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  • TREM2 and sTREM2 in Alzheimer’s disease: from mechanisms to . . .
    In amyloidosis mouse models, microglial activation follows a two-step process: an initial TREM2-independent phase characterized by the downregulation of homeostatic checkpoint genes and the upregulation of neurodegeneration-associated markers, followed by a TREM2-dependent phase essential for the induction of lipid metabolism and phagocytosis
  • TREM2-independent oligodendrocyte, astrocyte, and T cell . . .
    The effects of Trem2 disruption on tau pathology (in the absence of amyloid) vary in different studies, but amyloid-mediated exacerbation of tau pathology is further accelerated when Trem2 is absent from transgenic mouse models combining tau and amyloid aggregates (Bemiller et al , 2017; Lee et al , 2021; Leyns et al , 2017, 2019; Sayed et al
  • Elevating microglia TREM2 reduces amyloid seeding and . . .
    Here, by using microglia-specific inducible mouse models overexpressing human wild-type TREM2 (TREM2-WT) or R47H risk variant (TREM2-R47H), we show that TREM2-WT expression reduces amyloid deposition and neuritic dystrophy only during the early amyloid seeding stage, whereas TREM2-R47H exacerbates amyloid burden during the middle amyloid rapid
  • Transcriptome and proteome profiling reveals TREM2-dependent . . .
    Trem2-dependent regulation of genes expression and protein abundance in Aβ pathology A, Volcano plot illustrating DEGs when comparing the brain of App NL-G-F mice to that of App NL-G-F; Trem2 KO mice at 9 months of age (n = 3 per age group) Upregulated genes (FDR < 0 05) are represented as brown dots, and downregulated genes as navy dots)
  • Alzheimer’s disease modification mediated by bone marrow . . .
    Microglia and monocyte-derived macrophages (MDM) are key players in dealing with Alzheimer’s disease In amyloidosis mouse models, activation of microglia was found to be TREM2 dependent
  • New insights into the role of TREM2 in Alzheimer’s disease
    In AD, increased expression of TREM2 has been confirmed in patients [47, 57,58,59] and in mouse models of amyloid and tau pathology [45, 60,61,62,63] and seems to be associated with the recruitment of microglia to amyloid plaques [59, 64] Interestingly, aging is also a factor that increases TREM2 expression in both mice and humans [41, 60]
  • TREM2 is a receptor for β-amyloid which mediates microglial . . .
    Although a role for TREM2 in AD pathogenesis has been recently proposed, opposing effects on Aβ plaque deposition are observed with TREM2 deletion in differing AD models (Jay et al , 2015; Wang et al , 2015), which may be attributed to differences in genetic backgrounds, and or additional effects derived from APP PS1 overexpression (Cavanaugh





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