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Knockout punch: cardiolipin oxidation in trauma

Nature Neuroscience volume 15, pages 1325–1327 (2012)Cite this article

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During brain injury, mechanical injuries to neural cells initiate an apoptotic cascade through cardiolipin oxidation. Mitochondrially targeted electron scavenger compounds block this process, suggesting new therapeutic avenues.

Traumatic brain injury (TBI) is a major global health burden that cuts across demographics. In North America and Europe alone, TBI may affect 3–4 million people annually, with a fatality rate of 3–6% and an even higher incidence of long-term disabilities1. Furthermore, those afflicted by TBI may sustain an increased lifelong risk of amyotrophic lateral sclerosis, Parkinson's disease, dementia, substance abuse and other psychiatric disorders1. TBI results from blows or jolts to the head, typically as a result of falls, contact sports, motor vehicle accidents or assaults, including those frequently experienced by soldiers in wartime (http://www.ninds.nih.gov/disorders/tbi/tbi.htm). If severe, the primary injury sets in motion a complex series of secondary detrimental molecular and cellular events that do further damage in neurons. In this issue of Nature Neuroscience, Ji et al.2 provide elegant evidence for mitochondrial oxidative stress–associated lipid dysregulation as a landmark event that determines the balance between survival and death of neurons after TBI and suggest a new therapeutic avenue.

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Figure 1: Blocking cardiolipin peroxidation during acute brain injury prevents apoptotic cell death.

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Authors and Affiliations

  1. Robin B. Chan and Gilbert Di Paolo are in the Department of Pathology and Cell Biology, Taub Institute for Research on Alzheimer's Disease and the Aging Brain, Columbia University Medical Center, New York, New York, USA.,

    Robin B Chan & Gilbert Di Paolo

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  1. Robin B Chan
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  2. Gilbert Di Paolo
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Correspondence to Gilbert Di Paolo.

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Chan, R., Di Paolo, G. Knockout punch: cardiolipin oxidation in trauma. Nat Neurosci 15, 1325–1327 (2012). https://doi.org/10.1038/nn.3222

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