Undergraduate Course: Neurodegeneration, obesity and cancer: genetics and beyond (BIME10032)
|Deanery of Biomedical Sciences
|College of Medicine and Veterinary Medicine
|Credit level (Normal year taken)
|SCQF Level 10 (Year 4 Undergraduate)
|Available to all students
|In modern societies, the increase in life expectancy is accompanied by an increased risk of aging-associated diseases such as obesity, cancer and neurodegenerative disorders. These diseases pose enormous challenges in terms of life quality and economic burden so that it has become an urgent need for societies to address these health concerns. In an attempt to prevent or effectively treat these disorders, research interest in defining the molecular mechanisms underlying these diseases has been particularly intense. We will consider how studies on a variety of animal models have contributed to our growing understanding of the molecular basis of these diseases. In presenting the cellular processes that are disrupted in neurodegenerative disorders, obesity and cancer, particular emphasis will be given to molecular commonalities existing between these diseases, which, at a first glance, seem to have very little in common. We will also critically evaluate the advantages and pitfalls of every model system and the importance of using a variety of different models to gain a thorough understanding of the molecular mechanism underlying the pathogenesis of a given disease. This course will also highlight how the generation of disease models has made possible high-throughput genetic screens and large-scale proteomic and transcriptomic profiling both in health and disease states. Finally, we will discuss how computational analysis and experimental validation of these large data sets can lead to the identification of a large number of new disease-related genes and, possibly, to the development of innovative diagnostic and therapeutic approaches.
The course includes introductory lectures on the major cellular processes disrupted in cancer, neurodegenerative disorders and obesity. Particular emphasis will be given to mitochondria dynamics and RNA metabolism as emerging evidence indicate that these processes are common themes in the pathogenesis of these apparently divergent diseases. Among the neurodegenerative disorders, the role of animal models in prion diseases and in the motor neuron disease spinal muscular atrophy will be presented and critically evaluated. We will consider how a combination of computational analysis together with large-scale genetic and proteomic approaches on experimental models can streamline the identification of new genes and cellular processes involved in the pathogenesis of these diseases.
The course will have an ICA component. Students will be asked to outline an experimental approach to elucidate the role of a gene in a specific human disease. As a starting point, preliminary information on the gene and a few specific articles will be provided to the students. Each student will be required to give a 20 min presentation on this experimental outline in front of a committee of two lecturers.
Staff members involved in the teaching are: Dr. Andrew Gill, Prof. Tom Gillingwater, Dr. Mandy Jackson, Dr. Giusy Pennetta and Dr. Tom Wishart.
Entry Requirements (not applicable to Visiting Students)
Information for Visiting Students
|High Demand Course?
Course Delivery Information
|Academic year 2018/19, Not available to visiting students (SS1)
|Learning and Teaching activities (Further Info)
Lecture Hours 38,
Feedback/Feedforward Hours 1,
Summative Assessment Hours 3,
Programme Level Learning and Teaching Hours 4,
Directed Learning and Independent Learning Hours
|Assessment (Further Info)
|Additional Information (Assessment)
|30% in-course assessment and 70% degree examination
|Feedback will be given after the summative in course assement
|Hours & Minutes
|Main Exam Diet S1 (December)
On completion of this course, the student will be able to:
- Have an understanding of different ways to generate animal models of human diseases and be aware of the advantages and disadvantages of different models Be able to critically evaluate the contribution of animal models to the elucidation of the pathogenesis of complex human diseases and be able to formulate an experimental plan to model a human disease and study the importance of a cellular pathway in disease pathogenesis
- Have knowledge of how larger animals can be used to model cancer, diabetes and neurodegeneration and have an understanding of the complex patho-mechanism underlying prion diseases and Have an appreciation of how neurodegeneration, cancer and diabetes can share similar disrupted cellular mechanisms
- Be aware of how prion-like mechanisms may be responsible for the pathogenesis of other more common neurodegenerative diseases such as Alzheimer┐s and Parkinson┐s diseases
- Be aware of how modelling neurodegenerative diseases has implicated microRNAs and mitochondria dynamics in nerve cell dysfunction and degeneration
- Have knowledge of how models of neurodegeneration, cancer and diabetes have revealed a role for altered mitochondrial function and RNA metabolism in the disease process and Be aware of the contribution of large scale screens in the search for new disease related genes and potential biomarkers of disease progression Be able to discuss how modelling complex human diseases provides a better understanding of disease pathogenesis
|Lotti, F., Imlach, W.L., Saieva, L., Beck, E.S., Haole, T., Li, .D.K., Jiao, W., Mentis, G.Z., Beattie, C.E., McCabe, B.D. and Pellizzoni, L. (2012). An SMN-dependent U12 splicing event essential for motor circuit function. Cell. 12;151: :440-454.
|Graduate Attributes and Skills
|Dr Giuseppa Pennetta
Tel: (0131 6)51 3201
|Miss Emily Rowan
Tel: (0131 6)51 1515