Leticia Forny-Germano

TL;DR: It is shown that serine phosphorylation of IRS-1 (IRS-1pSer) is common to both diseases, and establishes molecular links between the dysregulated insulin signaling in AD and diabetes.

TL;DR: FNDC5/irisin is placed as a novel agent capable of opposing synapse failure and memory impairment in AD, and restoration of its expression can ameliorate these phenotypes in rodent models.

TL;DR: Results reveal pathogenic mechanisms shared by AD and diabetes and establish that proinflammatory signaling mediates oligomer-induced IRS-1 inhibition and PKR-dependent synapse and memory loss.

TL;DR: Generation of a macaque model of AD that links Aβ oligomers to tau and synaptic pathology has the potential to greatly advance the understanding of mechanisms centrally implicated in AD pathogenesis.

TL;DR: It is shown that liraglutide prevented the loss of brain insulin receptors and synapses, and reversed memory impairment induced by AD‐linked amyloid‐β oligomers (AβOs) in mice, and indicated that GLP‐1 receptor activation may be harnessed to protect brain insulin receptor, synaptic, and tau pathology in AD.