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Optimism for new targets of research

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I am currently a final year student at the University of Nottingham studying Neuroscience. One of the major influences on my life that encouraged me to study the brain was my Grandad, who was diagnosed with Alzheimer’s Disease when I was incredibly young. I became increasingly interested in the mechanisms of the brain and how they may contribute to my Grandfather’s diagnosis. I was incredibly excited at the beginning of my second year when I enrolled onto a module called ‘Neurobiology of Disease’. During the module, I learnt about a variety of medical conditions, from ADHD to epilepsy and of course Alzheimer’s Disease.

As someone who has a close family member with Alzheimer’s, I found it somewhat comforting to learn that scientists and researchers have an impressively strong understanding of the symptoms of Alzheimer’s as well as it’s underpinning mechanisms.

We learnt that the main indicator of Alzheimer’s Disease is the presence of ‘Extracellular Amyloid Plaques’ in the brain. These are collections of the protein called Amyloid that are toxic to the brain and can disrupt the mechanisms by which cells in the brain are able to communicate with each other, they can also cause the loss of brain cells in a process called brain atrophy. 

Brain atrophy in the early stages of Alzheimer’s Disease, takes place in an area of the brain called the hippocampus. The hippocampus region of the brain is vital for memories and so by losing cells in this region forgetfulness can often incur. This loss of cells can progress causing the symptoms of Alzheimer’s appear increasingly severe and effect behaviour more and more.

The loss of cells as a reason for many symptoms of Alzheimer’s Disease provides researchers and scientists with a clear target for treatment. Brain cells can be lost for a variety of reasons, but with the Amyloid Plaques indicators, we know that in Alzheimer’s a big reason for cell loss is a fault in how the brain breaks down the proteins that form the Amyloid Plaques. This protein is referred to as APP and is present in every brain cell where it is normally used for repairing the cell it inhabits. When APP is cut into smaller pieces by certain sites of a cell it has a protective role, but when the APP is metabolised by other sites, known to scientists as the beta-secretase, the APP and this site form Amyloid. This Amyloid is what leaves the cells in the brain vulnerable, increases toxicity and disrupts the balance of chemicals in the cells.

Although this may appear a potentially daunting idea, it does provide hope to those researching Alzheimer’s Disease. With these biomarkers identified, diagnosis can occur much sooner and targeting the sites on cells that combine with APP to form these amyloid plaques is a clear target that scientists are concentrating their work on. 

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Kate Swaffer

In the 1970’s when I commenced my nursing, most people with dementia were diagnosed nearer to the end stage of the disease process, and little was known about dementia.

Tom Dening

Developing dementia is dreaded more than any other medical condition, at least by people of middle age and upwards. It’s often said in conversation that we would rather be dead than live like that.

Fiona Marshall

Two things have recently made me think about the ways in which we as academics think about living with dementia; recent reading of wellbeing meanings in general and receiving a couple of battery hens.