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Human Cu/Zn superoxide dismutase (SOD1) overexpression in mice causes mitochondrial vacuolization, axonal degeneration, and premature motoneuron death and accelerates motoneuron disease in mice expressing a familial amyotrophic lateral sclerosis mutant SOD1

Further experimentation involved Annexin V-fluorescein isothiocyanate/propidium iodide labeling and flow cytometric analysis, which suggested that AHK-Cu may have reduced the number of apoptotic DPCs, although this decrease was not statistically significant and thus not conclusively confirmed

Boyton et al