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A recent dissertation from Charité – Universitätsmedizin Berlin by Lucie Yuanting Li explores the role of autoantibodies in autoimmune encephalitis, provides insights into mechanisms that disrupt the blood-brain barrier (BBB).
Key Findings of the Study
Led by Lucie Yuanting Li from Charité – Universitätsmedizin Berlin, the research explored the role of autoantibodies in autoimmune encephalitis, uncovering mechanisms of blood-brain barrier disruption:
Key Findings
- Diverse Autoantibodies Identified: Detection of various non-disease-defining autoantibodies in cerebrospinal fluid.
- Myosin-X as a Target Antigen: Monoclonal antibody 011-138 targets Myosin-X, reacting with brain blood vessels and cerebellar Purkinje cells.
- BBB Function Impairment: Monoclonal antibody 011-138 reduces the expression of tight junction protein Occludin, compromising BBB integrity both in vitro and in vivo.
This research highlights the significant impact of non-disease-defining antibodies on neurological conditions and advances our understanding of antibody-mediated BBB disruption.
PELOBiotech offers high-quality Solutions
The research relied on special media from PELOBiotech:
- Cellovations Microvascular Endothelial Cell Growth Medium Kit (PB-MH-100-4099)
These products ensured optimal cell growth and experimental reliability, enabling accurate in vitro blood-brain barrier function and integrity measurements.
The Path Forward in BBB Research
By exploring the impact of autoantibodies on blood-brain barrier integrity and identifying Myosin-X as a target antigen, this research provides a foundation for understanding antibody-mediated neurological disorders. Insights into BBB disruption mechanisms pave the way for developing targeted therapeutic strategies to prevent or mitigate damage caused by autoantibodies.
Congratulations to Lucie Yuanting Li on this contribution to neuroscience! PELOBiotech is glad to support innovative research that advances our understanding of the blood-brain barrier and neurological diseases.
Read the full dissertation: Link
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