Coinvolgimento del signaling β-adrenergico nella malattia di Alzheimer

Since 1907, when it was first described, Alzheimer’s disease (AD) has been one of the most studied diseases, in order to clarify its complex pathogenesis. Since AD will become increasingly widespread in the next decades, resulting in enormous health care costs. Since current treatments do not alter the course of the disease, acting temporarily on symptoms, it is essential to identify factors involved in the pathogenesis of disease. Among these, the β-adrenergic receptor (β-ARs) system might play a crucial role. The central noradrenergic system undergoes substantial changes in the course of AD and β-ARs have been implicated both in the formation of amyloid in brain and in amyloid-induced neurotoxicity. Furthermore, it has been shown that GRK2, a G protein-coupled receptor kinase which regulates receptor desensitization and downregolation, has been implicated in neuronal dysfunction caused by amyloid deposition. Finally, GRK2 levels in circulating lymphocytes, which correlate with cognitive impairment, may be used as a biomarker to monitor cognitive decline and response to therapy.