Jiali Sun
Current Organizations / Institutes
The organizations/institutes from the scholar's latest article
Jiali Sun has a total of 16 co-authors. Here are the top co-authors by number of shared publications:
- Huabing Wang
Department of Neurology, Beijing Tiantan Hospital Capital Medical University Beijing China
2 shared publications - Linlin Yin
Department of Neuroinfection and Neuroimmunology, Beijing Tiantan Hospital, Capital Medical University, Beijing, China
2 shared publications - Xinghu Zhang
Center for Neurology, Beijing Tiantan Hospital, Capital Medical University, Beijing, China
2 shared publications - De-Cai Tian
Department of Neurology, China National Clinical Research Center for Neurological Diseases, Beijing Tiantan Hospital, Capital Medical University, China
1 shared publication - Haoxiao Chang
Department of Neurology, Neuroinfection and Neuroimmunology Center, Beijing Tiantan Hospital, Capital Medical University, Beijing, China
1 shared publication - Jia Ma
Department of Neurology, Beijing Shunyi Hospital, Beijing, China
1 shared publication
Latest Publications
- 2 February 2025
- Published by Elsevier in Multiple Sclerosis and Related Disorders
- Vol. 95, 106313
Cerebrospinal fluid interleukin-6 may be a biomarker for conversion of clinically isolated syndrome to neuromyelitis optica spectrum disorder
- 2 February 2025
- Published by Elsevier in Multiple Sclerosis and Related Disorders
- Vol. 95, 106313
Cerebrospinal fluid interleukin-6 may be a biomarker for conversion of clinically isolated syndrome to neuromyelitis optica spectrum disorder
- Open Access
- 22 July 2023
- Published by Springer Nature in Journal of Neuroinflammation
- Vol. 20 (1) , 1-10
Elevated blood and cerebrospinal fluid biomarkers of microglial activation and blood‒brain barrier disruption in anti-NMDA receptor encephalitis
Background: Anti-NMDA receptor (NMDAR) encephalitis is an autoimmune disease characterized by complex neuropsychiatric syndrome and cerebrospinal fluid (CSF) NMDAR antibodies. Triggering receptor expressed on myeloid cells 2 (TREM2) has been reported to be associated with inflammation of the central nervous system (CNS). Matrix metalloproteinase-9 (MMP9) and cluster of differentiation (CD44) were measured to evaluate blood‒brain barrier (BBB) permeability in anti-NMDAR encephalitis. The roles of microglial activation and BBB disruption in anti-NMDAR encephalitis are not well known. Findings: In this work, we detected increased expression levels of CSF sTREM2, CSF and serum CD44, and serum MMP9 in anti-NMDAR encephalitis patients compared with controls. CSF sTREM2 levels were positively related to both CSF CD44 levels (r = 0.702, p < 0.0001) and serum MMP9 levels (r = 0.428, p = 0.021). In addition, CSF sTREM2 levels were related to clinical parameters (modified Rankin Scale scores, r = 0.422, p = 0.023, and Glasgow Coma Scale scores, r = − 0.401, p = 0.031). Conclusion: Increased sTREM2 levels in CSF as well as increased CD44 and MMP9 in serum and CSF reflected activation of microglia and disruption of the BBB in anti-NMDAR encephalitis, expanding the understanding of neuroinflammation in this disease. The factors mentioned above may have potential as novel targets for intervention or novel diagnostic biomarkers.
- 22 July 2023
- Published by Springer Nature in Journal of Neuroinflammation
- Vol. 20 (1) , 1-10
Open AccessElevated blood and cerebrospinal fluid biomarkers of microglial activation and blood‒brain barrier disruption in anti-NMDA receptor encephalitis
Background: Anti-NMDA receptor (NMDAR) encephalitis is an autoimmune disease characterized by complex neuropsychiatric syndrome and cerebrospinal fluid (CSF) NMDAR antibodies. Triggering receptor expressed on myeloid cells 2 (TREM2) has been reported to be associated with inflammation of the central nervous system (CNS). Matrix metalloproteinase-9 (MMP9) and cluster of differentiation (CD44) were measured to evaluate blood‒brain barrier (BBB) permeability in anti-NMDAR encephalitis. The roles of microglial activation and BBB disruption in anti-NMDAR encephalitis are not well known. Findings: In this work, we detected increased expression levels of CSF sTREM2, CSF and serum CD44, and serum MMP9 in anti-NMDAR encephalitis patients compared with controls. CSF sTREM2 levels were positively related to both CSF CD44 levels (r = 0.702, p < 0.0001) and serum MMP9 levels (r = 0.428, p = 0.021). In addition, CSF sTREM2 levels were related to clinical parameters (modified Rankin Scale scores, r = 0.422, p = 0.023, and Glasgow Coma Scale scores, r = − 0.401, p = 0.031). Conclusion: Increased sTREM2 levels in CSF as well as increased CD44 and MMP9 in serum and CSF reflected activation of microglia and disruption of the BBB in anti-NMDAR encephalitis, expanding the understanding of neuroinflammation in this disease. The factors mentioned above may have potential as novel targets for intervention or novel diagnostic biomarkers.