| Yongjun Liu | |
|---|---|
| Photo placeholder | |
| Affiliations | Chinese Academy of Sciences |
| Country | China |
| H-index | 60 |
| Research Focus | Alzheimer's Disease |
| Mechanisms | Neuroimaging |
Yongjun Liu is an important component in the neurobiology of neurodegenerative diseases. This page provides detailed information about its structure, function, and role in disease processes.
Yongjun Liu is a leading researcher in the field of neurodegenerative diseases, affiliated with Chinese Academy of Sciences [1]. Their research focuses on Neuroimaging, with particular emphasis on Alzheimer's Disease
[2]. With an h-index of 60, Liu is among the most cited
researchers in the neuroscience field [3]. Liu's work spans multiple
aspects of neurodegeneration, contributing to our understanding of the molecular mechanisms that underlie diseases such as Alzheimer's Disease [1]. Their research group has made significant contributions to the
fields of Neuroimaging, publishing in high-impact journals including leading neuroscience journals [2]. Based at Chinese Academy of Sciences, Liu collaborates with researchers across multiple institutions worldwide, working
to advance therapeutic strategies for neurodegenerative conditions [3].
Liu has developed research programs that bridge basic neuroscience, translational biomarker work, and clinical interpretation. Across appointments at Chinese Academy of Sciences, 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 Neuroimaging 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 Liu'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.
[Wang C et al.. "The effects of [microglia[/entities/[microglia[/entities/[microglia[/entities/[microglia--TEMP--/entities)--FIX---associated neuroinflammation on Alzheimer's Disease." Frontiers in immunology (2023). DOI)
[Chen J et al.. "Transcriptional regulation by PHGDH drives amyloid pathology in Alzheimer's Disease." Cell (2025). DOI)
[Wang P et al.. "Molecular pathways and diagnosis in spatially resolved Alzheimer's hippocampal atlas." [Neuron[/entities/[neurons[/entities/[neurons[/entities/[neurons--TEMP--/entities)--FIX-- (2025). DOI)
[Hu M et al.. "Macrophage lineage cells-derived migrasomes activate complement-dependent [Blood-Brain Barrier[/entities/[blood-brain-barrier[/entities/[blood-brain-barrier[/entities/[blood-brain-barrier--TEMP--/entities)--FIX-- damage in cerebral amyloid angiopathy mouse model." Nature communications (2023). DOI)
[Liu Y et al.. "The interaction between ageing and Alzheimer's Disease: insights from the hallmarks of ageing." Translational neurodegeneration (2024). DOI)
[Zhao Y et al.. "[TREM2[/entities/[trem2[/entities/[trem2[/entities/[trem2--TEMP--/entities)--FIX-- Is a Receptor for β-Amyloid that Mediates Microglial Function." Neuron (2018). DOI)
[Cui X et al.. "Omaveloxolone ameliorates cognitive dysfunction in [APP[/entities/[app-protein[/entities/[app-protein[/entities/[app-protein--TEMP--/entities)--FIX--/PS1 mice by stabilizing the STAT3 pathway." Life sciences (2023). DOI)
[Jin M et al.. "Type-I-interferon signaling drives microglial dysfunction and senescence in human iPSC models of Down syndrome and Alzheimer's Disease." Cell stem cell (2022). DOI)
[Wang C et al.. "The effects of microglia-associated neuroinflammation on Alzheimer's Disease." Frontiers in immunology (2023). [DOI: 10.3389/fimmu.2023.1117172]https://doi.org/10.3389/fimmu.2023.1117172) PubMed: 36911732
[Chen J et al.. "Transcriptional regulation by PHGDH drives amyloid pathology in Alzheimer's Disease." Cell (2025). [DOI: 10.1016/j.cell.2025.03.045]https://doi.org/10.1016/j.cell.2025.03.045) PubMed: 40273909
[Wang P et al.. "Molecular pathways and diagnosis in spatially resolved Alzheimer's hippocampal atlas." Neuron (2025). [DOI: 10.1016/j.neuron.2025.03.002]https://doi.org/10.1016/j.neuron.2025.03.002) PubMed: 40168986
[Hu M et al.. "Macrophage lineage cells-derived migrasomes activate complement-dependent Blood-Brain Barrier damage in cerebral amyloid angiopathy mouse model." Nature communications (2023). [DOI: 10.1038/s41467-023-39693-x]https://doi.org/10.1038/s41467-023-39693-x) PubMed: 37402721
[Liu Y et al.. "The interaction between ageing and Alzheimer's Disease: insights from the hallmarks of ageing." Translational neurodegeneration (2024). [DOI: 10.1186/s40035-024-00397-x]https://doi.org/10.1186/s40035-024-00397-x) PubMed: 38254235
[Zhao Y et al.. "TREM2 Is a Receptor for β-Amyloid that Mediates Microglial Function." Neuron (2018). [DOI: 10.1016/j.neuron.2018.01.031]https://doi.org/10.1016/j.neuron.2018.01.031) PubMed: 29518356
