Di Wen | Neuroscience | Best Researcher Award

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Dr. Di Wen | Neuroscience | Best Researcher Award

Dr. Di Wen | The Second Hospital of Hebei Medical University | China

Dr. Di Wen, a dedicated neurologist at the Second Hospital of Hebei Medical University, specializes in neurodegenerative diseases, particularly amyotrophic lateral sclerosis (ALS). Her research focuses on gene therapy, autophagy, and mitochondrial protection, with significant findings on the role of OPTN in regulating autophagy and mitophagy. She has contributed to multiple high-impact SCI-indexed publications and leads projects funded by the Hebei Natural Science Foundation. As a member of professional medical committees, Dr. Wen’s work advances therapeutic strategies for ALS, aiming to translate laboratory discoveries into effective clinical interventions that improve patient outcomes.

Author Profile

Scopus

Education

Dr. Di Wen’s journey into the world of neuroscience began with a strong academic foundation rooted in medical sciences, leading to her specialization in neurology. From the early stages of her education, she displayed a keen interest in understanding the complexities of the human nervous system, with a particular focus on neurodegenerative disorders. Her academic path was characterized by rigorous training, in-depth research engagements, and a determination to explore the molecular and cellular underpinnings of diseases like amyotrophic lateral sclerosis (ALS). During her early career, she cultivated expertise in advanced research methodologies, live-cell imaging techniques, and genetic intervention strategies, all of which laid the groundwork for her future breakthroughs in gene therapy and mitochondrial biology.

Experience

As a neurologist at the Department of Neurology, The Second Hospital of Hebei Medical University, Dr. Wen has combined clinical practice with high-level research. Her role bridges patient care and scientific discovery, ensuring that her laboratory findings are guided by real-world medical needs. Beyond her clinical duties, she actively engages in research projects funded by the Hebei Natural Science Foundation (Project Code: H2021206048), where she leads investigations into the genetic and molecular mechanisms underlying ALS. Dr. Wen also collaborates extensively with multidisciplinary teams, including molecular biologists, geneticists, and pharmacologists, to accelerate the translation of benchside discoveries into bedside therapies. Her professional trajectory demonstrates a rare balance of medical excellence and scientific innovation.

Research Focus

Dr. Wen’s research is centered on neurodegenerative diseases, with a primary emphasis on ALS, a condition marked by progressive motor neuron degeneration leading to paralysis. Her landmark studies have shed light on the role of the OPTN gene in regulating autophagy and mitophagy—two crucial cellular processes involved in maintaining neuronal health. Using advanced genetic tools such as LV-sgRNA-OPTN and confocal live-cell imaging, she demonstrated how loss of OPTN impairs mitochondrial function, decreases autophagic flux, and increases oxidative stress in neuronal cells. Her work extends beyond cellular models, exploring gene therapy interventions in SOD1-G93A transgenic mice, where she has shown that enhancing autophagy pathways can protect mitochondria and potentially slow ALS progression. In parallel, Dr. Wen has contributed to research on insulin-like growth factor 1 (IGF-1) as a neuroprotective agent, identifying its role in mitochondrial preservation and apoptosis inhibition. Her prolific publication record in high-impact journals like The FEBS Journal and Brain Research Bulletin underscores the depth and significance of her contributions to the global ALS research community.

Awards and Recognition

Dr. Wen’s dedication to advancing neurological research has been recognized through multiple scientific publications indexed in SCI and other reputable databases. Her papers, some of which have achieved high citation counts, reflect both her innovative approach and her influence in the field of neurobiology. She holds professional memberships in the Sleep and Mood Disorders Professional Committee of Hebei Geriatric Association and the Young Physicians Committee of Hebei Medical Association, affirming her active engagement in professional and academic communities. These affiliations enable her to contribute to collaborative research networks and participate in shaping clinical and research agendas at regional and national levels.

Impact and Influence

The impact of Dr. Wen’s work extends beyond the laboratory, influencing both clinical strategies and future research directions for ALS and related neurodegenerative disorders. By elucidating the molecular mechanisms behind impaired autophagy and mitochondrial dysfunction, she has opened new therapeutic avenues for slowing disease progression. Her studies on gene therapy interventions have the potential to revolutionize treatment protocols, offering hope to patients and their families. Furthermore, her research fosters cross-disciplinary collaboration, encouraging the integration of neurology, genetics, and molecular biology in tackling complex neurological conditions.

Publications

OPTN gene therapy increases autophagy and protects mitochondria in SOD1‐G93A‐expressing transgenic mice and cells.

Author:Wen D; Ji Y; Yuanyuan Li; Duan W; Wang Y; Li Z; Tao M; Li Y
Journal: The FEBS Journal
Year:  2024

The role of insulin-like growth factor 1 in ALS cell and mouse models: A mitochondrial protector.

Author: Wen D; Cui C; Duan W; Wang W; Wang Y; Liu Y; Li Z; Li C
Journal: Brain Research Bulletin
Year: 2019

Systemic administration of scAAV9-IGF1 extends survival in SOD1G93A ALS mice via inhibiting p38 MAPK and the JNK-mediated apoptosis pathway.

Author: Wang W; Wen D; Duan W; Yin J ; Cui C; Wang Y; Liu Y; Li C
Journal: Brain Research Bulletin
Year: 2017

TBK1 is involved in M-CSF-induced macrophage polarization through mediating the IRF5/IRF4 axis.

Author: Li Y, Ji L, Liu C, Li J, Wen D, Li Z , Yu L, Guo M, Zhang S, Duan W , Yi L, Y. Bi Y, Bu H, Li C and Liu Y
Journal:The FEBS Journal
Year: 2024

Intrathecal Delivery of ssAAV9-DAO Extends Survival in SOD1G93A ALS Mice.

