Massimo Tabaton of the University of Genoa, Italy, has been awarded this year's Alzheimer's Medal. The award is presented annually by the associate editors of the Journal of Alzheimer's Disease "for the best article published in the previous year's volume." The 2003 award is sponsored by Elan Pharmaceuticals. Dr. Tabaton received the recognition for his article, "Neuronal apoptosis is accompanied by amyloid-β-protein accumulation in the endoplasmic reticulum."

According to the journal's announcement of the award, "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 proapoptotic 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.

"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."—June Kinoshita


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Further Reading


  1. . Neuronal apoptosis is accompanied by amyloid beta-protein accumulation in the endoplasmic reticulum. J Alzheimers Dis. 2002 Feb;4(1):31-7. PubMed.
  2. . Heterogeneity of water-soluble amyloid beta-peptide in Alzheimer's disease and Down's syndrome brains. FEBS Lett. 1997 Jun 16;409(3):411-6. PubMed.
  3. . Amyloid-beta deposition in Alzheimer transgenic mice is associated with oxidative stress. J Neurochem. 1998 May;70(5):2212-5. PubMed.
  4. . Generation of an apoptotic intracellular peptide by gamma-secretase cleavage of Alzheimer's amyloid beta protein precursor. J Alzheimers Dis. 2000 Nov;2(3-4):289-301. PubMed.