson Disease/metabolism/pathology [MESH] |Protein Aggregation, Pathological [MESH] |Protein Binding [MESH] |Protein Transport [MESH]Potential Modes of Intercellular ?-Synuclein Transmission (epmc).pdf DeepDyve Pubget Overpricing