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10.1007/s00018-017-2463-7 http://scihub22266oqcxt.onion/10.1007/s00018-017-2463-7 C5425508!5425508!28197669     free     free     free Warning: file_get_contents(https://eutils.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&id=28197669&cmd=llinks): Failed to open stream: HTTP request failed! 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Clearance of cerebral A? in Alzheimer?s disease: reassessing the role of microglia and monocytes |pdf=|usr=}}{{28197669}} gab.com Text Clearance of cerebral A in Alzheimer s disease: reassessing the role of microglia and monocytes JO: Cell Mol Life Sci http://www.kidney.de/pget.php?&tw=1&pmid=28197669 #FOAvip Deficiency in cerebral amyloid ?-protein (A?) clearance is implicated in the pathogenesis of the common late-onset forms of Alzheimer?s disease (AD). Accumulation of misfolded A? in the brain is believed to be a net result of imbalance between its production and removal. This in turn may trigger neuroinflammation, progressive synaptic loss, and ultimately cognitive decline. Clearance of cerebral A? is a complex process mediated by various systems and cell types, including vascular transport across the blood?brain barrier, glymphatic drainage, and engulfment and degradation by resident microglia and infiltrating innate immune cells. Recent studies have highlighted a new, unexpected role for peripheral monocytes and macrophages in restricting cerebral A? fibrils, and possibly soluble oligomers. In AD transgenic (ADtg) mice, monocyte ablation or inhibition of their migration into the brain exacerbated A? pathology, while blood enrichment with monocytes and their increased recruitment to plaque lesion sites greatly diminished A? burden. Profound neuroprotective effects in ADtg mice were further achieved through increased cerebral recruitment of myelomonocytes overexpressing A?-degrading enzymes. This review summarizes the literature on cellular and molecular mechanisms of cerebral A? clearance with an emphasis on the role of peripheral monocytes and macrophages in A? removal. Twit Text FOAVip Clearance of cerebral A in Alzheimer s disease: reassessing the role of microglia and monocytes ????Cell Mol Life Sci http://www.kidney.de/pget.php?&tw=1&pmid=28197669 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=28197669 #FOAvip English Wikipedia <ref>{{Cite pmid|28197669}}</ref> Clearance of cerebral A? in Alzheimer?s disease: reassessing the role of microglia and monocytes #MMPMID28197669 Zuroff L; Daley D; Black KL; Koronyo-Hamaoui M Cell Mol Life Sci 2017[Jun]; 74 (12): 2167-201 PMID28197669show ga Deficiency in cerebral amyloid ?-protein (A?) clearance is implicated in the pathogenesis of the common late-onset forms of Alzheimer?s disease (AD). Accumulation of misfolded A? in the brain is believed to be a net result of imbalance between its production and removal. This in turn may trigger neuroinflammation, progressive synaptic loss, and ultimately cognitive decline. Clearance of cerebral A? is a complex process mediated by various systems and cell types, including vascular transport across the blood?brain barrier, glymphatic drainage, and engulfment and degradation by resident microglia and infiltrating innate immune cells. Recent studies have highlighted a new, unexpected role for peripheral monocytes and macrophages in restricting cerebral A? fibrils, and possibly soluble oligomers. In AD transgenic (ADtg) mice, monocyte ablation or inhibition of their migration into the brain exacerbated A? pathology, while blood enrichment with monocytes and their increased recruitment to plaque lesion sites greatly diminished A? burden. Profound neuroprotective effects in ADtg mice were further achieved through increased cerebral recruitment of myelomonocytes overexpressing A?-degrading enzymes. This review summarizes the literature on cellular and molecular mechanisms of cerebral A? clearance with an emphasis on the role of peripheral monocytes and macrophages in A? removal. �Clearance of cerebral A? in Alzheimer?s disease: reassessing the role (epmc).pdf DeepDyve Pubget Overpricing