Abstract

The more common sporadic form of Alzheimer disease (SAD) and the metabolic syndrome are two highly prevalent pathological conditions of Western society due to incorrect diet, lifestyle, and vascular risk factors. Due to the increasing aging of populations, prevalence of AD in western industrialized countries will rise in the near future and, thus, new knowledge in the area of molecular biology and epigenetics will probably help to reverse the neurodegenerative process. Recent data have suggested metabolic syndrome as an independent risk factor for SAD. Furthermore, biological plausibility for this relationship has been framed within the metabolic cognitive syndrome concept, and some authors designed SAD as a brain diabetes or diabetes 3. Then, impaired signaling of insulin and from some adipokines involved in the so called adipoinsular axis, like leptin, ghrelin or amylin could give a metabolic basis to explain the origin and progression of SAD. Thus, dipokines like leptin, ghrelin and amylin, or their mimetic compounds, could contribuite to inhibit apoptosis and inflammation processes and, thus, generate protective responses in the nervous system. Moreover, these adipokines might promote the activation of a cognitive process which may retard or even partially reverse selected aspects of Alzheimer’s disease or ageing memory loss.

Keywords: Sporadic Alzheimer disease, adipokines, leptin, ghrelin, amylin, prolactin