038-22 – Assessing the Potential of Specific Therapeutic Drugs to Prevent 6-OHDA Induced Mitochondrial Damage and Apoptosis, in HeLa Cells

Parkinson’s disease is the leading neurodegenerative motor disorder worldwide. It results from the loss of specific neurons within the substantia nigra, yet the cause of this neuronal death is not fully understood. It is suspected that mitochondrial damage resulting from oxidative stress may lead to the cell death that elicits disease-associated bradykinesia and tremors. Through use of the mitochondria specific fluorescence stain TMRM, and Annexin V-FITC, a marker for cellular apoptosis, the efficacy of neuroprotective drugs has been explored in vitro for their potential to prevent mitochondrial dysfunction and cellular apoptosis in the presence of 6-hydroxydopamine, a commonly used neurotoxic chemical employed to selectively kill dopaminergic neurons. In the present study, four treatments for neurological conditions; citalopram and venlafaxine (used to treat depression and anxiety), memantine (given for Alzheimer’s disease) and riluzole (prescribed for amyotrophic lateral sclerosis); and an anti-inflammatory compound that is considered to be neuroprotective, curcumin (a derivative of turmeric), have been investigated. During live cell TMRM stained imaging, no drug compound used was able to prevent significant reduction of whole cell pixel density in the presence of 6-hydroxydopamine, suggesting no compound was neuroprotective against mitochondrial membrane damage. In fixed cell Annexin V-FITC stained samples, only memantine and venlafaxine did not produce a statistically significant increase in the presence of apoptotic cells, therefore suggesting further research into these compounds should be conducted to assess their neuroprotective potential in Parkinson’s disease.