Molecular Interplay between Mammalian Target of Rapamycin (mTOR), Amyloid-β, and Tau

摘要: Accumulation of amyloid-β (Aβ) and Tau is an invariant feature Alzheimer disease (AD). The upstream role Aβ accumulation in the pathogenesis widely accepted, there strong evidence showing that causes cognitive impairments. However, molecular mechanisms linking to decline remain be elucidated. Here we show buildup increases mammalian target rapamycin (mTOR) signaling, whereas decreasing mTOR signaling reduces levels, thereby highlighting interrelation between Aβ. pathway plays a central controlling protein homeostasis hence, neuronal functions; indeed regulates different forms learning memory. Using animal model AD, pharmacologically restoring with rescues deficits ameliorates pathology by increasing autophagy. Indeed, further autophagy induction necessary for rapamycin-mediated reduction levels. results presented here provide basis Aβ-induced and, moreover, rapamycin, FDA approved drug, improves memory pathology.