| Title | Developing novel treatment for Alzheimer’s disease through understanding the disease immunopathogenesis |
|---|---|
| Supervisors | Hui-Rong Jiang Shuzo Sakata |
| Research Area | Neuroscience, immunology, neurodegenerative diseases |
| Description | Alzheimer’s disease (AD) is the biggest cause of dementia, a disease with dramatic increase in its prevalence in recent years due to increased life expectancy. The 2014 Dementia UK report suggest that 850,000 people in UK were living with dementia by 2015 and the number of people living with dementia will increase to over 1 million by 2021 and over 2 million by 2051 in the UK. Currently dementia costs the UK £26 billion a year. Thus it has become a major global challenge on the healthcare and the society. Although the cause of AD is currently unknown, accumulating research evidence confirmed that AD pathology is closely associated with immune-inflammation in the central nervous system (CNS). Thus a better understanding of the specific roles of immune cells and molecules and their interaction between the CNS and the immune system in AD pathogenesis is the key for the development of novel therapeutic strategies for patients. This project therefore aims to investigate how the phenotype and function of various immune cells in the periphery immune system and in the CNS are modulated at the early, peak and late stages of AD disease using genetically modified AD mouse model. The findings may lead to the development of a novel therapeutic strategy for AD patients through modulating neuro-immune responses. The students will have access to state-of-the-art equipment during their studies. In addition they will receive the excellent training programme designed for PhD students in SIPBS in: data handling and statistical interpretation, information and database searching, research skills in data presentation and scientific writing. |
| Techniques Used | • In vitro techniques: primary and cell line culture, molecular biology assays (e.g. RNA extraction, real-time PCR), immunohistochemical staining, histology, microscope imaging, various immunoassays such as ELISA, flow cytometry. • In vivo techniques: PIL course training, murine AD model, evaluation of disease severity, tissue dissection and processing for specific immunoassays. |
| References | 1. Hardy J, Selkoe DJ. The amyloid hypothesis of Alzheimer's disease: progress and problems on the road to therapeutics. Science. 2002; 297: 353-356. 2. Ransohoff RM. How neuroinflammation contributes to neurodegeneration. Science. 2016; 353: 777-783. 3. Deczkowska A , Schwartz M. Targeting Neuro-Immune Communication in Neurodegeneration: Challenges and Opportunities. J Exp Med. 2018;215, 2702-2704. 4. Fairlie-Clarke K, Barbour M, Wilson C, et al., Expression and Function of IL-33/ST2 Axis in the Central Nervous System Under Normal and Diseased Conditions. Front Immunol. 2018;9:2596. doi: 10.3389/. 5. Unger MS, Schernthaner P, Marschallinger J, et al. Microglia prevent peripheral immune cell invasion and promote an anti-inflammatory environment in the brain of APP-PS1 transgenic mice. J v. 2018; 15: 1304-1314. 6. Keren-Shaul H, Spinrad A, Weiner A, et al. A unique microglia type associated with restricting development of Alzheimer's disease. Cell. 2017; 169: 1276-1290. |
| Conditions | Applicants should possess or be about to obtain a 1st class or 2:1 Honours degree or equivalent in a relevant discipline in addition to receipt of satisfactory references and an IELTS score of 6.5 where appropriate. |
| Bench Fee | Running costs of £12000 p.a. will be associated with this project in addition to University tuition fees. |
| Suitable For | Degree in biomedical science and related subjects |
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