Accumulation of amyloid-β (Aβ) and Tau is an invariant feature of Alzheimer disease (AD).
The upstream role of Aβ accumulation in the disease pathogenesis is widely accepted, and
there is strong evidence showing that Aβ accumulation causes cognitive impairments.
However, the molecular mechanisms linking Aβ to cognitive decline remain to be elucidated.
Here we show that the buildup of Aβ increases the mammalian target of rapamycin (mTOR)
signaling, whereas decreasing mTOR signaling reduces Aβ levels, thereby highlighting an …