INmune Bio Inc. Announces Publication in Cell Reports Demonstrating XPro? Promotes Remyelination

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INmune Bio, Inc.
INmune Bio, Inc.

Data from Animal Model Study Demonstrate XPro? converts microglia from a demyelinating cell to a remyelinating cell

Multi-year study published has implications for many CNS diseases including Alzheimer’s

Boca Raton, Florida, Oct. 24, 2024 (GLOBE NEWSWIRE) --  INmune Bio, Inc. (NASDAQ: INMB) (the “Company”), a clinical-stage inflammation and immunology company focused on developing treatments that harness the patient’s innate immune system to fight disease, announces the publication of a seminal paper in the journal Cell Reports that demonstrates XPro1595 promotes remyelination in an animal model of demyelinating disease. The study, Microglia Regulate Cortical Remyelination via ΤNFR1-Dependent Phenotypic Polarization, was performed under the direction of Leslie Probert PhD, Head of Immunology at the Hellenic Pasteur Institute in Athens Greece, and is the culmination of several years of work supported by EU research grants.

Myelin is necessary for fast and efficient communication between neurons. Loss of myelin compromises neuron function and communication and is a key step in the neurodegenerative process of many CNS diseases, including Alzheimer’s Disease.

“Activated microglia play a central role in both demyelination and remyelination,” said Dr. Probert, senior author of the publication. “Our data identify solTNF as a critical cytokine checkpoint that converts microglia from a reparative, remyelinating cell to a damaging, demyelinating cell. These data suggest that blocking soluble TNF is a promising strategy for treating demyelinating diseases.”

“Demyelination is a core mechanism of neurodegeneration that has been overlooked in Alzheimer's disease, despite the evidence that it’s a critical element of the disease's pathology,” said RJ Tesi MD, CEO of INmune Bio. “These new data further support the potential for XPro1595 in neurodegenerative diseases by restoring glia function to improve key components of neurodegeneration at multiple levels, including restoration of synaptic function, remyelination, and ceasing cell loss.”

INmune anticipates reporting top-line cognitive results of an ongoing blinded randomized Phase II in Early AD patients in the first half of 2025.

About Demyelination in Alzheimer's Disease

Research shows that demyelination occurs in various brain regions critical for cognition in AD patients. This damage is often associated with the presence of amyloid-beta (Aβ) plaques, suggesting that myelin loss may precede or accompany the classic pathological changes seen in AD. Changes in myelin structure can be detected even before the onset of typical AD symptoms. Advanced imaging techniques have revealed alterations in myelin density and integrity in individuals at risk for AD, indicating that demyelination might serve as an early biomarker for the disease. The mechanisms underlying myelin damage in AD involve oligodendrocyte dysfunction, which can lead to the breakdown of myelin sheaths. This breakdown not only affects neuronal health but may also contribute to the accumulation of Aβ, creating a feedback loop that exacerbates both myelin loss and neurodegeneration. Studies utilizing techniques like myelin water fraction imaging have shown significant reductions in myelin integrity among individuals with mild cognitive impairment and dementia, reinforcing the notion that demyelination is prevalent in AD.