I fiddle about with cells in a dish
This is the short, succinct, and yet still pretty accurate description of what I do at work! This is the description I roll out at parties following a few glasses of wine, when there is only time for a five minute interaction, and when bumping into distant acquaintances who have only asked me what I do to be polite.
And while it very effectively sums up what I and many others do, the details of those cells and how they came to be in that dish are pretty awesome.
I research Huntington’s Disease – and although this will most likely be the subject of a future post, I’ve put some of the main points that you might be interested in at the end of this post.
So the big question is; what’s the relevance of a bunch of cells in a lab to a complicated, devastating human disease?
Well, a major roadblock to investigating any disease that affects the brain is that it isn’t considered particularly ethical or practical to cut into a live person’s brain and cut out a bit to take a look at.
So that’s where fiddling about with cells in a dish come in. The particular cells I work with have been engineered to carry the mutation that causes Huntington’s Disease – making it a cell model of Huntington’s Disease.
A particularly cool bit of this process is that the cells are ‘immortalised’. This is exactly as it sounds – the cells are made immortal so that they continue to grow and divide instead of dying after a week or so. This is done by forcing the cell to follow its internal programs for growth and survival that would normally be turned off.
The advantage of using a cell model is that people like me can investigate what is different between those cells that carry the mutation and those that don’t. The idea behind this is to try to understand the disease on a molecular and cellular level – that means we ask things like; how do they look different? Do they react differently to treatments? Do they have different levels of protein? Are they communicating differently? How can we fix it?
Perhaps more importantly, this never-ending supply of cells means that we can look for something that might prevent the effects of the Huntington’s Disease mutation – or whatever mutation is being investigated – and this (after many years of work and plenty of failures!) may then sow the seeds for the development of new treatments and cures.
That’s the ultimate goal.
Cell models are a crucial starting point for understanding how individual cells work, or rather stop working, in the context of a disease – especially when that disease attacks the very inaccessible cells in the brain! The endless supply of cells also gives fantastic flexibility – experiments can be relatively easily repeated and new techniques can be trialled without losing valuable source material – because you can just grow some more!
Compare this with animal work (another future blog post!) – where each individual animal is a precious resource and the numbers used must be kept to a minimum – and with human studies – where only so many people with the disease exist or have been identified, only a proportion will be willing or able to take part in research programs, and will understandably only consent to so many blood samples and tests.
Of course, cell models are by no means perfect – the brain is incredibly complicated, and a lot of cells in a dish can’t possibly replicate that (but there are people working on it!). But that’s not to say there’s no point in using them – I’m not wasting my time, I swear!! They are a brilliant spring board; a preliminary stage in the investigation of new ideas, and they can be manipulated (i.e. fiddled about with) in ways that aren’t possible in animals or people. Although they aren’t the perfect model and cannot be considered as an exact replication of human disease, cell models are still a crucial and valuable resource in scientific research.
Please feel free to comment if you want to know any more about cell models in research, or more about Huntington’s Disease!
Huntington’s Disease – The basics
- Huntington’s Disease is caused by a mutation on the (imaginatively named) ‘huntingtin’ gene. It typically starts to develop in mid-life (around 40-50 years old).
- The child of a person carrying the mutated gene has a 50% chance of inheriting the gene.
- The gene is ‘dominant’ – which means that anyone who has the mutation will develop the disease in their lifetime. If the gene is not passed down from parent to child, that child will not develop Huntington’s Disease, and they in turn cannot pass it on to their children.
- The cells in a particular region of the brain – the striatum – no longer function properly and start to die. This is called ‘neurodegeneration.’
- The striatum controls muscle movement, so losing its function means that people with Huntington’s Disease slowly lose control of their bodies – typically this starts with ‘chorea,’ also described as ‘dance-like movements.’
- The disease spreads throughout the brain, so sufferers also lose some cognitive abilities such as decision making, problem solving & memory.
- Although the genetic cause for the disease is known, there is currently no cure.