| Min Wang | |
|---|---|
| Photo placeholder | |
| Affiliations | Shanghai Jiao Tong University |
| Country | China |
| H-index | 60 |
| Research Focus | Alzheimer's Disease |
| Mechanisms | Stem cells, Regenerative medicine |
Min Wang is an important component in the neurobiology of neurodegenerative diseases. This page provides detailed information about its structure, function, and role in disease processes.
Min Wang is a leading researcher in the field of neurodegenerative diseases, affiliated with Shanghai Jiao Tong University [1]. Their research focuses on Stem cells, Regenerative medicine, with particular emphasis on Alzheimer's Disease [2]. With an h-index of 60, Wang is among the most cited researchers in the
neuroscience field [3]. Wang's work spans
multiple aspects of neurodegeneration, contributing to our understanding of the molecular mechanisms that underlie diseases such as Alzheimer's Disease. Their research group has
made significant contributions to the fields of Stem cells, Regenerative medicine, publishing in high-impact journals including leading neuroscience journals. Based at Shanghai
Jiao Tong University, Wang collaborates with researchers across multiple institutions worldwide, working to advance therapeutic strategies for neurodegenerative conditions.
Wang has developed research programs that bridge basic neuroscience, translational biomarker work, and clinical interpretation. Across appointments at Shanghai Jiao Tong University, their group has helped define how mechanistic discoveries are converted into robust disease models and clinically actionable hypotheses.
The laboratory's approach combines rigorous experimental design with broad collaboration across disease-focused teams. This includes hypothesis-driven studies, replication across independent cohorts, and careful interpretation of effect sizes, heterogeneity, and confounding factors that often complicate neurodegeneration research.
The publication portfolio is being expanded from primary literature databases, with emphasis on high-impact studies and longitudinal research programs.
Their program contributes to translational and mechanistic work in [Alzheimer's disease[/diseases/[alzheimers[/diseases/[alzheimers[/diseases/[alzheimers--TEMP--/diseases)--FIX--.
The lab emphasizes Stem cells to connect molecular findings with patient outcomes. The lab emphasizes Regenerative medicine to connect molecular findings with patient outcomes.
These efforts support clearer disease taxonomy, stronger biomarker validation pipelines, and prioritization of therapeutic targets with human biological relevance. The work also contributes to cross-disease comparisons that reveal shared pathways and disease-specific vulnerabilities.
Current priorities in Wang's research ecosystem include improving reproducibility across cohorts, integrating multi-omic and longitudinal clinical datasets, and clarifying which biological signals are most predictive of near-term progression and treatment response. A recurring challenge across neurodegeneration is separating causal drivers from downstream correlates, especially when molecular pathology and clinical symptoms evolve over long time horizons.
Another central objective is translation: defining how mechanistic discoveries can be converted into practical diagnostics and intervention strategies. This includes identifying robust stratification markers, benchmarking assays across sites, and aligning trial endpoints with biologically meaningful changes rather than only late-stage clinical decline.
Collaborator network pending enrichment.
