Massimo Tabaton, M.D., is Professor of Neurology at the University of Genoa, Italy, where he directs a research group involved in studies of various aspects of Alzheimer's disease. In the early 1990s, Dr. Tabaton was the first to identify the molecular components of soluble amyloid-β (Aβ), an early, toxic, and diffusible oligomer, in the brain. Later on, he further characterized the type, binding, and accumulation of soluble Aβ in several pathologic conditions. Another focus of Dr. Tabaton's studies is the amyloidogenic processing of amyloid-β protein precursor (AβPP) following oxidative stress and other pro-apoptotic agents. He first described the overproduction of Aβ in neurons undergoing apoptosis and then identified the cellular mechanisms that underlie this event. His work has led to over 90 peer-reviewed publications in leading journals.

Importance of published article

This work published in the Journal of Alzheimer's Disease clarified an event that was previously revealed by Dr. Tabaton's group, i.e., the amyloidogenic processing of AβPP in the course of apoptosis. Indeed, it is known that Aβ can cause neuronal apoptosis, which, in turn, further fosters Aβ production. This toxic loop may be a critical event of AD pathogenesis. The present study published in JAD showed that apoptosis increases the intracellular content of Aβ, which accumulates in the endoplasmic reticulum, the site of production of the more toxic Aβ42 species. Moreover, this work demonstrated that the caspase cleavage in the C-terminus of AβPP, previously indicated as the key event of Aβ overproduction, is not associated with the increased Aβ production.