Probing the molecular mechanisms of neuronal degeneration: importance of mitochondrial dysfunction and calcineurin activation View Full Text


Ontology type: schema:ScholarlyArticle     


Article Info

DATE

2008-08

AUTHORS

Hiroyuki Uchino, Yasuhiro Kuroda, Saori Morota, Go Hirabayashi, Nagao Ishii, Futoshi Shibasaki, Yukiho Ikeda, Magnus J. Hansson, Eskil Elmér

ABSTRACT

Cerebral injury is a critical aspect of the management of patients in intensive care. Pathological conditions induced by cerebral ischemia, hypoxia, head trauma, and seizure activity can result in marked residual impairment of cerebral function. We have investigated the potential mechanisms leading to neuronal cell death in pathological conditions, with the aim of discovering therapeutic targets and methods to minimize neuronal damage resulting from insults directed at the central nervous system (CNS). Over the years, deeper understanding of the mechanisms of neuronal cell death has indeed evolved, enabling clinical critical care management to salvage neurons that are at the brink of degeneration and to support recovery of brain function. However, no substantial breakthrough has been achieved in the quest to develop effective pharmacological neuroprotective therapy directed at tissues of the CNS. The current situation is unacceptable, and preservation of function and protection of the brain from terminal impairment will be a vital medical issue in the twenty-first century. To achieve this goal, it is critical to clarify the key mechanisms leading to neuronal cell death. Here, we discuss the importance of the calcineurin/immunophilin signal transduction pathway and mitochondrial involvement in the detrimental chain of events leading to neuronal degeneration. More... »

PAGES

253-262

References to SciGraph publications

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  • Identifiers

    URI

    http://scigraph.springernature.com/pub.10.1007/s00540-008-0617-3

    DOI

    http://dx.doi.org/10.1007/s00540-008-0617-3

    DIMENSIONS

    https://app.dimensions.ai/details/publication/pub.1014763810

    PUBMED

    https://www.ncbi.nlm.nih.gov/pubmed/18685932


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