[Iliff JJ et al.. "A paravascular pathway facilitates CSF flow through the brain parenchyma and the clearance of interstitial solutes, including amyloid β." Science translational medicine (2012). DOI)
[Tcw J et al.. "Cholesterol and matrisome pathways dysregulated in [astrocytes[/entities/[astrocytes[/entities/[astrocytes[/entities/[astrocytes--TEMP--/entities)--FIX-- and [microglia[/entities/[microglia[/entities/[microglia[/entities/[microglia--TEMP--/entities)--FIX--." Cell (2022). DOI)
[Choi I et al.. "[Autophagy[/entities/[autophagy[/entities/[autophagy[/entities/[autophagy--TEMP--/entities)--FIX-- enables microglia to engage amyloid plaques and prevents microglial senescence." Nature cell biology (2023). DOI)
[Bai B et al.. "Deep Multilayer Brain Proteomics Identifies Molecular Networks in Alzheimer's Disease Progression." [Neuron[/entities/[neurons[/entities/[neurons[/entities/[neurons--TEMP--/entities)--FIX-- (2020). DOI)
[Johnson ECB et al.. "Large-scale proteomic analysis of Alzheimer's Disease brain and cerebrospinal fluid reveals early changes in energy metabolism associated with microglia and astrocyte activation." Nature medicine (2020). DOI)
[Wang M et al.. "Non-invasive modulation of meningeal lymphatics ameliorates ageing and Alzheimer's Disease-associated pathology and cognition in mice." Nature communications (2024). DOI)
[Hur JY et al.. "The innate immunity protein IFITM3 modulates γ-secretase in Alzheimer's Disease." Nature (2020). DOI)
[Chen G et al.. "ApoE3 R136S binds to [Tau[/entities/[tau-protein[/entities/[tau-protein[/entities/[tau-protein--TEMP--/entities)--FIX-- and blocks its propagation, suppressing neurodegeneration in mice with Alzheimer's Disease." Neuron (2025). DOI)
[Iliff JJ et al.. "A paravascular pathway facilitates CSF flow through the brain parenchyma and the clearance of interstitial solutes, including amyloid β." Science translational medicine (2012). [DOI: 10.1126/scitranslmed.3003748]https://doi.org/10.1126/scitranslmed.3003748) PubMed: 22896675
[Tcw J et al.. "Cholesterol and matrisome pathways dysregulated in astrocytes and microglia." Cell (2022). [DOI: 10.1016/j.cell.2022.05.017]https://doi.org/10.1016/j.cell.2022.05.017) PubMed: 35750033
[Choi I et al.. "Autophagy enables microglia to engage amyloid plaques and prevents microglial senescence." Nature cell biology (2023). [DOI: 10.1038/s41556-023-01158-0]https://doi.org/10.1038/s41556-023-01158-0) PubMed: 37231161
[Bai B et al.. "Deep Multilayer Brain Proteomics Identifies Molecular Networks in Alzheimer's Disease Progression." Neuron (2020). [DOI: 10.1016/j.neuron.2019.12.015]https://doi.org/10.1016/j.neuron.2019.12.015) PubMed: 31926610
[Johnson ECB et al.. "Large-scale proteomic analysis of Alzheimer's Disease brain and cerebrospinal fluid reveals early changes in energy metabolism associated with microglia and astrocyte activation." Nature medicine (2020). [DOI: 10.1038/s41591-020-0815-6]https://doi.org/10.1038/s41591-020-0815-6) PubMed: 32284590
[Wang M et al.. "Non-invasive modulation of meningeal lymphatics ameliorates ageing and Alzheimer's Disease-associated pathology and cognition in mice." Nature communications (2024). [DOI: 10.1038/s41467-024-45656-7]https://doi.org/10.1038/s41467-024-45656-7) PubMed: 38365740
[Hur JY et al.. "The innate immunity protein IFITM3 modulates γ-secretase in Alzheimer's Disease." Nature (2020). [DOI: 10.1038/s41586-020-2681-2]https://doi.org/10.1038/s41586-020-2681-2) PubMed: 32879487
[Chen G et al.. "ApoE3 R136S binds to Tau and blocks its propagation, suppressing neurodegeneration in mice with Alzheimer's Disease." Neuron (2025). [DOI: 10.1016/j.neuron.2024.12.015]https://doi.org/10.1016/j.neuron.2024.12.015) PubMed: 39814008