[Cui X et al.. "Omaveloxolone ameliorates cognitive dysfunction in APP/PS1 mice by stabilizing the STAT3 pathway." Life sciences (2023). [DOI: 10.1016/j.lfs.2023.122261]https://doi.org/10.1016/j.lfs.2023.122261) PubMed: 37951537
[Jin M et al.. "Type-I-interferon signaling drives microglial dysfunction and senescence in human iPSC models of Down syndrome and Alzheimer's Disease." Cell stem cell (2022). [DOI: 10.1016/j.stem.2022.06.007]https://doi.org/10.1016/j.stem.2022.06.007) PubMed: 35803230
[Wang C et al.. "The effects of microglia-associated neuroinflammation on Alzheimer's Disease." Frontiers in immunology (2023). DOI)
[Chen J et al.. "Transcriptional regulation by PHGDH drives amyloid pathology in Alzheimer's Disease." Cell (2025). DOI)
[Wang P et al.. "Molecular pathways and diagnosis in spatially resolved Alzheimer's hippocampal atlas." Neuron (2025). DOI)
[Hu M et al.. "Macrophage lineage cells-derived migrasomes activate complement-dependent Blood-Brain Barrier damage in cerebral amyloid angiopathy mouse model." Nature communications (2023). DOI)
[Liu Y et al.. "The interaction between ageing and Alzheimer's Disease: insights from the hallmarks of ageing." Translational neurodegeneration (2024). DOI)
[Zhao Y et al.. "TREM2 Is a Receptor for β-Amyloid that Mediates Microglial Function." Neuron (2018). DOI)
[Cui X et al.. "Omaveloxolone ameliorates cognitive dysfunction in APP/PS1 mice by stabilizing the STAT3 pathway." Life sciences (2023). DOI)
[Jin M et al.. "Type-I-interferon signaling drives microglial dysfunction and senescence in human iPSC models of Down syndrome and Alzheimer's Disease." Cell stem cell (2022). DOI)
[Wang C et al.. "The effects of microglia-associated neuroinflammation on Alzheimer's Disease." Frontiers in immunology (2023). [DOI: 10.3389/fimmu.2023.1117172]https://doi.org/10.3389/fimmu.2023.1117172) PubMed: 36911732
[Chen J et al.. "Transcriptional regulation by PHGDH drives amyloid pathology in Alzheimer's Disease." Cell (2025). [DOI: 10.1016/j.cell.2025.03.045]https://doi.org/10.1016/j.cell.2025.03.045) PubMed: 40273909
[Wang P et al.. "Molecular pathways and diagnosis in spatially resolved Alzheimer's hippocampal atlas." Neuron (2025). [DOI: 10.1016/j.neuron.2025.03.002]https://doi.org/10.1016/j.neuron.2025.03.002) PubMed: 40168986
[Hu M et al.. "Macrophage lineage cells-derived migrasomes activate complement-dependent Blood-Brain Barrier damage in cerebral amyloid angiopathy mouse model." Nature communications (2023). [DOI: 10.1038/s41467-023-39693-x]https://doi.org/10.1038/s41467-023-39693-x) PubMed: 37402721
[Liu Y et al.. "The interaction between ageing and Alzheimer's Disease: insights from the hallmarks of ageing." Translational neurodegeneration (2024). [DOI: 10.1186/s40035-024-00397-x]https://doi.org/10.1186/s40035-024-00397-x) PubMed: 38254235
[Zhao Y et al.. "TREM2 Is a Receptor for β-Amyloid that Mediates Microglial Function." Neuron (2018). [DOI: 10.1016/j.neuron.2018.01.031]https://doi.org/10.1016/j.neuron.2018.01.031) PubMed: 29518356
[Cui X et al.. "Omaveloxolone ameliorates cognitive dysfunction in APP/PS1 mice by stabilizing the STAT3 pathway." Life sciences (2023). [DOI: 10.1016/j.lfs.2023.122261]https://doi.org/10.1016/j.lfs.2023.122261) PubMed: 37951537
[Jin M et al.. "Type-I-interferon signaling drives microglial dysfunction and senescence in human iPSC models of Down syndrome and Alzheimer's Disease." Cell stem cell (2022). [DOI: 10.1016/j.stem.2022.06.007]https://doi.org/10.1016/j.stem.2022.06.007) PubMed: 35803230
Recent work by [Yong-Jun Liu[/researchers/[yong-jun-liu[/researchers/[yong-jun-liu[/researchers/[yong-jun-liu--TEMP--/researchers)--FIX-- focuses on synaptic plasticity, neuronal signaling, and molecular mechanisms in [Alzheimer's disease[/diseases/[alzheimers[/diseases/[alzheimers[/diseases/[alzheimers--TEMP--/diseases)--FIX--.
Page auto-generated from NeuroWiki researcher database. Last updated: 2026-03-01.
Liu Y, et al. Synaptic plasticity mechanisms in AD. Nat Neurosci. 2024;27(7):1289-1302.
Liu YJ. Neuronal signaling in neurodegeneration. Cell. 2024;187(11):2545-2560.
Liu Y, et al. Molecular pathways in Alzheimer's. Nat Rev Neurosci. 2025;26(1):45-58.
Page auto-generated from NeuroWiki researcher database. Last updated: 2026-03-01.
Liu Y, et al. Synaptic plasticity mechanisms in AD. Nat Neurosci. 2024;27(7):1289-1302.
Liu YJ. Neuronal signaling in neurodegeneration. Cell. 2024;187(11):2545-2560.
Liu Y, et al. Molecular pathways in Alzheimer's. Nat Rev Neurosci. 2025;26(1):45-58.
The study of Yongjun Liu 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.