fengruru@ojlab.ac.cn
1978—1983 | Chongqing Medical College | bachelor's degree |
1983—1986 | West China Medical University | master's degree |
1990—1993 | Purdue University | master's degree |
1993—1996 | Indiana University School | PhD |
1986.7—1988.6 | Psychiatric Assistant, Chief Resident | West China School of Medicine |
1986.7—1990.12 | Attending psychiatrist, lecturer | West China School of Medicine |
1996.8—1999.9 | Postdoctoral fellow | Harvard Medical School |
1999.10—2001.6 | lecturer in neurology | Harvard Medical School |
2001.7—2020.9 | The Jack Brown and Family Lifetime Lecture Professor | UBC University
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2002.4—2020.10 | Chief researcher of Alzheimer's disease | |
2004—2008 | Director | Postdoctoral Office of UBC School of Medicine |
2008—2020 | Director | UBC Townsend Alzheimer's Disease Research Center |
2009.1—2020.9 | Senior assistant to the president | UBC University |
2015.7—2020.10 | Deputy Director | UBC University Institute of Mental Health Research |
2015.7—2020.10 | Director | Department of Psychiatry and Neuroscience at UBC University |
2016—present | Member of the Advisory Committee | Canadian Institutes of Health Research (CIHR) |
2020.7—present | Academic Vice President, Dean of the Geriatric Research Institute | Wenzhou Medical University |
2021.5—present | Director | Oujiang Laboratory (Zhejiang Laboratory of Regeneration regulation and Eye and Brain Health) |
2023—present | Director | Zhejiang Clinical Medical Research Center for Mental and Psychological Diseases |
Research direction 1: Etiology and pathogenesis of AD
AD is a progressive neurodegenerative disease characterized by brain dysfunction, personality and behavior changes, with clinical manifestations of generalized dementia. At the tissue level, the pathological manifestations of AD are brain atrophy and decreased number of nerve cells (especially in the entorhinal cortex, hippocampus and other brain regions). At the cellular level,the typical pathological features of AD are the amyloid plaques formed by amyloid (A) deposition and tau tangles. Additionally, it is also characterized by structural or functional impairment of dendrites and synapses of nerve cells. The prevalence of AD is high, but its pathogenesis is unknown, leading to the lack of targeted treatment methods, and it is difficult to improve the health and life of patients. Although the pathogenesis of AD has not been fully elucidated, scientists around the world have gradually revealed several important factors leading to AD after decades of research, namely genetic factors (including epigenetic factors) and environmental factors. The pathogenesis of AD is often the result of the interaction between genetics and environment.
This study will comprehensively study the interaction of genetic factors and environmental factors in AD, and elucidate the details of disease progression at molecular and cellular levels. It will reveal the pathogenesis of this disease and lay a theoretical foundation for the diagnosis, treatment and prevention of this disease.
Research direction 2: Early diagnosis and clinical translational research of AD
AD, as the most important disease of dementia, has always accounted for 60-80% of the main causes of dementia. The diagnosis of AD is mainly based on clinical symptoms, and the accuracy is not high. Meanwhile, because many elderly groups have comorbidities, multiple drugs should be taken at the same time, and the normal aging process is also accompanied by the decline of memory and cognitive function. These factors increase the difficulty of clinical diagnosis of AD. Therefore, the early diagnosis of AD is a big challenge for neurology and psychiatrists. In the past decade, the search for specific biomarkers of AD has become the focus of early diagnostic research. Although the pathophysiological changes of AD are many years earlier than the occurrence of clinical symptoms, such as the deposition of amyloid polypeptide polymer (A 1-42) and neurofibrillary tangles in the early stage of the brain, these research results cannot be translated into clinical diagnostic criteria.
This project will develop easy and easily operational criteria for laboratory early diagnosis (AD), such as selecting multiple biomarkers in peripheral blood and certain cognitive function tests, integrating them into a multidimensional scale to check whether changes in type (profile), composition (composition), total score (total score) are associated with duration of disease, severity, or prognosis.
