INmune Bio, Inc., Virginia Commonwealth University, and Barrow Neurological Institute Receive Department of Defense Funding to Study the Role of Traumatic Brain Injury in the Development of Alzheimer’s Disease

On December 22, 2022 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 in concert with Virgina Commonwealth University (VCU) and Barrow Neurological Institute have received a grant from the Department of Defense (DoD) (Press release, INmune Bio, DEC 22, 2022, View Source [SID1234625540]). The grant is titled: Novel solTNF inhibitor improves outcomes in a mouse model of TBI-induced AD. The funding covers a collaboration that studies the impact of traumatic brain injury (TBI) in the development of Alzheimer’s disease (AD) related pathology. These DoD funded studies are a collaboration between Dr. Kirsty Dixon, Associate Professor of Surgery and director of Surgery’s Neurotrauma Repair Laboratory at Virginia Commonwealth University, and Dr. Elliott Mufson, Professor of Neurobiology and the director of the Alzheimer’s disease research laboratory at Barrow Neurological Institute and INmune Bio.

Schedule your 30 min Free 1stOncology Demo!
Discover why more than 1,500 members use 1stOncology™ to excel in:

Early/Late Stage Pipeline Development - Target Scouting - Clinical Biomarkers - Indication Selection & Expansion - BD&L Contacts - Conference Reports - Combinatorial Drug Settings - Companion Diagnostics - Drug Repositioning - First-in-class Analysis - Competitive Analysis - Deals & Licensing

                  Schedule Your 30 min Free Demo!

"This is a great example of collaboration for innovation," said RJ Tesi MD, CEO of INmune. "Two stellar academic institutions combine with industry (INMB) and government (DoD) to answer an important medical question."

TBI is a risk factor for developing AD, although reasons for this remains largely unknown. The ApoE4 allele is the strongest known risk factor for late onset AD, and the presence of human ApoE4 following TBI results in accumulation of AD pathology (soluble Aβ and tau/p-tau levels). Evidence suggests a role for soluble tumor necrosis factor (sTNF) and its receptor TNFR1 in the development of AD in patients with previous TBI, especially in individuals carrying the APOE4 allele. These studies will use XPro1595 to determine the contribution of ApoE4 and TBI on sTNF/TNFR1-induced hippocampal inflammation, AD pathology and dendritic spine plasticity, that collectively promote cognitive impairment.

"Much of the neurologic damage after TBI is driven by neuroinflammation," said Kirsty Dixon, PhD, associate professor in the Department of Surgery at the VCU School of Medicine. "This study aims to confirm that neuroinflammation caused by an acute neurologic injury has long-term consequences that contribute to dementia and that early intervention can prevent disability later in life."

"We know that traumatic brain injury can accelerate the onset of Alzheimer’s disease, however little is known about the association between the two diseases," says Elliott Mufson, PhD, researcher at Barrow Neurological Institute. "This study is an important step toward helping us better understand the relationship between these disorders and to develop effective therapies."