Accessibility Skip to Global Navigation Skip to Local Navigation Skip to Content Skip to Search Skip to Site Map Menu

Alzheimers essay wins Otago Medical School Research Society essay prize

Monday 4 January 2016 11:36am

Nikita_PotemkinBrain Health Research Centre student Nikita Potemkin won the Otago Medical Research Society's prize for science writing at the end of year competition in December.

Thirty-one people entered the essay contest, which asked them to explain why their research matters, in a way that would interest a non-scientific audience.

Nikita is a Masters student in the departments of Anatomy and Biochemistry, supervised by Dr Joanna Williams.

Here is his essay:

Helping the fight against Alzheimer’s disease: Beating the bullies

Our memories are what make us who we are – that one summer on the beach when you were six; your first day at high school; your first kiss. Our personalities are a product of our experiences. So what happens when those defining memories are lost? When you can’t remember your partner’s face, or even your own name? This is exactly what happens in Alzheimer’s disease – memories start to fade, it becomes harder to make new memories, planning and organization skills deteriorate and even language and speech are affected. This means that most people affected by Alzheimer’s disease require residential care, their past lives only discernible through their photos around them, shadows of their former selves.

Alzheimer’s disease is a horrendous illness affecting nearly 36 million people worldwide, mostly over the age of 60, and costing over US$600 billion in care costs, according to the World Health Organization. In New Zealand alone the cost to the taxpayer is in excess of NZ$1 billion (Alzheimer’s New Zealand) because of the high level of care required for the 150,000 people suffering from the disease. These numbers will only increase as the global population ages. Currently there is no cure for the disease, or even particularly effective treatments to alleviate the symptoms. Researchers have tried for decades to develop drugs and lifestyle interventions to combat Alzheimer’s, but with little success. The main problem is that we still have a poor understanding of what causes the disease. However, what we have discovered has helped guide the development of potential treatments and new research directions into the causes and progression of the disease.

In very rare cases, Alzheimer’s disease runs in families (only 12 families worldwide) – individuals affected develop Alzheimer’s before their 40s and the symptoms tend to be quite severe. Study of these people have provided a starting point for looking into the cause and development of the disease, and this has led to the identification of genes that are involved, and some of the biological processes that might underlie the more common sporadic cases, with no known common genetic origin.

Research over the last century into Alzheimer’s has highlighted the importance of a protein called Amyloid-Beta, which is a defining feature of the disease. Amyloid-Beta proteins are like the schoolyard bullies - they congregate together in the brain and interfere with the normal working of brain cells, damaging them in the process. The more the disease progresses, the more Amyloid-Beta there is, the more brain cells die, the worse the symptoms get. However, it’s not all bad news - Amyloid-Beta has a cousin called sAPPα, who’s very against bullying. Amyloid-Beta and sAPPα are both derived from the same grandparent protein, but while the former is damaging to brain cells, the latter actually helps protect them - it stands up to the bullies and doesn’t let them get away with it. In our hypothetical schoolyard is another molecule, zinc, which is like a social chameleon. In some cases it hangs out with the Amyloid-Beta, binding onto the protein when it groups together, but at other times it might actually help sAPPα protect brain cells.

My research aims to figure out how sAPPα and Amyloid-Beta interact on the molecular level, and the contribution of zinc to both the damage done by Amyloid-Beta and the protection given by sAPPα. SAPPα and Amyloid-Beta, as relatives, share a length of their protein sequence, which contains a number of locations where zinc can bind. The zinc encourages Amyloid-Beta to clump together, but somehow prevents some of the damage it would otherwise do to brain cells. The aim of my research is to determine how zinc changes the toxicity of Amyloid-Beta and how it changes the ability of sAPPα to protect brain cells. Furthermore, I am investigating whether the shared sequence between sAPPα and Amyloid-Beta is necessary for their interaction, especially in the context of their mutual relationship with zinc.

My research should shed light on the complex relationship between these molecules in the brain, an area which, while quite extensively explored, lacks clarity and consensus. On top of that, if zinc turns out to be a major player in the brain’s “schoolyard” dynamics, it may also highlight novel treatment strategies for Alzheimer’s. For example, sAPPα therapies are in very early stages of development and if zinc plays a role in regulating its protective function, these therapies may be improved or enhanced by manipulating zinc.

Alzheimer’s is a disease which will impact our lives and the lives of our loved ones, directly or indirectly. This is a very exciting area of research and the possibility of changing millions of lives for the better is as good a reason as any to go down this road.