It would be very easy to feel intimidated by Dr Kerri Kinghorn (OA 1996). Not only is she an Associate Professor at University College London (UCL), where she leads a research group dedicated to finding a cure for Parkinson’s disease, but she is also a Consultant Neurologist at the National Hospital for Neurology and Neurosurgery in London. 

Versa spoke to Kerri about her research now, and her journey from St Albans School to studying Medicine at Gonville & Caius College, University of Cambridge, where she completed the MB/ PhD programme. 

Have you always loved science and what made you want to become a doctor?
I have always had a deep passion for science, which has been a driving force throughout my career. The combination of patient interaction and the potential for scientific discovery is what initially drew me to studying medicine. A medical career offers the unique privilege of applying scientific knowledge to real-world challenges, where the impact on individuals is both immediate and profound. It also provides the opportunity to engage in research, a critical aspect of advancing healthcare. 

How did you become interested in research? 
In my first few years of studying medicine, I became fascinated by how the brain functions at a cellular level, especially in neurodegenerative diseases like Parkinson’s and Alzheimer’s. Motivated by this interest, I enrolled in the MB/PhD programme midway through my clinical training. This programme offers a select group of students the opportunity to pursue a PhD alongside their medical studies. My research contributed to the discovery of previously unknown proteins that accumulate in the brains of individuals with Alzheimer’s disease. 

What attracted you to neurology?
Given my strong interest in neuroscience and neurodegenerative disorders such as Parkinson’s disease, pursuing a career in neurology felt like a natural fit (or perhaps a no-brainer!). Neurology is a complex and challenging field that focuses on diseases and conditions of the nervous system. One of its most appealing aspects is the potential for translational research, bridging the gap between laboratory science and clinical practice.

How did you combine research with medicine? 
After two years of clinical training in several London hospitals, I was fortunate to gain an academic post, which allowed me to balance my time between research and working in the hospital. I applied to two Professors at UCL: Sir John Hardy, a pioneering figure in Alzheimer’s and Parkinson’s genetics, and Dame Linda Partridge, an expert in using the fruit fly (Drosophila melanogaster) to model human disease. With the support of a research fellowship from a charity called The Wellcome Trust, I was able to split my time between their two world-renowned laboratories, developing novel fruit fly models of Parkinson’s disease. Many people are unfamiliar with the use of fruit flies in research and often wonder how such tiny insects can contribute to our understanding of Parkinson’s disease and similar disorders. Yet, these models have arguably - in many areas - provided greater insights into the cellular abnormalities underlying these conditions than traditional mouse models.

How did you reach your current role as an academic neurologist and what does it involve?
After 12 years of clinical training within the NHS, including five years dedicated to scientific research, I became a consultant neurologist in 2017. Shortly thereafter, I established my own research group at UCL. I now divide my work time between seeing patients in the clinic, leading my research group, and teaching. I run an undergraduate course at UCL on the genetics of neurological disease and I am also responsible for the smooth running of all research projects in my department as project tutor. 
Research in my group has led to many new insights into what goes wrong in the cell in Parkinson’s disease and related disorders. Indeed, one of our projects led to a new therapy for the treatment of a rare neurodegeneration condition caused by alterations in a gene called PLA2G6. Changes in this gene can cause Parkinson’s disease and are also linked to a devastating neurodegenerative condition in children known as infantile neuroaxonal dystrophy (INAD). 
Upon examining the brain cells of flies lacking the PLA2G6 gene, we found that their mitochondria - the energy-producing organelles in all cells - were damaged. Specifically, the lipids in their membranes were oxidized, impairing the function of these critical structures. Our research showed that a drug, RT001, could block this damage and reverse the disease in both flies and cells derived from patients. This drug was subsequently tested in clinical trials, where it significantly reduced mortality and morbidity in children with INAD. It was later licensed by the FDA and remains the only available treatment for the disease. 
Subsequently, one of the most fulfilling moments in my career came when I met the parents of children affected by INAD at a conference focused on this condition. Knowing that my work had contributed to the hope brought by treatments like RT001 was deeply gratifying. The next step is to investigate whether this drug could also benefit individuals with the more common neurodegenerative condition, Parkinson’s disease.

Some of your recent research has looked at the gut-brain axis. The idea of gut health as a factor in overall wellbeing is an area that is very popular at the moment, to the extent that the gut is being described as a second brain. As a neurologist, do you agree with this, and do you think we take gut health seriously enough?
The role of gut health in disease is an exciting and rapidly evolving area of research. In recent years, scientists have become increasingly interested in the gut-brain axis and its implications for various conditions, including Parkinson’s disease. It has long been suspected that gut health may influence the progression of Parkinson's, as the protein that accumulates in the brains of individuals with the disease - alpha-synuclein - often begins to build up in the gut wall before appearing in the brain. Additionally, the gut microbiome, which consists of billions of microbes living in our intestines, has garnered significant attention. Many of these microbes perform essential functions and help protect against disease.
In our Parkinson’s fly models, we observed significant alterations in the gut microbiome compared to healthy flies. Remarkably, we found that eliminating the gut microbiome with an antibiotic cocktail extended the lifespans of Parkinson’s flies, promoting health and even reducing their overactive immune responses. Additionally, modifying the gut microbiome had an impact on the brain, decreasing inflammation. 
This research highlights the critical connection between the gut and brain and has been further supported by an intriguing new study just published showing that people who took multiple courses of antibiotics had a moderately reduced risk of developing Parkinson’s disease. The challenge for scientists is now to determine whether altering the microbes in the gut could potentially reduce the risk of Parkinson’s disease or help alter the progression of the disease. 

What does success look like to you? 
Without a doubt, from a professional perspective, success would be prescribing the first disease-modifying drug to a newly diagnosed patient with Parkinson's disease in my clinic, knowing that my research team had contributed to its development.