Professor David Lewis outlines how model organisms such as mice can help uncover the interplay of the genetic components in schizophrenia.
Transcript:
One of the major challenges in the field is how best to use animal model studies to inform our understanding of schizophrenia. One way to approach that, now that we are discovering genes that confer risk for schizophrenia, is to look at mice that have been manipulated in such a way so that the genes that seem to confer risk in schizophrenia have been altered in mice. In that situation we can then study what are the downstream effects – what other changes occur in the brain as a result of that genetic manipulation?
That helps us to understand whether changes in molecules, different molecules, say, molecule X and molecule Y, may both be changed in individuals with schizophrenia. But, in studying the illness, all we can say is that those two things changed together. But in a mouse, we can change gene X and see if that change produces the same change in gene Y that we observed in the illness. So, another way of saying this is that studies in animals enable us to convert correlations, or things that co-occur in the illness into an understanding of cause and effect.
Professor David Lewis explains that although many symptoms of schizophrenia are not reproducible in animals, animal models can help understand the disorder.
Professor David Lewis discusses how the diversity of symptoms in schizophrenia is reflected in the diversity of genetic and neural causes of the disorder.
Students will experiment with an interactive animation to compare mutant and wild-type mice in a water maze. They will analyze data and discuss findings of a research paper.