INmune Bio, Inc. (NASDAQ: INMB) announced the publication of a peer-reviewed preclinical study in the Journal of Neurotrauma examining the biological link between traumatic brain injury (TBI) and Alzheimer's disease, according to a press release from the company.

The Department of Defense-funded study, conducted in 3xTg-AD mice, found that a single moderate TBI raised brain levels of tumor necrosis factor (TNF), its receptor TNFR1, and the neurotoxic protein amyloid beta (Aβ42). Animals that received the company's drug candidate XPro1595 showed reduced TNF levels, no injury-induced rise in Aβ42, improved learning and memory within one week of injury, and reduced pain compared to vehicle-treated injured animals.

The study identifies soluble TNF as a potential biological link between head injury and Alzheimer's pathology. XPro1595 selectively neutralizes soluble TNF without affecting transmembrane TNF or its receptors.

"For a long time we've known that a traumatic brain injury raises the risk of Alzheimer's disease without really understanding why," said study author Dr. Kirsty Dixon, Associate Professor of Surgery at Virginia Commonwealth University. "These data point to soluble TNF as a key part of that link: neutralizing it early kept the injury from triggering the rise in amyloid-related proteins and prevented the memory and pain deficits that usually follow."

The study is preclinical and conducted in animal models. XPro1595 has not been approved by the FDA or any other regulatory body. INmune Bio has received FDA Fast Track designation for XPro1595 and is planning a Phase 2b/3 registrational program in neuroinflammation-enriched early Alzheimer's disease.