The Role of mitochondrial dynamics and metabolism in cellular senescence.

Senescence is the unavoidable consequence of cumulative deterioration on biological units or individuals due to the progression of time. Incremental organic deterioration triggers the risk to develop serious neurological diseases such as Alzheimer or Parkinson disease. Due to the sustained augmentation of life expectancies worldwide, there is a concomitant increase in aging associated pathologies. As a consequence, it is critical to design strategies to guarantee health in this near future context of extended active life individuals.

Cellular aging is associated to certain molecular markers such as unusual telomere shortening and cumulative oxidative damage, a by-product of mitochondrial activity. The so-call progeroid syndromes, diseases associated with early onset aging, are considered natural models of accelerated senescence that may give clues to better understand normal aging. Among them, Down Syndrome (DS), caused by genomic unbalance (the presence of an extra copy of chromosome 21) is the most prevalent in humans. In our group we combine expertise in biochemistry, microscopy and molecular biology to better understand mitochondrial function, oxidative stress and cellular metabolism, in DS cells and equivalent mouse models. The achievement of these goals will allow the identification of relevant risk factors of aging and their potential as therapeutic targets





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Zamponi N, Zamponi E, Cannas S, Billoni O, Helguera P, and Chialvo D. 2017. Mitochondrial network complexity results from fission/fusion balance. Scientific Reports, In Press.

Coskun P, Helguera P, Nemati Z, Bohannan RC, Thomas J, Samuel SE, Argueta J, Doran E, Wallace DC, Lott IT, Busciglio J. 2016. Metabolic and Growth Rate Alterations in Lymphoblastic Cell Lines Discriminate Between Down Syndrome and Alzheimer’s Disease. J Alzheimers Dis. Nov 19;55(2):737-748.

Helguera P, Seiglie J, Rodriguez J, Hanna M, Helguera G and Busciglio J. 2013.

Adaptive downregulation of mitochondrial function in Down’s syndrome. Cell Metabolism, 17:132–140