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Publication(s) | Type of study | Observations |
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Martin et al., 2008 [41] | Epidemiologic | No primary prevention of AD in an NSAID clinical trial; weak evidence for lower cognitive scores in naproxen users. |
Schenk et al., 1999 [45] | Mouse models | Aβ immunotherapy mitigates β-amyloid plaque pathology in PDAPP mice; phagocytic microglia colocalize with remaining Aβ deposits. |
Janus et al., 2000 [46]; Morgan et al., 2000 [47] | Mouse models | Behavioral impairment is reduced in Aβ-immunized TgCRND8 or APP/PS1 transgenic mice. |
Bard et al., 2000 [48] | Mouse models | Passive Aβ immunotherapy reduces cerebral amyloidosis in PDAPP mice. Remaining Aβ deposits colocalize with phagocytic microglia. |
Nicoll et al., 2003 [50] | Neuropathologic | AN-1792 Aβ immunotherapy results in striking reduction of amyloid pathology; remaining plaques colocalize with phagocytic microglia. |
Tan et al., 2000 [53] | Mouse models | Microglial CD45 negatively regulates microglial activation and opposes activated microglia-induced neuronal cell injury. |
Zhu et al., 2011 [54] | Mouse models | Microglial CD45 endorses phagocytosis and clearance of Aβ peptides and oligomers in PSAPP mice. |
Shaftel et al., 2007 [55] | Mouse models | Forcing brain IL-1β expression using IL-1β XAT transgenic mice activates “good” neuroinflammation and dramatically reduces amyloid plaque pathology in APP/PS1 mice. |
Chakrabarty et al., 2010 [56] | Mouse models | Forcing cerebral IFN-γ expression leads to profound neuroinflammation and clears amyloid plaques in TgCRND8 mice via microglial phagocytosis. |
Chakrabarty et al., 2010 [57] | Mouse models | Overexpressing brain IL-6 leads to massive gliosis and clears amyloid plaques in TgCRND8 mice via microglial phagocytosis. |
Chakrabarty et al., 2011 [58] | Mouse models | Increasing cerebral proinflammatory TNF-α expression clears amyloid pathology in TgCRND8 mice. |
DiCarlo et al., 2001 [59] | Mouse models | Acute intrahippocampal injection of LPS reduces Aβ plaque load in APP/PS1 transgenic mice. |
Wilcock et al., 2008 [60] | Mouse models | APPSwDI mice deficient in proinflammatory NOS2 have tau pathology and neuronal loss. |
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