On Our Work at the Intersection of Acute and Chronic Cognitive Disease
A class of cognitive injury that medicine has treated as transient — and a class that medicine has treated as terminal — share more biology than either field assumed. Our work sits at that intersection.
Several million patients each year experience cognitive impairment following surgery, critical illness, sepsis, severe systemic infection, or chemotherapy. The clinical literature has labelled these events transient: most patients recover, the impairment resolves, the diagnosis closes. Several million more carry permanent cognitive impairment from neurodegenerative disease, post-stroke injury, or unresolved acute insult. The clinical literature has treated these as separate populations, separate research programmes, and largely separate therapeutic pipelines.
They are not as separate as the textbooks suggest. The inflammatory cascades that drive transient cognitive impairment after acute medical events share regulatory machinery with the cascades that drive chronic neurodegenerative decline. The microglial states that respond to a single severe insult resemble the states that sustain themselves through decades of progressive disease. Neuroinflammation is the common substrate. Resolving it cleanly in the acute setting and modulating it durably in the chronic setting are different problems — but they are related problems, and they reward a related set of therapeutic tools.
Our work is built around that observation. We develop multispecific biologics that target multiple inflammatory pathways simultaneously, designed to act on the regulatory nodes that the cognitive disease literature has converged on over the past decade. We engineer for engagement across the blood-brain barrier, because no neuroinflammatory therapeutic can succeed without it. We work in protein modalities that allow precise control of mechanism, dosing, and resolution — properties the field has historically struggled to combine.
The clinical rationale extends in both directions from the mechanism. Transient cognitive impairment — particularly the cognitive sequelae of surgery, critical illness, and severe systemic infection — is a population of millions, with measurable endpoints, shorter regulatory horizons, and almost no current standard of care. Permanent neurocognitive dysfunction and neurodegenerative disease constitute the long-horizon opportunity the field has been trying to address for forty years. Few therapeutic programmes are positioned to engage both. Ours is.
This is preclinical work. The horizons are long. We have organised the work, the team, and the science accordingly.