摘要：SummaryAs an insidious and slowly progressive neurodegenerative disorder, Alzheimer’s disease (AD) uniquely develops in humans but fails in other species. Therefore, it has been challenged to rebuild human AD in animals, including in non-human primates. Here, we bilaterally delivered synthetic Aβ oligomers (AβOs) into the cerebral parenchyma of cynomolgus monkeys, which rapidly drove the formation of massive Aβ plaques and concomitant neurofibrillary tangles in the cynomolgus brain. The amyloid and tau pathology as well as their co-occurrence in AβO-monkeys were reminiscent of those in patients with AD. In addition, the activated astrocytes and microglia surrounding Aβ plaques indicated the triggered neuroinflammation. The degenerative neurons and synapses around Aβ plaques also emerged in cynomolgus brain. Together, soluble AβOs caused the cascade of pathologic events associated with AD in monkeys as occurred in patients at the early phase, which could facilitate the development of a promising animal model for human AD in non-human primates.Graphical abstractDisplay OmittedHighlights•The Aβ oligomers (AβOs) drive to develop massive Aβ plaque in the monkey brain•Neurofibrillary tangles form in multiple brain regions of AβO-monkeys•The co-occurrence of amyloid and tau pathology in AβO-monkeys as in patients with AD•The neuroinflammation and neurodegeneration are triggered in AβO-monkeysNeuroscience; Model organism; Synthetic biology
