Synaptic mitochondria are more susceptible to traumatic brain injury-induced oxidative damage and respiratory dysfunction than non-synaptic mitochondria: neuroprotective effects of cyclosporine a
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Therefore, as central mediators of the secondary injury cascade, mitochondria are promising therapeutic targets for prevention of cellular death and dysfunction after TBI. ... Synaptic mitochondria are considered essential for proper neurotransmission and synaptic plasticity,62–64 processes that are impaired after TBI.
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