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.


Research Description:

Dr. Juang’s laboratory employs a multidisciplinary approach involving Drosophila genetics, along with mouse and cell line models, to delve into the molecular intricacies of Alzheimer’s disease (AD) and explore potential therapeutic avenues. The current research endeavors are centered on two primary research directions:

  1. Inter-organ Crosstalk in AD Development: Dr. Juang’s team is dedicated to uncovering the intricate interplay between various organs in the context of AD. They delve into how signaling cues triggered by adverse environmental or cellular factors in one organ can exert a profound impact on the brain, ultimately contributing to the onset and progression of AD. Notably, their groundbreaking work has highlighted the pivotal role of the gut-brain axis as a foundational factor driving the development of AD.
  2. Metabolic Dysfunction in AD: Within this research avenue, the lab’s focus is on the exploration of metabolic pathways in the context of AD. Their investigations have revealed the significant involvement of beta amyloid in modulating metabolic processes within peripheral organs. This connectivity between the brain’s metabolism and immune function and peripheral organs assumes paramount importance during AD development.

Through these dynamic research pursuits, Dr. Juang’s laboratory is at the forefront of expanding our understanding of AD. The overarching objective is to not only unravel the complexities of this devastating neurodegenerative disorder but also to identify potential therapeutic interventions that can make a meaningful impact in the ongoing battle against AD.


1. Unraveling the Gut-Brain Axis in AD: Pioneering Insights from a Drosophila Model Organism

The paper titled “Intestinal Microbial Dysbiosis and Alzheimer’s Progression,” published in Nature Communications (2017), significantly advances our grasp of the gut-brain axis in Alzheimer’s research. Using Drosophila (fruit fly) as a model, the study probes how gut microbial changes impact Alzheimer’s progression. The gut-brain axis, a bidirectional link between the gut and brain, is gaining recognition for its potential role in neurodegenerative conditions like Alzheimer’s.

This work strongly demonstrates how gut microbial imbalance impacts AD-like symptoms in Drosophila. Altering gut microbiota worsens toxic protein buildup and memory issues in these flies, mirroring Alzheimer’s traits. The study illuminates the gut’s potential influence on AD and suggests microbial imbalances could impact disease development. It enriches our understanding of the gut-brain axis as a crucial facet of AD, potentially guiding novel therapies.

With the gut microbiome gaining attention in neurological disorders, this research reaches beyond fruit flies, underlining the importance of gut-brain interactions in neurodegenerative diseases. Ultimately, this paper enhances our grasp of Alzheimer’s and unveils new avenues for addressing AD-related issues through the gut microbiome.

2. Challenging Conventions: Vitamin D Supplementation and Alzheimer’s Progression

Recent studies link vitamin D deficiency to higher AD risk. Vitamin D is considered beneficial for maintaining adult brain health genomically, as it binds with and activates a vitamin D-binding receptor (VDR)/retinoid X receptor (RXR) transcriptional complex. Whether VDR’s genomic role changes in AD brains is unknown.

Juang’s lab found higher VDR levels in AD brains despite low serum vitamin D. VDRs colocalized with Aβ plaques, gliosis, and autophagosomes in AD patients’ hippocampi, suggesting non-genomic VDR activation’s role in AD. The molecular determinants underlying the activation of the non-genomic VDR signaling pathway were closely examined, revealing that Aβ-induced VDR protein formed a complex with p53 in the cytosol, not with its canonical heterodimer partner RXR in the nucleus. Significantly, Aβ-induced VDR-p53 signaling appeared to play a crucial role in modulating AD neurodegeneration.

Moreover, animal model studies demonstrated that vitamin D supplementation resulted in increased Aβ depositions and exacerbated AD-like pathology, revealing unexpected and adverse outcomes. Human cohort studies further validated these findings, showing a similar trend of vitamin D supplementation exacerbating dementia. The convergence of evidence from both animal and human studies strengthens the credibility of this work and raises critical considerations for future research and clinical practice.

These findings call for a reevaluation of the current approach to vitamin D supplementation in AD, urging researchers and healthcare practitioners to critically examine the underlying mechanisms of vitamin D’s actions in the context of AD.


  1. Lai RH, Hsu CC, Yu BH, Lo YR, Hsu YY, Chen MH and Juang JL*. (2022) Vitamin D supplementation worsens Alzheimer’s progression: animal model and human cohort studies. Aging Cell. doi: 10.1111/acel.13670. Online ahead of print. (IF: 11.001)
  2. Lai, RH;Chow YH;Chung NH; Chen TC; Shie FS; Juang JL*. (2022) Neurotropic EV71 causes encephalitis by engaging intracellular TLR9 to elicit neurotoxic IL12-p40-iNOS signaling. Cell Death and Disease. 13(4):328 (IF: 9.705)
  3. Lai RH, Hsu YY, Shie FS , Huang CC, Chen MH and Juang JL (2021) Non-genomic rewiring of vitamin D receptor to p53 as a key to Alzheimer’s disease. Aging Cell 20(12):e13509(IF: 11.001)
  4. Wu TH, Lai RH, Yao CN, Juang JL* (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: 16.823)
  5. 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: 12.353)
  6. Wu SC, Liao CW, Pan RL, Juang JL*. (2012) Infection-induced intestinal oxidative stress triggers organ-to-organ immunological communication in Drosophila. Cell Host & Microbe. 11(4): 410–417. (featured by Cell Host & Microbe. 11: 323-324) (IF: 13.728)
  7. 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).
  8. 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).
  9. 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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