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10.15252/embj.201694591 http://scihub22266oqcxt.onion/10.15252/embj.201694591 C5331757!5331757!28007893     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       EMBO+J 2017 ; 36 (5): 583-603 Nephropedia Template TP {{tp|p=28007893|t=2017. Young microglia restore amyloid plaque clearance of aged microglia |pdf=|usr=}}{{28007893}} gab.com Text Young microglia restore amyloid plaque clearance of aged microglia JO: EMBO J http://www.kidney.de/pget.php?&tw=1&pmid=28007893 #FOAvip Alzheimer?s disease (AD) is characterized by deposition of amyloid plaques, neurofibrillary tangles, and neuroinflammation. In order to study microglial contribution to amyloid plaque phagocytosis, we developed a novel ex vivo model by co?culturing organotypic brain slices from up to 20?month?old, amyloid?bearing AD mouse model (APPPS1) and young, neonatal wild?type (WT) mice. Surprisingly, co?culturing resulted in proliferation, recruitment, and clustering of old microglial cells around amyloid plaques and clearance of the plaque halo. Depletion of either old or young microglial cells prevented amyloid plaque clearance, indicating a synergistic effect of both populations. Exposing old microglial cells to conditioned media of young microglia or addition of granulocyte?macrophage colony?stimulating factor (GM?CSF) was sufficient to induce microglial proliferation and reduce amyloid plaque size. Our data suggest that microglial dysfunction in AD may be reversible and their phagocytic ability can be modulated to limit amyloid accumulation. This novel ex vivo model provides a valuable system for identification, screening, and testing of compounds aimed to therapeutically reinforce microglial phagocytosis. Twit Text FOAVip Young microglia restore amyloid plaque clearance of aged microglia ????EMBO J http://www.kidney.de/pget.php?&tw=1&pmid=28007893 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=28007893 #FOAvip English Wikipedia <ref>{{Cite pmid|28007893}}</ref> Young microglia restore amyloid plaque clearance of aged microglia #MMPMID28007893 Daria A; Colombo A; Llovera G; Hampel H; Willem M; Liesz A; Haass C; Tahirovic S EMBO J 2017[Mar]; 36 (5): 583-603 PMID28007893show ga Alzheimer?s disease (AD) is characterized by deposition of amyloid plaques, neurofibrillary tangles, and neuroinflammation. In order to study microglial contribution to amyloid plaque phagocytosis, we developed a novel ex vivo model by co?culturing organotypic brain slices from up to 20?month?old, amyloid?bearing AD mouse model (APPPS1) and young, neonatal wild?type (WT) mice. Surprisingly, co?culturing resulted in proliferation, recruitment, and clustering of old microglial cells around amyloid plaques and clearance of the plaque halo. Depletion of either old or young microglial cells prevented amyloid plaque clearance, indicating a synergistic effect of both populations. Exposing old microglial cells to conditioned media of young microglia or addition of granulocyte?macrophage colony?stimulating factor (GM?CSF) was sufficient to induce microglial proliferation and reduce amyloid plaque size. Our data suggest that microglial dysfunction in AD may be reversible and their phagocytic ability can be modulated to limit amyloid accumulation. This novel ex vivo model provides a valuable system for identification, screening, and testing of compounds aimed to therapeutically reinforce microglial phagocytosis. äYoung microglia restore amyloid plaque clearance of aged microglia (epmc).pdf DeepDyve Pubget Overpricing