[Iliff JJ et al.. "A paravascular pathway facilitates CSF flow through the brain parenchyma and the clearance of interstitial solutes, including amyloid β." Science translational medicine (2012). DOI)
[Tcw J et al.. "Cholesterol and matrisome pathways dysregulated in astrocytes and microglia." Cell (2022). DOI)
[Choi I et al.. "Autophagy enables microglia to engage amyloid plaques and prevents microglial senescence." Nature cell biology (2023). DOI)
[Bai B et al.. "Deep Multilayer Brain Proteomics Identifies Molecular Networks in Alzheimer's Disease Progression." Neuron (2020). DOI)
[Johnson ECB et al.. "Large-scale proteomic analysis of Alzheimer's Disease brain and cerebrospinal fluid reveals early changes in energy metabolism associated with microglia and astrocyte activation." Nature medicine (2020). DOI)
[Wang M et al.. "Non-invasive modulation of meningeal lymphatics ameliorates ageing and Alzheimer's Disease-associated pathology and cognition in mice." Nature communications (2024). DOI)
[Hur JY et al.. "The innate immunity protein IFITM3 modulates γ-secretase in Alzheimer's Disease." Nature (2020). DOI)
[Chen G et al.. "ApoE3 R136S binds to Tau and blocks its propagation, suppressing neurodegeneration in mice with Alzheimer's Disease." Neuron (2025). DOI)
[Iliff JJ et al.. "A paravascular pathway facilitates CSF flow through the brain parenchyma and the clearance of interstitial solutes, including amyloid β." Science translational medicine (2012). [DOI: 10.1126/scitranslmed.3003748]https://doi.org/10.1126/scitranslmed.3003748) PubMed: 22896675
[Tcw J et al.. "Cholesterol and matrisome pathways dysregulated in astrocytes and microglia." Cell (2022). [DOI: 10.1016/j.cell.2022.05.017]https://doi.org/10.1016/j.cell.2022.05.017) PubMed: 35750033
[Choi I et al.. "Autophagy enables microglia to engage amyloid plaques and prevents microglial senescence." Nature cell biology (2023). [DOI: 10.1038/s41556-023-01158-0]https://doi.org/10.1038/s41556-023-01158-0) PubMed: 37231161
[Bai B et al.. "Deep Multilayer Brain Proteomics Identifies Molecular Networks in Alzheimer's Disease Progression." Neuron (2020). [DOI: 10.1016/j.neuron.2019.12.015]https://doi.org/10.1016/j.neuron.2019.12.015) PubMed: 31926610
[Johnson ECB et al.. "Large-scale proteomic analysis of Alzheimer's Disease brain and cerebrospinal fluid reveals early changes in energy metabolism associated with microglia and astrocyte activation." Nature medicine (2020). [DOI: 10.1038/s41591-020-0815-6]https://doi.org/10.1038/s41591-020-0815-6) PubMed: 32284590
[Wang M et al.. "Non-invasive modulation of meningeal lymphatics ameliorates ageing and Alzheimer's Disease-associated pathology and cognition in mice." Nature communications (2024). [DOI: 10.1038/s41467-024-45656-7]https://doi.org/10.1038/s41467-024-45656-7) PubMed: 38365740
[Hur JY et al.. "The innate immunity protein IFITM3 modulates γ-secretase in Alzheimer's Disease." Nature (2020). [DOI: 10.1038/s41586-020-2681-2]https://doi.org/10.1038/s41586-020-2681-2) PubMed: 32879487
[Chen G et al.. "ApoE3 R136S binds to Tau and blocks its propagation, suppressing neurodegeneration in mice with Alzheimer's Disease." Neuron (2025). [DOI: 10.1016/j.neuron.2024.12.015]https://doi.org/10.1016/j.neuron.2024.12.015) PubMed: 39814008
Page auto-generated from NeuroWiki researcher database. Last updated: 2026-03-01.
Page auto-generated from NeuroWiki researcher database. Last updated: 2026-03-01.
The study of Min Wang has evolved significantly over the past decades. Research in this area has revealed important insights into the underlying mechanisms of neurodegeneration and continues to drive therapeutic development.
Historical context and key discoveries in this field have shaped our current understanding and will continue to guide future research directions.