Last week I had the pleasure of reporting on an adboard for a neuroprotective agent. I’m semi-confident with my neurology experience, but the sessions blew my microglia. I listened to fascinating debates about how the brain degenerates in certain diseases and how drugs are thought to slow the process.
Like many people going all the way back to Aristotle, songwriter Morrissey once asked “Does the body rule the mind, or does the mind rule the body?” Morrissey would not be pleased with the fact that much of our contemporary neuroscience understanding is rooted in the brains of mice and monkeys, but he might agree that it shapes a definitive answer: mind and body are one and the same. What’s on your mindbody? What’s the mindbody of evidence in this case? If I told you you had a beautiful mindbody, would you….etc.
In the opening remarks, the clinicians on the ad-board were unanimously neutral on the drug under question. By the end of the day, all but one held some degree of positive opinion. Two standard acceptances we make in healthcare comms are 1) Doctors don’t care about MOA and 2) Doctors want simple maths and pretty p-values. These doctors were looking to the MOA to swing their opinion on efficacy. I know there are regulatory restrictions on supporting clinical efficacy by way of MOA, but in no other instance have I ever seen a preclinical and clinical story so intertwined. There is plenty of conjecture in this particular neurodegenerative framework, and clinicians positively have to understand what is driving results.
For a flavour: the photograph here is of a human foetal astrocyte. This is a brain cell that nurtures the well-being of nearby neurons. Under certain conditions it changes its shape entirely, becoming leaner, meaner, neglectful. Swathes of neurons die when astrocytes go bad. Let’s not forget that all of our mindbodies have the ability to turn against us in ways like this.
In terms of the maths, neurologists are geniuses. When a biostatistician presented after lunch, I expected this to be a snooze session. Instead my typing became ever more frantic as clinicians weighed in on sensitivity analyses, artefacts and noise, imbalance and consistency across studies. With the ABPI also recently speaking out about absolute vs relative risk reduction, I felt compelled to refresh my regulatory knowledge.
Neurology is a big one and I’ve resolved to keep digging deeper into the science of all my brands: Parkinsons, BDD, schizophrenia, epilepsy – whether, like a neurodegenerative disease , they are currently active or not. There is a world of debate out there. I’m not qualified to challenge: my job is instead to transform proof and hypothesis into benefits for ill people. And, in my own nerdy downtime, to ponder the possible connections between these different and very unfortunate diseases.