Dr. Jyh-Lyh Juang


Jyh-Lyh(Jerry) Juang, Ph.D.

Institute of Molecular and Genomic Medicine


Ph.D., Neuroscience, University of Wisconsin-Madison (1993)
M.S., Entomology, National Taiwan University (1985)
B.S., Entomology, National Chung-Hsing University (1983)


2009-current   Investigator; Institute of Molecular and Genomic Medicine, NHRI

2009-current Joint Appointment Professor, Biotechnology Center, National Chung Hsing University

2009-current   Joint Appointment Professor, Graduate Institute of Basic Medical Science, China Medical University

2011-current   Adjunct Professor, Institute of Molecular & Cellular Biology, National Taiwan University

2012-current   Joint Appointment Professor; Graduate Institute of Life Sciences, National Defense Medical Center

2004-2009     Associate investigator; Division of Molecular and Genomic Medicine, NHRI

1997-2012     Adjunct Associate Professor; Graduate Institute of Life Sciences, National Defense Medical Center

1997-2004     Assistant investigator; Division of Molecular and Genomic Medicine, NHRI

1993-1997     Research Associate; McArdle Laboratory for Cancer Research, U.S.A.


Molecular pathogenesis of Alzheimer’s disease

We use Drosophila and mouse model systems to investigate the molecular pathogenesis of Alzheimer’s disease (AD). Genetic studies of transgenic fly overexpressing amyloid b (Ab42), a principal constituent of senile plaques in AD, have suggested that Abl signaling is important for the Alzheimer’s pathogenesis via the activation of Cdk5/p35 (Cell Death Differ., 2007). The focus of the current work is to identify novel therapeutic targets and diagnostic biomarker of human AD.


Inter-organ communication in modulation of aging and diseases

Inter-organ communication has long been recognized as an important mechanism in maintaining systematic homeostasis in the body. However, its role in aging and diseases has only just being explored. Drosophila is an excellent genetic model system to perform in vivo and genetic experiments for the understanding of inter-organ immune communication. Our recent work shows that intestinal ROS triggers inter-organ immunological communication between gut and fat body (analogous to human liver). We find that immune hemocytes function as an important signal relay between intestinal ROS-NO signaling and fat body antimicrobial response to intestinal infection (Cell Host & Microbe, 2012). This unique signaling profile underlines the importance of the oxidative stress in an organ to the activation of systemic immune responses in remote organs. Our lab current research efforts are now directed toward studying gut-brain axis in modulation of aging and neurodegeneration.


Immunological cross talks between gut and other organs in the body

Immunological cross-talk between organs helps maintain the homeostasis of immune responses, thereby, enhancing immune protection of the host. For instance, when intestines are infected with harmful microbes, it not only would hamper intestinal health, but also trigger immunological reactions in other organs. Yet, the molecular mechanisms underlying the immunological communication remain unclear. Drosophila shares a similar innate immune system with humans and is an excellent genetic model system for studying inter-organ communication. Dr. Juang’s lab found that after the gut experiences bacterial stress, the increase of ROS in gut initiates an innate immune response in a remote organ fat body (analogous to human liver). This communication pathway is done via nitric oxide and hemocytes and another unknown messenger in carrying the ROS signal in the gut to the fat body, which then activates the Relish/NF-KB transcription factors and induces an antimicrobial peptide response in the fat body. The results of this study have been published in Cell Host & Microbe (2012), and is one of the stories that received a preview. This study’s importance is that it reveals that when an organism experience microbial threats in the gut, how would it signal other organs to induce immune response and protect it from harm, letting us better understand how to prevent immune-related diseases and further to therapeutic drug development.


1. Phi-Tao-Phi Scholastic Honor Society (1985)
2. Sigma Xi Best Ph.D. Thesis Award (1993)
3. NHRI Outstanding Research Achievement Award (2013)


  1. RH Lai, YY Hsu, CC Hsu , FS Shie , BH Yu, YK Chang, MH Chen and JL Juang* (2021) Vitamin D Receptor Dysfunction and the Exacerbation of Alzheimer’s Disease by Vitamin D Supplementation. Aging Cell 20(12):e13509(IF:9.304)
  2. Te-Haw Wu,† Rai-Hua Lai, ‡ Chun-Nien Yao,† Jyh-Lyh Juang* (co-corresponding author), and Shu-Yi Lin,* (2020) A supramolecular bait to trigger non-equilibrium co-assembly and clearance of Aβ42. Angewandte Chemie. 60(8):4014-4017 (IF:12.959)
  3. Wu SC, Cao ZS, Chang KM, Juang JL*. (2017) Intestinal microbial dysbiosis aggravates the progression of Alzheimer’s disease in Drosophila. Nature Comm. 8(1):24. doi:10.1038/s41467-017-00040-6 (IF: 12)
  4. Wu SC, Liao CW, Pan RL, Juang JL*. (2012) Infection-induced intestinal oxidative stress triggers organ-to-organ immunological communication in Drosophila. Cell Host & Microb 11(4): 410–417. (featured by Cell Host & Microbe. 11: 323-324) (IF: 13.728)
  5. Chen PC, Huang YY, and Juang JL*. (2011) MEMS microwell and microcolumn arrays: novel methods for high-throughput cell-based assays. Lab Chip. 11(21): 3619-3625 (IF: 6.260)
  6. Lin TY, Huang CH, Kao HH, Liou GG, Yeh, SR, Cheng CM, Chen MH, Pan, RL, Juang JL*. (2009) Abi plays an opposing role to Abl in Drosophila axonogenesis and synaptogenesis. Development. 136(18): 3099-107 (IF: 7.194).
  7. Liu SC, Jen YM, Jiang SS, Chang JL, Hsiung CA, Wang CH, Juang JL*. (2009) Ga12-mediated pathway promotes invasiveness of nasopharyngeal carcinoma by modulating actin cytoskeleton reorganization. Cancer Research. 69(15): 6122-30 (IF: 7.54).
  8. Huang CH, Lin TY, Pan RL, Juang JL*. (2007) The involvement of Abl and PTP61F in the regulation of Abi protein localization and stability and lamella formation in Drosophila S2 cells. J. Biol. Chem. 282(44):32442-32452. (IF: 5.8)
  9. Chen TC, Lai YK, Yu CK, and Juang JL*. (2007) Enterovirus 71 triggering of neuronal apoptosis through activation of Abl-Cdk5 signaling. Cell. Micro 9(11): 2676–2688. (IF: 5.07)
  10. Lin H, Lin TY, and Juang JL*. (2007) Abl deregulates Cdk5 kinase activity and subcellular localization for amyloid-induced Drosophila Cell Death Differ. 14:607-615. (IF: 8.254)


  1. Juang, J.L., Lee, D.F. (2004) Baculovirus-based expression system. United States Patent. Patent No.: US6,814,963 B2.
  2. Juang, J.L., Lee, D.F. (2006) Internal ribosome entry site of the labial gene for protein expression. United States Patent. Patent No.: US US7119187
  3. 莊志立, 李東芳。(2006) 可供重組蛋白質表現之Labial基因的內部核糖體結合位置。中華民國發明第I 260346號。
  4. 莊志立,熊昭,林仲彥。(2007) 跨種核酸探針。中華民國發明第I 286573號。
  5. 莊志立, 李東芳。(2010) 重組桿狀病毒感染非宿主細胞的方法。中華民國發明第I 330198號。
  6. 莊志立,林赫。(2011) 抑制神經退化性疾病的方法。中華民國發明第I343806號。

Lab Members

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