Dr. Paul Edison, more than likely brought on board for the indication of Alzheimer's Disease and possibly epilepsy. His work in assessing microglial activation and amyloid load showed that both these are increased in Alzheimer's disease, and microglial activation correlates with cognition, while amyloid load does not correlate with cognition. https://www.imperial.nhs.uk/consultant-directory/paul-edison



Remember, Leronlimab crosses the blood brain barrier on its own. (It does not need to first be bound to a WBC). It is small enough to cross to bind to the Microglial cells in the Brain. If they were bound to WBC, they couldn't then bind to the Microglial cells and therefore, how would it work? Microglial cells contain CCR5. Therefore LL will block the activation of microglial cells.

As in NASH, Dr. Paul Edison will likely advise the employment of Brain MRI in determining Leronlimab effectiveness by measuring reduction in Alzheimer's plaques. It is now evaluating the relationship between neuroinflammation, tau, glucose metabolism, and structural and functional changes measured by MRI. He is evaluating novel microglial agents in mild cognitive impairment and Alzheimer's disease.