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10.1007/s00401-018-1868-1 http://scihub22266oqcxt.onion/10.1007/s00401-018-1868-1 C6015111!6015111!29934873     free     free     free Deprecated: Implicit conversion from float 231.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 231.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 231.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 231.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 231.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534       Acta+Neuropathol 2018 ; 136 (1): 41-56 Nephropedia Template TP {{tp|p=29934873|t=2018. Alzheimer?s disease pathology propagation by exosomes containing toxic amyloid-beta oligomers |pdf=|usr=}}{{29934873}} gab.com Text Alzheimer s disease pathology propagation by exosomes containing toxic amyloid-beta oligomers JO: Acta Neuropathol http://www.kidney.de/pget.php?&tw=1&pmid=29934873 #FOAvip The gradual deterioration of cognitive functions in Alzheimer?s disease is paralleled by a hierarchical progression of amyloid-beta and tau brain pathology. Recent findings indicate that toxic oligomers of amyloid-beta may cause propagation of pathology in a prion-like manner, although the underlying mechanisms are incompletely understood. Here we show that small extracellular vesicles, exosomes, from Alzheimer patients? brains contain increased levels of amyloid-beta oligomers and can act as vehicles for the neuron-to-neuron transfer of such toxic species in recipient neurons in culture. Moreover, blocking the formation, secretion or uptake of exosomes was found to reduce both the spread of oligomers and the related toxicity. Taken together, our results imply that exosomes are centrally involved in Alzheimer?s disease and that they could serve as targets for development of new diagnostic and therapeutic principles.Electronic supplementary material: The online version of this article (10.1007/s00401-018-1868-1) contains supplementary material, which is available to authorized users. Twit Text FOAVip Alzheimer s disease pathology propagation by exosomes containing toxic amyloid-beta oligomers ????Acta Neuropathol http://www.kidney.de/pget.php?&tw=1&pmid=29934873 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=29934873 #FOAvip English Wikipedia <ref>{{Cite pmid|29934873}}</ref> Alzheimer?s disease pathology propagation by exosomes containing toxic amyloid-beta oligomers #MMPMID29934873 Sardar Sinha M; Ansell-Schultz A; Civitelli L; Hildesjö C; Larsson M; Lannfelt L; Ingelsson M; Hallbeck M Acta Neuropathol 2018[]; 136 (1): 41-56 PMID29934873show ga The gradual deterioration of cognitive functions in Alzheimer?s disease is paralleled by a hierarchical progression of amyloid-beta and tau brain pathology. Recent findings indicate that toxic oligomers of amyloid-beta may cause propagation of pathology in a prion-like manner, although the underlying mechanisms are incompletely understood. Here we show that small extracellular vesicles, exosomes, from Alzheimer patients? brains contain increased levels of amyloid-beta oligomers and can act as vehicles for the neuron-to-neuron transfer of such toxic species in recipient neurons in culture. Moreover, blocking the formation, secretion or uptake of exosomes was found to reduce both the spread of oligomers and the related toxicity. Taken together, our results imply that exosomes are centrally involved in Alzheimer?s disease and that they could serve as targets for development of new diagnostic and therapeutic principles.Electronic supplementary material: The online version of this article (10.1007/s00401-018-1868-1) contains supplementary material, which is available to authorized users. äAlzheimer?s disease pathology propagation by exosomes containing toxic(epmc).pdf DeepDyve Pubget Overpricing