A metabolic perspective of late onset Alzheimer’s disease

Publication date: Available online 7 May 2019Source: Pharmacological ResearchAuthor(s): Miren Ettcheto, Amanda Cano, Oriol Busquets, Patricia Regina Manzine, Elena Sánchez-López, Rubén D. Castro-Torres, Carlos Beas-Zarate, Ester Verdaguer, María Luisa García, Jordi Olloquequi, Carme Auladell, Jaume Folch, Antoni CaminsAbstractAfter decades of research, the molecular neuropathology of Alzheimer’s disease (AD) is still one of the hot topics in biomedical sciences. Some studies suggest that soluble amyloid β (Aβ) oligomers act as causative agents in the development of AD and could be initiators of its complex neurodegenerative cascade. On the other hand, there is also evidence pointing to Aβ oligomers as mere aggravators, with an arguable role in the origin of the disease.In this line of research, the relative contribution of soluble Aβ oligomers to neuronal damage associated with metabolic disorders such as Type 2 Diabetes Mellitus (T2DM) and obesity is being actively investigated. Some authors have proposed the endoplasmic reticulum (ER) stress and the induction of the unfolded protein response (UPR) as important mechanisms leading to an increase in Aβ production and the activation of neuroinflammatory processes. Following this line of thought, these mechanisms could also cause cognitive impairment.The present review summarizes the current understanding on the neuropathological role of Aβ associated with metabolic alterations induced by an obesogenic high fat diet...
Source: Pharmacological Research - Category: Drugs & Pharmacology Source Type: research