A research study published in Neuroscience in 1996 by Dugan et al. investigates the potential of buckminsterfullerenols, a type of water-soluble, polyhydroxylated C60 fullerene derivatives, to protect brain cells (neurons) from damage caused by excitotoxicity and apoptosis. The study demonstrates that these fullerene-based compounds act as powerful antioxidants, offering significant neuroprotection in lab-grown cortical neuron cultures.

In consumer-friendly terms, excitotoxicity occurs when neurons are overstimulated by chemicals like NMDA, AMPA, or kainate, leading to cell damage or death, often linked to conditions like stroke or brain injury. Apoptosis, on the other hand, is a programmed cell death process, which can be triggered by stressors like nutrient deprivation. The researchers tested two fullerenol compounds, C60(OH)12 and C60(OH)18-20 with hemiketal groups, and found they neutralized harmful free radicals (unstable molecules that damage cells) using a technique called electron paramagnetic spectroscopy.

The results were impressive: fullerenols reduced neuronal death by 80% after NMDA exposure, 65% after AMPA, and 50% after kainate. They also protected neurons from apoptosis caused by serum deprivation. Importantly, the study confirmed that fullerenols work as antioxidants, not by blocking NMDA or AMPA/kainate receptors, meaning they target oxidative stress—a key driver of both excitotoxic and apoptotic damage.

This research highlights the potential of buckminsterfullerenols as a new class of antioxidant compounds for protecting brain cells, with possible future applications in treating neurological disorders or brain injuries where oxidative stress plays a role. 

Link to research study

• Buckminsterfullerenol free radical scavengers reduce excitotoxic and apoptotic death of cultured cortical neurons