Author: Wang W, Duan W, Wang Y, Wen D, Liu Y, Li Z, Hu H, Cui H, Cui C, Lin H, Li C
Journal: Neurochem Research
Year: 2017

Conclusion

Dr. Di Wen, of The Second Hospital of Hebei Medical University, stands as a dedicated clinician–scientist whose work seamlessly bridges advanced research and compassionate patient care. Through her pioneering studies on autophagy, mitophagy, and gene therapy in amyotrophic lateral sclerosis, she has significantly advanced the understanding of disease mechanisms and potential therapeutic strategies. Her contributions, reflected in high-impact publications, professional leadership roles, and collaborative projects, underscore her influence in the neurological research community. With a clear vision for future innovations in personalized neurotherapies, Dr. Wen continues to inspire progress toward effective treatments for complex neurodegenerative diseases.

Chao Peng | Neurodegenerative disease | Best Researcher Award

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Prof. Chao Peng | Neurodegenerative disease | Best Researcher Award

Prof. Chao Peng, Department of Neurology UCLA, United States

“Prof. Chao Peng is an Assistant Professor at the Department of Neurology, UCLA, USA. His research focuses on neurodegenerative diseases, particularly the transmission and spread of pathological proteins like alpha-synuclein and tau. Prof. Peng has received numerous awards and grants for his work, including the Michael J. Fox Foundation Grant and the CurePSP Grant.”

Profile

Scopus

Early Academic Pursuits 🎓

Dr. Chao Peng’s journey into the world of biomedical sciences began at Wuhan University, China, where he pursued a B.Sc. in Life Science (2002–2006). His keen interest in developmental biology led him to Fudan University, Shanghai, China, where he earned his Ph.D. (2006–2012) under the mentorship of Dr. Wufan Tao, with co-mentors Min Han, Yuan Zhuang, and Tian Xu. During his Ph.D. studies, he established groundbreaking piggyBac transposon-based genetic screening systems to identify metastasis genes, tumor suppressors, and drug resistance-related genes. His work also included generating Vps18 conditional knockout mice, which played a pivotal role in understanding late endocytosis in neural cell survival and dendrite development.

Professional Endeavors 🏛️

Dr. Peng has had an illustrious career in neuroscience, focusing on molecular mechanisms underlying neurodegenerative diseases. After completing his doctoral studies, he embarked on a rigorous postdoctoral fellowship (2013–2018) at the University of Pennsylvania, Dr. Virginia Lee’s Laboratory, where he made seminal discoveries regarding the pathological α-synuclein strains and their role in neurodegeneration. His tenure at Pennsylvania continued as a Research Associate (2018–2019), where he refined methodologies for studying protein aggregation and transmission in neurodegenerative conditions.

In January 2020, Dr. Peng joined the prestigious University of California, Los Angeles (UCLA) as an Assistant Professor. Here, his research delves into the molecular machinery of pathological α-synuclein and tau transmission, their genetic and environmental risk factors, and their structural diversity in diseased brains. His work aims to develop novel disease models for neurodegenerative disorders, offering new therapeutic avenues.

Contributions and Research Focus 🔬

Dr. Peng’s research is dedicated to unraveling the complexities of protein misfolding and aggregation in neurodegenerative diseases, particularly Parkinson’s disease and tauopathies. Some of his most notable contributions include:

  • Pathological α-synuclein strains: He demonstrated the biological and structural diversity of α-synuclein strains, which has significant implications for diagnostics and targeted therapies.
  • Cross-seeding of pathological proteins: His studies revealed interactions between α-synuclein, tau, and TDP-43, which may provide insight into disease progression and overlapping pathologies.
  • Post-translational modifications (PTMs) of α-synuclein: He systematically examined PTMs and their role in protein aggregation, shedding light on their functional significance in disease pathogenesis.
  • Development of disease models: His work on oligodendrocyte-mediated α-synuclein transmission has led to advanced models for studying Multiple System Atrophy (MSA) and related disorders.
  • High-throughput screening systems: He has pioneered screening techniques to evaluate protein aggregation inhibitors, paving the way for potential therapeutics.

Accolades and Recognition 🏆

Dr. Peng’s impactful research has been widely recognized in the scientific community. Some of his notable honors include:

  • Invited Speaker at Prestigious Conferences & Institutions: NIH (2024), University of Pennsylvania (2024), UT Southwestern (2023), Tiantan International Movement Disorder Symposium (2022), King’s College London (2020), Cornell University (2020), and more.
  • Editorial & Peer Review Contributions: He serves as a reviewer for renowned journals such as Science Translational Medicine, Nature Chemical Biology, and Molecular Neurodegeneration.
  • Highly Cited Publications: His studies have been published in Nature, Neuron, Nature Neuroscience, JBC, and Nature Reviews Neurology, influencing global research in neurodegeneration.

Publication Top Notes

Post-translational modifications of soluble α-synuclein regulate the amplification of pathological α-synuclein

Author: Zhang, S., Zhu, R., Pan, B., Xu, H., Olufemi, M., Gathagan, R., Li, Y., Zhang, L., Zhang, J., Xiang, Q., Kagan, E., Cao, X., Yuan, C., Kim, S., Williams, C., Magaki, S., Vinters, H., Lashuel, H., Garcia, B., Petersson, J., Trojanowski, J.Q., Lee, V.M.,* Peng, C.*

Journal: Nature Nueroscience

Year: 2023

Cellular milieu imparts distinct pathological α-synuclein strains in α-synucleinopathies

Author: Peng, C., Gathagan, R.J., Covell, D.J., Medellin, C., Stieber, A., Robinson, J.L., Zhang, B., Pitkin, R.M., Olufemi, M.F., Luk, K.C.,

Journal: Neurodegeneration

Year: 2018