Mitochondria, calcium and cell death: a deadly triad in neurodegeneration.

Fulvio Celsi, Paola Pizzo, Marisa Brini, Sara Leo, Carmen Fotino, Paolo Pinton, Rosario Rizzuto

Journal: Biochimica et biophysica acta 2009;1787(5):335-44

PMID: 19268425

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Abstract

Mitochondrial Ca(2+) accumulation is a tightly controlled process, in turn regulating functions as diverse as aerobic metabolism and induction of cell death. The link between Ca(2+) (dys)regulation, mitochondria and cellular derangement is particularly evident in neurodegenerative disorders, in which genetic models and environmental factors allowed to identify common traits in the pathogenic routes. We will here summarize: i) the current view of mechanisms and functions of mitochondrial Ca(2+) homeostasis, ii) the basic principles of organelle Ca(2+) transport, iii) the role of Ca(2+) in neuronal cell death, and iv) the new information on the pathogenesis of Alzheimer's, Huntington's and Parkinson's diseases, highlighting the role of Ca(2+) and mitochondria.

Address: Department of Experimental and Diagnostic Medicine, Interdisciplinary Center for the Study of Inflammation, Italy.

DOI: 10.1016/j.bbabio.2009.02.021

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MeSH Terms: Alzheimer Disease, Calcium, Cell Death, Cytosol, Humans, Huntingtin Protein, Huntington Disease, Mitochondria, Mitochondrial Membranes, Mutation, Nerve Degeneration, Nerve Tissue Proteins, Nuclear Proteins, Parkinson Disease, Presenilins, Signal Transduction, Ubiquitin-Protein Ligases