Why do we use mice?
Over eight out of ten animals used in research at Cambridge are mice. Their short life span and fast reproductive rate make it possible to investigate biological processes in many areas, at all stages of the life cycle.
The mouse makes an excellent model for human disease because the organisation of their DNA and their gene expression is similar to humans, with ninety-eight percent of human genes having a comparable gene in the mouse. They have similar reproductive and nervous systems to humans, and suffer from many of the same diseases such as obesity, cancer and diabetes.
It is possible to manipulate the DNA of mice either through cross-breeding or using techniques that ‘knock out’ certain genes, or edit their genes using recently-developed CRISPR-Cas techniques. This enables us to study novel genes of interest in the specific areas of the body without the need for generating new GM mice, which will dramatically reduce the number of animals needed to perform research. Manipulating their genes can lead the mice to develop other diseases that do not naturally affect them. As a result research on mice has helped the understanding of both human physiology and the causes of disease.
Information adapted from AnimalResearch.info
What do we study?
Understanding abnormalities in embryo development
Our researchers have used mice to model aneuploidy, where some cells in the embryo contain an abnormal number of chromosomes. Normally, each cell in the human embryo should contain 23 pairs of chromosomes, but some can carry multiple copies of chromosomes, which can lead to developmental disorders. For example, children born with three copies of chromosome 21 will develop Down’s syndrome.
Pregnant mothers – particularly older mothers, whose offspring are at greatest risk of developing such disorders – are offered tests to predict the likelihood of genetic abnormalities. Until very recently, little was understood about the fate of embryos containing abnormal cells and about the fate of these abnormal cells within the developing embryos.
Our researchers developed a mouse model of aneuploidy by mixing 8-cell stage mouse embryos in which the cells were normal with embryos in which the cells were abnormal and showed that the embryo has an amazing ability to correct itself. This means that even when early indications suggest a child might have a birth defect because there are some abnormal cells in its embryonic body, this isn’t necessarily the case.
Atherosclerosis is a severe disease of the arteries, responsible for heart attack and stroke. The disease is initiated by accumulation of fatty deposits in the artery wall. This leads to the stimulation of our defences through the activation of the white blood cells. Our researchers are trying to find out which set of white blood cells is responsible for damaging the artery wall and how this alters tissue response to injury. Knowing this will enable us to design new treatments that stimulate the cells that protect our arteries without stimulating the damaging ones. If we can do this we may be able to develop a ‘vaccine’ against atherosclerosis, which could reduce the incidence of heart attacks and strokes.
The research involves a combination of tissue culture to understand cell-cell communication and genetically-modified mice to mimic human disease and to test potential new medicines. Animals are necessary to reproduce the complex network involved in atherosclerosis and aneurysm formation.