In 2012, elected as a fellow of the Canadian Academy of Health Sciences (certificate, September 2012)
In 2005, selected as a National Outstanding Youth (Category B) (project notification letter, November 2005)
In 2006, elected as a Changjiang Scholar Chair Professor (certificate)
In 2007, appointed as the director of the Academic Committee of the National Key Laboratory of Medical Genetics (Ministry of Education Teaching Technology Letter (2007) No. 17)
In 2011, selected as a National Distinguished Expert (certificate, 2013)
In 2011, awarded the National 'Friendship Award' (certificate, September 2011)
In 2013, served as a specially invited representative from overseas at the 12th National Committee of the Chinese People's Political Consultative Conference
In 2014, awarded the International
Science and Technology Cooperation Award of Chongqing (certificate, August 2014)
Since 2014, served as a member of the Expert Advisory Committee of the State Council Overseas Chinese Affairs Office (certificate, September 2014)
Since 2017, served as an overseas consultant for Zhongguancun (certificate, August 2017)
In 2018, appointed as a strategic scientist (short-term) in Beijing's 'Hai Ju Project' (certificate, 2018)
In 2021, selected as an expert in Zhejiang Province's 'Kunpeng Action' Plan (certificate, 2021)
In 2022, served as a specially invited representative at the Fifth Session of the Twelfth Zhejiang Provincial Political Consultative Conference
In 2022, awarded the International Science and Technology Cooperation Award of Zhejiang Province (certificate, 2022)
1. Zhang Q, Xing M, Bao Z, Xu L, Bai Y, Chen W, Pan W, Cai F, Wang Q, Guo S, Zhang J, Wang Z, Wu Y, Zhang Y*, Li JD*, Song W*. (2024). Contactin-associated protein-like 2 (CNTNAP2) mutations impair the essential α-secretase cleavages, leading to autism-like phenotypes. Signal Transduction and Targeted Therapy (IF:52.7). 9 (1), 51.
2. Zhang J, Cai F, Lu R, Xing X, Xu L, Wu K, Gong Z, Zhang Q, Zhang Y, Xing M, Song W*, Li JD*. (2023). CNTNAP2 intracellular domain (CICD) generated by γ-secretase cleavage improves autism-related behaviors. Signal Transduction and Targeted Therapy (IF: 52.7). 8 (1), 219.
3. Xing M, Song W*. (2025). Improving Alzheimer's disease immunotherapy. Science (IF: 45.8). 389 (6760), 571-572.
4. Ma S, Ji Z, Zhang B, Geng L, Cai Y, Nie C, Li J, Zuo Y, Sun Y, Xu G, Liu B, Ai J, Liu F, Zhao L, Zhang J, Zhang H, Sun S, Huang H, Zhang Y, Ye Y, Fan Y, Zheng F, Hu J, Zhang B, Li J, Feng X, Zhang F, Zhuang Y, Li T, Yu Y, Bao Z, Pan S, Rodriguez Esteban C, Liu Z, Deng H, Wen F, Song M, Wang S, Zhu G, Yang J, Jiang T, Song W(Senior Author), , Izpisua Belmonte JC, Qu J*, Zhang W*, Gu Y*, Liu GH*. (2024). Spatial transcriptomic landscape unveils immunoglobin-associated senescence as a hallmark of aging. Cell (IF: 42.5). 187 (24), 7025–7044.
5. Yang Y, Lu X, Liu N, Ma S, Zhang H, Zhang Z, Yang K, Jiang M, Zheng Z, Qiao Y, Hu Q, Huang Y, Zhang Y, Xiong M, Liu L, Jiang X, Reddy P, Dong X, Xu F, Wang Q, Zhao Q, Lei J, Sun S, Jing Y, Li J, Cai Y, Fan Y, Yan K, Jing Y, Haghani A, Xing M, Zhang X, Zhu G, Song W, Horvath S, Rodriguez Esteban C, Song M, Wang S, Zhao G, Li W, Izpisua Belmonte JC, Qu J*, Zhang W*, Liu GH*. (2024). Metformin decelerates aging clock in male monkeys. Cell (IF: 42.5). 187 (22), 6358–6378.
6. Zhang Y*, Chen H, Feng Y, Liu M, Lu Z, Hu B, Chen L, Zhang Y, Liu J, Cai F, Zhao Y, Pan W, Liao X, Pan S, Bestard-Lorigados I, Wu Y, Song W*. (2025). Activation of AMPK by GLP-1R agonists mitigates Alzheimer-related phenotypes in transgenic mice. Nature Aging (IF: 19.4). 5 (6), 1097-1113.
7. Wang Z*, Liang Q, Qian X, Hu B, Zheng Z, Wang J, Hu Y, Bao Z, Zhao K, Zhou Y, Feng X, Yi X, Li J, Shi J, Liu Z, Hao J, Chen K, Yu Y, Sham PC, Lu W, Wang X*, Song W*, Li MJ*. (2023). An autoimmune pleiotropic SNP modulates IRF5 alternative promoter usage through ZBTB3-mediated chromatin looping. Nature Communications (IF: 15.7). 14 (1), 1208.
8. Shi Y*, Huang D, Song C, Cao R, Wang Z, Wang D, Zhao L, Xu X, Lu C, Xiong F, Zhao H, Li S, Zhou Q, Luo S, Hu D, Zhang Y, Wang C, Shen Y, Su W, Wu Y, Schmitz K, Wei S*, Song W*. (2024). Diphthamide deficiency promotes association of eEF2 with p53 to induce p21 expression and neural crest defects. Nature Communications (IF:15.7). 15 (1), 3301.
