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Genes and dementia

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The final year research project allows neuroscience students at The University of Nottingham to delve deep with hands-on experience into their particular area of interest. Following my training in dementia research (https://idea.nottingham.ac.uk/blogs/posts/my-experience-dementia-research) I knew I wanted to continue exploring this subject more in my final year project. I started looking for a supervisor who could help me get closer to answering questions such as “How are neurodegenerative diseases coded in our genes and would it be possible to hack into that code and somehow control it?”.

After some research, I found out about a group run by Kevin Morgan, who is the Professor of Human Genomics and Molecular Genetics at the University. His pioneering work has helped to better understand how personal genetic make-up can influence the risk of developing Alzheimer’s disease, the most common cause of dementia. Prof Kevin was kind enough to agree to take me under his wing.

Although the exact number is difficult to estimate, each one of us has about 20,000 various genes. Those are instructions on how proteins are made and regulated in each cell in our body. Each gene can come in different flavours, so that same genes can slightly differ amongst people.

Based on large scale studies with thousands of participants, scientists now know that some genes can come in variations, and that some of these variants are more often seen in people with dementia. We call these variants associated with dementia genetic risk factors. My project focuses on what strength of influence those variants have when we add them up together, which allows us to see a cumulative effect (polygenic risk score), taking into account variations in almost each of 20,000 human genes. The higher polygenic risk score in an individual, the higher risk of developing Alzheimer’s disease. This scoring system has many potential applications, including in clinical trials that can enrol participants at higher risk.

Although Alzheimer’s disease has a strong genetic component, genetic risk factors are not usually sufficient to cause the disease. People with a high polygenic risk do not always develop the disease (and vice versa, people with a low genetic risk can still be diagnosed with dementia). Environmental factors, such as diet and exposure to toxins amongst others can all contribute to the likelihood of developing the disease. Understanding exactly how these impact an individual’s risk will be crucial to overcome dementia.

My final year project has provided me with great insight into why dementia can express itself so differently from person to person. Firstly, genetic make-up inherited from our parents is unique to each individual. Secondly, genes interact with environmental and lifestyle factors in yet not well understood way. This stresses why everyone should be treated with a personalised, individual-based approach.

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