Fullerenols Prevent Neuron Death and Reduce Oxidative Stress in Huntington's Disease Model.

Huntington's disease (HD) is one of the human neurodegenerative diseases for which there is no effective treatment. Therefore, there is a strong demand for a novel neuroprotective agent that can alleviate its course. Fullerene derivatives are considered to be such agents; however, they need to be comprehensively investigated in model organisms.

Reduction of the α-synuclein expression promotes slowing down early neuropathology development in the model of Parkinson's disease.

Parkinson's disease (PD) is a neurodegenerative disease characterised by the formation of Lewy bodies and progressive loss of dopaminergic (DA) neurons in the substantia nigra. Lewy bodies mainly consist of α-synuclein, which plays a critical role in the pathophysiology of PD. The α-synuclein is encoded by the gene and is the first identified gene associated with hereditary PD.

The neuroprotective effect of fullerenols on a model of Parkinson's disease in Drosophila melanogaster.

Neuroprotective properties of fullerenols С(OH) and С(OH) have been shown in a Drosophila melanogaster model of Parkinson's Disease (PD). Fullerenols used in this work demonstrated negligible toxicity even at high concentrations as a result of a specifically developed manufacturing process. It has been shown that the drugs promote restoration of dopamine levels, reduce oxidative stress in transgenic flies expressing the human alpha-synuclein gene, prevent death of dopaminergic neurons in the brain and alleviate aggregation of alpha-synuclein.

In vitro and in vivo study of the toxicity of fullerenols С, С and СО obtained by an original two step method.

The toxicity of C(OH), C(OH), and CO(OH) fullerenols, prepared by a new original method, has been studied. This method allowed us to obtain high-purity fullerenols and eliminate the risks of synthesis of preparations containing insoluble fractions contaminated with impurities such as fullerenes not completely reacted by hydroxylation. All fullerenols were detected inside cultured cells.

Yeast red pigment modifies cloned human α-synuclein pathogenesis in Parkinson disease models in Saccharomyces cerevisiae and Drosophila melanogaster.

Recently, we identified the yeast red pigment (RP), a polymer of 1-(5'-Phosphoribosyl)-5-aminoimidazole, as a novel potential anti-amyloid agent for the therapy of neurodegenerative diseases. The purpose of this study was to further validate RP for treatment of Parkinson's disease (PD) and to clarify molecular mechanisms involved in the reduction of amyloid cytotoxicity. We investigated RP effects in vivo using Saccharomyces cerevisiae and Drosophila melanogaster PD models.