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XPro™ Reduces Amyloid and Enhances Behavior Post Traumatic Brain Injury in an Animal Model of Alzheimer’s Disease: Supported by Department of Defense

Core Insights - INmune Bio, Inc. is collaborating with Virginia Commonwealth University to study the effects of Traumatic Brain Injury (TBI) on Alzheimer's disease (AD) and the potential of XPro™ treatment to mitigate these effects [1][2][4] - The study indicates that TBI increases amyloid deposition and neuroinflammation, which are linked to AD progression, and that XPro™ significantly reduces amyloid formation and improves brain function [1][3][4] Group 1: Study Findings - TBI leads to a transient increase in TNFR1, BACE1, and Aβ42 expression in the hippocampus, peaking three days post-injury [3] - Administering XPro™ shortly after TBI inhibits solTNF/TNFR1 activity, preventing elevations in TNFR1, BACE1, Aβ42, and caspase-3 levels [3] - XPro™ treatment reduces intracellular neuronal amyloid accumulation and improves neurological outcomes in treated animals [3][4] Group 2: Implications for Alzheimer's Disease - The findings suggest that targeting TBI-induced solTNF/TNFR1 signaling could mitigate Aβ42 production and neuronal loss, linking TBI and AD [2][4] - XPro™ is positioned as a promising treatment to reduce AD pathology risk following TBI, particularly for the elderly population at risk for dementia [4] Group 3: Company Overview - INmune Bio, Inc. is a clinical-stage biotechnology company focused on developing treatments that target the innate immune system to combat diseases [6][7] - The company has three product platforms, including XPro™, which is in clinical trials for Mild Alzheimer's disease and other conditions [7]