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Nature Publication by Heneka and colleagues

Inflammatory Processes Drive Progression of Alzheimer's and Other Brain Diseases

Report in "Nature" Inflammation drives the progression of neurodegenerative brain diseases and plays a major role in the accumulation of tau proteins within neurons. An international research team led by Prof. Michael Heneka (DZNE), member of cluster of excellence ImmunoSensation, and the University of Bonn comes to this conclusion in the journal "Nature". The findings are based on the analyses of human brain tissue and further lab studies. In the particular case of Alzheimer's the results reveal a hitherto unknown connection between Abeta and tau pathology. Furthermore, the results indicate that inflammatory processes represent a potential target for future therapies. ies. In the particular case of Alzheimer's the results reveal a hitherto unknown connection between Abeta and tau pathology. Furthermore, the results indicate that inflammatory processes represent a potential target for future therapies.

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NLRP3 inflammasome activation drives tau pathology

Christina Ising et al., Nature (2019), DOI: 10.1038/s41586-019-1769-z

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—An international research team involving Bonn scientist has made an important contribution to understanding the human immune response to poxviruses: The scientists were able to show for the first time that different human cell types recognize poxviruses via different sensors in order to trigger inflammatory responses. At the same time, the team developed the world's first nanobodies that can specifically block the DNA sensor AIM2 – a tool that opens up new possibilities for inflammation and infection research. The paper has now been published in The EMBO Journal.
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Multiple Sclerosis: Potential biomarker linked to progression and brain inflammation identified

—Better ways to detect ongoing brain damage in multiple sclerosis (MS) are urgently needed. An international team of scientists, including ImmunoSensation³ member Prof. Anne-Katrin Pröbstel, has identified a molecular circuit that drives brain injury in MS. In a mouse model, blocking the enzyme Bruton's tyrosine kinase prevented harmful clustering of immune cell and brain tissue demage. Patient data revealed the same immune signaling pattern, suggesting strong translational potential for diagnosis. The study was recently published in Nature Immunology.
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Instructions for building antibodies decoded

—MOG Antibody-associated Disease (MOGAD) is a rare autoimmune disease of the central nervous system. The blood of patients contains antibodies against myelin oligodendrocyte glycoprotein (MOG), a protein in the myelin layer that surrounds the neurons in the brain. It is believed that these antibodies contribute to the destruction of this protective layer in the brain. Researchers at the University Hospital Bonn (UKB) and the Universities of Basel and Bonn, in collaboration with an international team, have now deciphered the construction plan of the anti-MOG antibodies.
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