Research Background
1. I am a PhD graduate, with a master degree major in Neuroscience.
2. My interest is neurodegeneration and anti-inflammation research in both the central nervous system (CNS) and peripheral nervous system (PNS).
3. I have versatile background of studying neuro-degeneration in Alzheimer's Disease (AD), cerebral ischemic stroke, multiple sclerosis (MS) and spinal cord injury (SCI).
4. Instead of conventional strategies with mild effects on repairs, I want to focus on innovative ones for AD, the most common neurodegenerative disorders.
5. Base on our lab's non-transgenic AD mouse model, I would like to explore the gastrointestinal (GI) in AD from a pathological perspective, and the co-relationship between the enteric nervous system (ENS) and CNS, assessing whether the ENS can mirror the neuropathology in CNS.
2. My interest is neurodegeneration and anti-inflammation research in both the central nervous system (CNS) and peripheral nervous system (PNS).
3. I have versatile background of studying neuro-degeneration in Alzheimer's Disease (AD), cerebral ischemic stroke, multiple sclerosis (MS) and spinal cord injury (SCI).
4. Instead of conventional strategies with mild effects on repairs, I want to focus on innovative ones for AD, the most common neurodegenerative disorders.
5. Base on our lab's non-transgenic AD mouse model, I would like to explore the gastrointestinal (GI) in AD from a pathological perspective, and the co-relationship between the enteric nervous system (ENS) and CNS, assessing whether the ENS can mirror the neuropathology in CNS.
PhD Project
Effect of Ghrelin on Beta-Amyloid-Induced-Degeneration in the Mouse
The occurrence of enteric pathology in AD is well recognized, and presence of beta-amyloid (AD) deposits have been confirmed in the GI tract during aging in transgenic mice. But for sporadic AD, a non-transgenic mouse model should be a better choice. Ghrelin, which can promote GI motility as a gastrointestinal hormone, has recently been show to have an association with cognitive function in elderly patients with AD. Thus we wish to explore the mechanism and potential protection of its effects on both gastric function and cognition via the GI tract in our novel AD model.
Publications
1. Sun Y, Sommerville NR, Liu JYH, Ngan MP, Poon D, Ponomarev ED, Lu Z, Kung JSC, Rudd JA* (2020) Intra-gastrointestinal amyloid-β1-42 Oligomers Perturb Enteric Function and Induce Alzheimer's Disease Pathology. The Journal of Physiology. [PMID: 32617993]
2. Liu JYH, Sun Y, Sommerville N, Ngan MP, Ponomarev ED, Lin G, Rudd JA* (2020) Soy flavonoids prevent cognitive deficits induced by intra-gastrointestinal administration of beta-amyloid. Food and Chemical Toxicology. 141: 111396. [PMID: 32417364]
3. SUN Y*, Fang M, Davies H, et al. Mifepristone: a potential clinical agent based on its anti-progesterone and anti-glucocorticoid properties. Gynecological Endocrinology. 2014;30:169-73. [PMID: 24205903]
4. Fang M*, Sun Y, Hu Z, et al. C16 peptide shown to prevent leukocyte infiltration and alleviate detrimental inflammation on in acute allergic encephalomyelitis model. Neuropharmacology. 2013;70:83-99. [PMID: 23352465]
2. Liu JYH, Sun Y, Sommerville N, Ngan MP, Ponomarev ED, Lin G, Rudd JA* (2020) Soy flavonoids prevent cognitive deficits induced by intra-gastrointestinal administration of beta-amyloid. Food and Chemical Toxicology. 141: 111396. [PMID: 32417364]
3. SUN Y*, Fang M, Davies H, et al. Mifepristone: a potential clinical agent based on its anti-progesterone and anti-glucocorticoid properties. Gynecological Endocrinology. 2014;30:169-73. [PMID: 24205903]
4. Fang M*, Sun Y, Hu Z, et al. C16 peptide shown to prevent leukocyte infiltration and alleviate detrimental inflammation on in acute allergic encephalomyelitis model. Neuropharmacology. 2013;70:83-99. [PMID: 23352465]