INmune Bio Inc. Announces Data Presented at the 16th European Meeting on Glial Cells in Health and Disease Shows that XPro Promotes Remyelination by Affecting Astroglial and Microglial Biology

Neutralizing soluble TNF with XPro promotes remyelination in cuprizone model after increasing astrocyte and microglia activation responses

Boca Raton, Florida, July 10, 2023 (GLOBE NEWSWIRE) --  INmune Bio, Inc. (NASDAQ: INMB) (the “Company”), a clinical-stage immunology company focused on developing treatments that harness the patient’s innate immune system to fight disease, announces important findings from data presented at The 16^th European Meeting on Glial Cells in Health and Disease.  The conference runs July 8-12 in Berlin, Germany.

Myelin is a specialized lipid produced by oligodendrocytes that forms the myelin sheath of axons.  Axons are the projections that allow neurons to communicate with each other and with other tissues such as muscle, skin, retina, nose and the ear for sight, smell and hearing respectively.  An intact and healthy myelin sheath is necessary for axons to work properly.  Any damage to the myelin sheath compromises axon function preventing nerve cells from communicating and can result in nerve cell death.  Although the pathology of demyelination is easy to see, the biology of demyelination and remyelination is poorly understood.  Drug therapy to prevent demyelination are available, but there are no therapies that promote remyelination.  Therapies that promote remyelination will be needed to effectively treat many neurodegenerative diseases.

“Demyelination is an important part of the pathology of many neurodegenerative diseases including multiple sclerosis (MS) and Alzheimer’s disease (AD).  In the past, microglia cells were thought to drive demyelination,” said Prof. Lesley Probert Ph.D. from the Hellenic Pasteur Institute in Athens, Greece.  “This work shows that astrocytes, the most abundant cell in the brain after neurons, like microglia, are intimately involved in driving the neuroinflammation component in demyelinating diseases, and that blocking soluble TNF with XPro promotes remyelination.”  Prof. Probert’s team has previously shown that XPro promotes remyelination in the cuprizone model – a standard model for studying myelin biology in the brain.  Work continues to determine how XPro affects microglia and astrocyte responses to promote disease resolution and repair.  The data presented today demonstrate new findings.  First, astrocytes are rapidly activated in response to demyelination. Second, preventing soluble TNF and TNFR1 function in mice using microglia- or astrocyte-specific TNFR1 knockout mice mirrors the effects of XPro in increasing beneficial glial responses that results in better remyelination. The third surprise is that traditional biomarkers of astroglial and microglial activation, GFAP and Iba1 respectively, are increased in these myelin-promoting glial cells.