Paula I. Moreira

TL;DR: The data show that although diabetes induces some alterations in brain mitochondrial activity, those alterations do not interfere significantly with mitochondria functional efficiency and insulin seems to prevent the decline in mitochondrial oxidative phosphorylation efficiency and avoids an increase in oxidative stress, improving or preserving the function of neurons under adverse conditions, such as Alzheimer's disease.

TL;DR: The involvement of ER stress in the pathogenesis of AD is discussed, focusing the processing and trafficking of the AD-related amyloid precursor protein (APP) during disease development.

TL;DR: Mechanistically speaking, an increasing body of evidence suggests that the detrimental effects of oxidative RNA damage to protein synthesis are attenuated, at least in part, by the existence of mechanisms that avoid the incorporation of the damaged ribonucleotides into the translational machinery.

TL;DR: Some of the recent developments on the common features between T2D and AD are reviewed, namely on insulin signaling and its participation in the regulation of amyloid β (Aβ) plaque and neurofibrillary tangle formation (the two major neuropathological hallmarks of AD).

TL;DR: Evidence for the protective effects of metformin against diabetes-associated complications mainly cerebral and vascular complications is presented and the few known side effects associated to this antidiabetic agent are described.