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News > Alumni > RESEARCH FOCUS: PARNAZ SHARIFI

RESEARCH FOCUS: PARNAZ SHARIFI

Parnaz Sharifi (2022, Medicine) discusses her cutting-edge research into the mechanisms underlying disorders like Parkinson's at Christ Church, where she is supported by the Pitts-Tucker Scholarship.
1 Jul 2024
Alumni
Parnaz Sharifi
Parnaz Sharifi

Thanks to generous support from Nick Pitts-Tucker (1968, Classics) and his family, Parnaz has a fully-funded DPhil place at Christ Church. The money given by the Pitts-Tucker family trust is matched by College funds. For information about other opportunities to fund research in this way, please contact: laura.jostins-dean@chch.ox.ac.uk.

Parnaz writes:

'My academic journey started at King's College London, where I studied Biomedical Sciences. Eager to specialise further, I pursued a Master’s degree in Translational Neuroscience at Imperial College London, where I was introduced to the pivotal work on cell vulnerability in diseases like Parkinson's. My interest for cutting-edge research led me to the Department of Physiology, Anatomy, and Genetics at Oxford University. Here, I was introduced to the innovative stem cell technologies that are revolutionizing our approach to understanding neurodegenerative disorders. I am privileged to be associated with Christ Church, where my work is generously funded by the Pitts-Tucker Scholarship. This support allows me to continue my research in an esteemed academic environment, and further understand the mechanisms underlying disorders like Parkinson's.

I am deeply interested in understanding why certain brain cells are more vulnerable to death and degeneration in Parkinson’s. This is a challenging research area, but I believe that investigating the sources of vulnerability in these cells and identifying the pathways that lead to their compromised state are crucial steps that can help us develop more effective therapies for people with Parkinson’s.

To delve deeper, my research focuses on the role of calcium and the channels that allow its entry into the cell. Calcium is a crucial ion that controls practically all vital processes within brain cells. Therefore, even the slightest imbalance in their levels can have significant toxic effects, leading to disease. In the lab, I study how calcium behaves using a special type of stem cell called human induced pluripotent stem cells (iPSCs). These iPSCs are made from ordinary skin or blood cells that are “reprogrammed” to return to a flexible state, where they can develop into any type of human cells. Specifically, I use these iPSCs to make and study dopaminergic neurons, the type of brain cells that are affected in Parkinson's. 

My data so far shows that as healthy neurons age, the number of calcium channels gradually increases. This finding is interesting, as it suggests a greater use of these channels, making the neurons more prone to degeneration, perhaps because they have to deal with more calcium coming into the cell. I'm now exploring this theory using electrical stimulation, a new technique I’m learning. 

These calcium channels also control a pattern of calcium movement called calcium oscillations. While these oscillations help the cells stay alive, they can also become harmful when triggers for Parkinson’s are present, causing cells to deteriorate and die. With an experimental setup I developed, I've not only observed these flickering calcium oscillations but have also demonstrated that certain calcium channels play a part in these harmful patterns. More importantly, I've found altered calcium behaviour in Parkinson’s patients compared to healthy individuals, including increased expression of certain channels and a different calcium oscillation pattern. These results are fascinating as disruptions in calcium levels have been shown to cause a range of cellular dysfunctions linked to disease. It's important to consider that the increased expression of certain channels might be behind these shifts in calcium activity seen in Parkinson’s, emphasising their role in cell vulnerability.

In terms of real-world applications, some of the drugs I use in my research are already FDA-approved for other conditions, highlighting the potential of repurposing existing drugs for PD treatment. Since many calcium channel blockers are safe and well-tolerated, exploring their potential protective effects against PD in both pre-clinical (human and animal models) and clinical trials is particularly promising.

Thank you to the Pitts-Tucker and JPT Family Trust for this incredible scholarship and for their generous support, enabling me to pursue my passion.'

 

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