It’s sad but true that most of us have witnessed the devastating impacts of neurodegenerative conditions such as Alzheimer’s Disease (AD) and Parkinson’s Disease (PD) on our friends and relatives. Generally associated with ageing and characterised by the progressive death of neurones (nerve cells) in the brain, these diseases gradually destroy basic human abilities such as thinking, remembering, speaking and moving.
Since the early findings about C60’s remarkable super-antioxidant and anti-ageing properties, researchers have been exploring the possibility that it may help to explain and possibly prevent the neural damage that underpins these aggressive diseases.
Not long after Kroto, Smalley and Curl’s Nobel Chemistry Prize-winning ‘buckyball’ research, Laura L Dugan and her ten-strong team published a paper in the Proceedings of the National Academy of Sciences (PNAS) which further strengthened the evidence that C60 is “a potent free radical scavenger” (ie a super-antioxidant). They also showed that it inhibited disease onset and lengthened life in mice affected by FALS (familial amyotrophic lateral sclerosis), a neurodegenerative motor disorder. The team concluded that their work around this exciting finding clearly demonstrated that C60 derivatives could protect neurones from damage in the living body. (Dugan, L. et al, 1997).
A few years later, Dugan’s work with a different team revealed that C60 derivatives protected neurones against biochemical, metabolic and bio-electrical damage. One particularly encouraging result was that when rats with Parkinson’s were treated for one month with a form of C60, they showed significant improvements in their symptoms. (Dugan, L. et al, 2001).
With C60’s neuroprotective properties evident in many studies (Vorobyov et al, 2015), the scientific and medical community continues to work on identifying and understanding the exact pathways and processes by which C60 is able to achieve these remarkable effects.
A good deal of research is now targeted at understanding how C60 affects neurones, and in 2016, Bednarikova et al explored the production of ‘amyloid plaques’. These plaques – sticky clumps which block the connections between neurones in the brain – are a hallmark of Alzheimer’s Disease. Crucially, the research results indicated that C60 could disrupt the formation of these plaques, and the team concluded that the C60 was therefore “a promising candidate as a therapeutic for Alzheimer’s Disease”.
The development of drugs and treatments is nearly always slow and laborious, but there is now global excitement in the medical and scientific community about C60 and its potential for preventing the devastation of Alzheimer’s, Parkinson’s and other neurodegenerative diseases.
Bednarokova Z, Huy PD, Mocanu MM, Fedunova D, Li MS & Gazova Z., Phys Chem Chem Phys 18(28), 2016, Fullerenol C60(OH)16 prevents amyloid fibrillization of AB40-in vitro and in silico approach
Dugan, LL, Lovett EG, Quick KL, Lotharius, J, Lin TT & O’Malley KL, Parkinsonism & Related Disorders (7), 2001, Fullerene-based antioxidants and neurodegenerative disorders
Dugan, LL, Turetsky, DM, Du C, Lobner D, Wheeler M, Almli CR, Shen CK, Luh TY, Choi DW, Lin TS, Proceedings of the National Academy of Sciences USA (94:22), 1997, Carboxyfullerenes as neuroprotective agents
Vorobyov V, Kaptsov V, Gorden R, Makarova R, Podolski I & Sengpiel F, Journal of Alzheimer’s Disease 45(1), 2015, Neuroprotective Effects of Hydrated Fullerene C-60: Cortical and Hippocampal EEG Interplay in an Amyloid-infused Rat Model of Alzheimer’s Disease