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Restraint stress increases neuroinflammation independently of amyloid ? levels in amyloid precursor protein/PS1 transgenic mice.
Nitration of tyrosine 10 critically enhances amyloid ? aggregation and plaque formation.
Selective loss of noradrenaline exacerbates early cognitive dysfunction and synaptic deficits in APP/PS1 mice.
PPAR?/RXR?-induced and CD36-mediated microglial amyloid-? phagocytosis results in cognitive improvement in amyloid precursor protein/presenilin 1 mice.
Induced LC degeneration in APP/PS1 transgenic mice accelerates early cerebral amyloidosis and cognitive deficits.
Imaging microglial activation and glucose consumption in a mouse model of Alzheimer's disease.
Mrp14 deficiency ameliorates amyloid ? burden by increasing microglial phagocytosis and modulation of amyloid precursor protein processing.
Ear2 deletion causes early memory and learning deficits in APP/PS1 mice.
Pan-PPAR modulation effectively protects APP/PS1 mice from amyloid deposition and cognitive deficits.
Intramembranous processing by ?-secretase regulates reverse signaling of ephrin-B2 in migration of microglia.
Microglia-derived ASC specks cross-seed amyloid-? in Alzheimer's disease.
Left frontal hub connectivity delays cognitive impairment in autosomal-dominant and sporadic Alzheimer's disease.