Neuroprotective properties of transition metal dichalcogenide nanoflowers alleviate acute and chronic neurological conditions linked to mitochondrial dysfunction.

Mitochondrial dysfunction is an expected cause of etiology and progression in numerous human neurological pathologies, including stroke, Alzheimer's, and Parkinson's diseases. Therefore, a neuroprotective treatment is an urgent and unmet need. Transition metal dichalcogenide nanoflowers (TMD NFs) exhibit unique biological properties. However, neuroprotective properties of these nanomaterials remain poorly understood. In the current study, the biological effect of molybdenum disulfide and molybdenum diselenide TMD NFs on neurons and astrocytes was investigated. It was found that both nanomaterials lowered reactive oxygen species levels, reduced mitochondrial impairment, and increased mitochondrial biogenesis. Neuroprotective effects of both TMD NFs resulted from upregulation of the peroxisome proliferator-activated receptor gamma coactivator 1 alpha pathway, the biological system responsible for mitochondrial biogenesis. Furthermore, administration of TMD NFs to Caenorhabditis elegans extended lifespan of the nematodes. These results indicate that TMD NFs can be used as novel neuroprotective therapeutic agents against acute and chronic neurological condition linked to mitochondrial dysfunction.