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Alzheimer’s: calcium accumulation in mitochondria under the lens of UniPd and CNR

Alzheimer’s: calcium accumulation in mitochondria under the lens of UniPd and CNR

Exploring the mechanisms behind genetic forms of Alzheimer’s disease is the goal of a new all-Italian research project that received 360,000 euro in funding from Fondazione Telethon.


The project, proposed by Rosario Rizzuto from the University of Padua, will be carried out in partnership with the research team led by Tullio Pozzan, Department of Biomedical Sciences of the National Research Council. With a duration of three years, the research is one of the 17 projects submitted in 2016 and selected for funding by Telethon.

The researchers will investigate the possible role of calcium accumulation in mitochondria ‒ the power plants of the cell ‒ in the development of the most known and common type of dementia. In particular, the hypothesis is that this fact can contribute to the death of nerve cells, representing one of the mechanisms underlying genetic forms of Alzheimer’s.

A slowly progressive dementia caused by the death of nerve cells, Alzheimer’s disease involves loss of memory, loss of language, loss of autonomy and, finally, premature death of patients. The disease usually occurs sporadically, without any apparent specific cause, but in 1 case out of 10 it is caused by specific genetic defects. The mechanisms that trigger the death of nerve cells, however, are still unknown, although some hypotheses have been proposed.

The research activity focuses on Ca2+ ion accumulation in mitochondria: small structures found in all cells whose main function is to provide energy to the cell. The accumulation of this cation within the mitochondria is essential to maintain a high energy production but excessive levels can lead to cell death. Nerve cells, on the other hand, need a lot of energy to function, for which reason they are particularly susceptible to mitochondrial Ca2+ overload.

Hence the idea, behind the research, to understand if blocking mitochondrial Ca2+ overload can actually prevent the death of nerve cells in mice models affected by genetic forms of Alzheimer’s. This has not been directly explored yet because the molecular identity of the channels that transport Ca2+ into mitochondria has been revealed only recently by the same researcher proposing this project. If the hypothesis is correct, a cellular component will be identified that will become a novel target for the development of innovative drugs.

The research will be conducted by senior researchers Diego De Stefani, Anna Raffaello, Cristina Mammucari, Giorgia Pallafacchina of Rizzuto’s team and by Paola Pizzo, Cristina Fasolato, Diana Pendin and Elisa Greotti of Pozzan’s team. Thanks to Telethon funding, two other young researchers will be recruited who will contribute to the project.



Publication date 04/14/2017
Tag Health