Amyloid plaques in the brains are the pathological hallmark of Alzheimer's disease (AD).
Amyloid-β (Aβ), the central component of amyloid plaques, is generated from amyloid-β
protein precursor (AβPP), following β-and γ-secretase cleavage. The molecular mechanism
underlying the pathogenesis of AD is still unknown and there has been no effective
treatment for AD. Clinical data showed that brain cerebral perfusion of most AD patients was
reduced before memory and cognitive impairment incurred. Hypoxia is the direct …