TTR and Alzheimer disease: The glycation of abnormal accumulating proteins (i.e., amyloid beta, tau, prions, and transthyretin) in brains of patients with neurodegenerative diseases is supposed to be associated with crosslinking formation, leading to more stable protein aggregates and then exacerbating their neurotoxicity [30,31]; accordingly, the positive modulation of AGEs-targeting detoxifying systems, such as GLO1, has been demonstrated to contrast cognitive decline in a mouse model of Alzheimer’s disease (AD) [32].