- UCAS course code
- B940
- UCAS institution code
- M20
Bachelor of Science (BSc)
BSc Biomedical Sciences
- Typical A-level offer: AAA-AAB including specific subjects
- Typical contextual A-level offer: AAB-ABC including specific subjects
- Refugee/care-experienced offer: ABB-ABC including specific subjects
- Typical International Baccalaureate offer: 36-35 points overall with 6, 6, 6 to 6, 6, 5 at HL, including specific requirements
Course unit details:
Neuroinflammation in Health & Disease
Unit code | BIOL31612 |
---|---|
Credit rating | 10 |
Unit level | Level 3 |
Teaching period(s) | Semester 2 |
Available as a free choice unit? | No |
Overview
This unit will provide you with an extensive knowledge of the role of inflammation in nervous system health and disease. You will gain an understanding of the important role of inflammatory molecules as key mediators of central nervous system (CNS) functions and of inflammatory responses to, and pathogenesis of, acute and chronic nervous system disorders. The development of new therapeutic interventions to treat all major nervous system disorders (i.e. stroke, epilepsy, and Alzheimer's disease) is a major field of research in neuroinflammation of which you will be acquainted with. The topics covered in this unit range from 'Introduction to Neuroinflammation' to 'Chronic CNS Disorders'.
Pre/co-requisites
Unit title | Unit code | Requirement type | Description |
---|---|---|---|
Excitable Cells: the Foundations of Neuroscience | BIOL10832 | Pre-Requisite | Compulsory |
Drugs & the Brain | BIOL21312 | Pre-Requisite | Recommended |
Aims
The aim of the unit is to provide an extensive knowledge of the role of inflammation in nervous system health and disorders. Inflammation is involved in many central nervous system (CNS)-regulated physiological processes (including, e.g. memory and synaptic plasticity), and is a key host defense response to acute and chronic peripheral and central disorders. Research into neuroinflammation is a major field that aims to develop new therapeutic interventions to treat all major nervous system disorders including stroke, brain trauma, epilepsy, Alzheimer's disease and neuropathies (for which there is currently no or limited treatments). This unit will cover the important role of inflammatory molecules as key mediators of CNS functions and will provide basic knowledge on the pathogenesis of, and inflammatory responses to acute and chronic nervous system disorders.
Learning outcomes
Students will be able to:
- Describe the role of inflammation in key biological functions and pathological conditions.
- Describe the main inflammatory mediator families and the role of some key inflammatory molecules.
- Describe CNS-regulated physiological functions that are mediated by inflammatory mediators.
- Describe the pathogenesis of, and inflammatory response to acute and chronic central and peripheral nervous system disorders.
- Describe the methods available for evaluating CNS and peripheral inflammation in patients after stroke and in people at risk of stroke.
Syllabus
Introduction to neuroinflammation - These lectures will provide a general introduction to neuroinflammation, including description of inflammatory mediators (cytokines, chemokines and adhesion molecules), mechanisms of production and action in the brain (receptors, signalling pathways and downstream effects) and cell-cell interactions.
Peripheral inflammation - These lectures will describe the mechanisms of neuropathic pain with a focus on neuroimmune interactions in peripheral nerve. Neuroimmune interactions and normal brain functions - These lectures will describe the function of inflammatory mediators during memory, long-term potentiation, synaptic plasticity, and host defense response to infection and injury. Communications from the immune system to the brain and associated behavioural changes including fever, anorexia, lethargy, depression and sickness behaviour will also be covered. Inflammation in chronic brain disorders - These lectures will describe the mechanisms of inflammation during chronic brain disorders including epilepsy, and Alzheimer's disease, with an emphasis on disease pathogenesis and current therapeutic approaches. Inflammation in acute brain injury - These lectures will describe the acute neuroinflammatory response that occurs during acute brain injury such as stroke. The mechanisms of neurovascular unit dysfunction, neuronal plasticity, glial scar, neurogenesis and angiogenesis will be addressed. Finally, these lectures will provide knowledge on the use of brain imaging (e.g. MRI, PET) and clinical assessment of neuroinflammation (CSF and plasma markers) used in patient management and therapeutic applications.
Employability skills
- Problem solving
- Students have to solve some problems based on some e-learning exercises.
- Research
- The lectures the students are given contain some current research that in some cases is the lecturers own research.
Assessment methods
Method | Weight |
---|---|
Other | 10% |
Written exam | 90% |
Feedback methods
There will be 4 eLearning activities (cases related to 4 themes of lectures). Students will review online material on several topics (enquiry-based learning) and, will answer MCQs through Blackboard. A feedback session for each e-learning case will provide answers and give more information each topic, and students will be able to receive immediate feedback on their activity and performance by talking to teaching staff. In addition, students will receive feedback on overall performance in the form of the final mark for the unit.
Recommended reading
David, S. (2015) Neuroinflammation: New Insights into Beneficial and Detrimental Functions. John Wiley & Sons, New Jersey.
Peterson, P.K and Toborek M. (2014) Neuroinflammation and Neurodegeneration. Springer, New York.
Wood, P, Understanding Immunology (3rd Edition), Prentice Hall, 2011, (Optional, Background)
Study hours
Scheduled activity hours | |
---|---|
Lectures | 18 |
Independent study hours | |
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Independent study | 82 |
Teaching staff
Staff member | Role |
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Catherine Lawrence | Unit coordinator |