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I'm Cautiously Optimistic a Treatment Which Could Slow Alzheimer's Disease Is Not Far From Discovery

23/05/2016 12:27 | Updated 23 May 2016

Inspired by my dad's science books when I was little, I grew up to develop a deep passion for science. During my undergraduate degree in Human Anatomy, I found the brain and it was my first love! I became particularly interested in how our brain cells communicate to make us who we are and how we lose these functions in brain diseases. I realised this needed knowledge of how the brain cells work and this was how I got to do my Masters in Cellular and Molecular Neuroscience and now my Neuroscience Ph.D. in one of the UK's leading Neuroscience Research Centres - Sussex Neuroscience. With over 50 research groups, the Sussex Neuroscience demonstrates a reputation of working to find answers to how our brain operates in health and diseases.

I am currently in the third year of my research PhD in the Serpell Laboratory, Dementia Research Group, at the University of Sussex where I work on trying to understand one of the most devastating brain diseases, Alzheimer's. It is a progressive neurodegenerative disease, the most common of dementias, that affects learning and memory, personality, communication skills and many other behavioral functions.

One of the common but debilitating symptoms patients encounter is the loss of memory - the memory of who we are, our family and many more. The major hallmarks of the disease in the brains of sufferers are two protein deposits called amyloid plaques comprised of a protein called amyloid beta and neurofibrillary tangles made up of a protein called Tau. Decades of research has implicated these proteins in the disease. However, we still don't have a complete understanding of the function and involvement of these proteins in triggering or driving the disease. The research in our lab tries to understand the normal role of these proteins and how they turn deviant in brain cells of people with Alzheimer's disease. To find efficient therapies that could slow or cure the disease, we need to understand more about how brain cells become affected by the disease.

With support from both the University of Sussex's Neuroscience Centre and the Sussex Genome Damage and Stability Centre, using cell models, my project, has employed a wide range of cell and molecular biology techniques to identify how amyloid beta and Tau may interact to prevent brain cells from functioning in a healthy manner. These findings recapitulate what happens in the different stages of the disease, indeed confirming the relevance of our findings. I hope that by the end of my Ph.D, my research will enhance our understanding of the disease and how to best therapeutically target it.

As a scientist, I cannot express how exciting it is to think about a problem in the laboratory, design experiments, and seek and find answers to these problems, in ways that are relevant to finding an end to the tyranny of diseases like Alzheimer's. This, to me, is the most rewarding gift for one's passion in science. As the most common cause of dementia, causing severe emotional, economic and healthcare burden, David Cameron has pledged more support for research into the disease and hopes for a cure by 2025. Considering the high number of scientists working to solve the mystery of this complex disease, I am cautiously optimistic that treatment that could slow the disease is not far from discovery.

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