I am a neurologist, and for most of my career, my real subject hasn't been disease — it's been flow.

That probably sounds strange. Neurologists are supposed to talk about neurons, plaques, tangles, the parts of the brain that light up on a scan. And I do. But underneath nearly every patient I've ever cared about, there has been a quieter, less glamorous question: is the blood getting where it needs to go?

I trained as both a physician and a scientist — an MD-PhD, with my doctoral research focused on diffusion tensor imaging, a technique for visualizing the brain's white matter, the wiring that connects one region to another. My dissertation work, done at the University of Minnesota's Center for Magnetic Resonance Research, was about understanding how that wiring breaks down — and how to measure it before someone notices anything is wrong. One of the studies that shaped my thinking most was on patients with longstanding type 1 diabetes: people with no diagnosed brain disease, who nonetheless showed measurable disruption in their white matter, tightly correlated with reduced cognitive performance. The vessels were the story. They just hadn't been asked yet.

I completed my neurology residency at UCLA, where I researched diffusion imaging in acute stroke and helped develop natural language processing tools to identify stroke patients eligible for treatment — work that won UCLA's Department of Neurology Resident Research Award. Since then, I've spent my career in clinical neurology: as Director of Neurologic Care at UCLA's Ashe Center, as Team Neurologist for the Los Angeles Wildcats, as co-director of a Normal Pressure Hydrocephalus clinic addressing one of the few reversible causes of dementia, and most days, simply in clinic — sitting across from people who are frightened about their minds.

Here is the problem I kept running into, year after year.

A patient comes in. She's in her sixties. Sharp, accomplished, a little scared. Her memory is slipping — not dramatically, but enough that she's noticed, and that's enough to keep her up at night. We do the full workup: history, exam, MRI. And often, what comes back isn't Alzheimer's. It isn't a tumor, a stroke, anything with a name and a treatment protocol. It's something quieter: white matter hyperintensities. Small bright spots on the scan, signs of damage to the brain's smallest blood vessels — the microvasculature.

I can tell her what it is. I usually can't tell her what to do about it. There's no pill for microvascular disease. We manage blood pressure. We talk about exercise and sleep. But the honest truth is that mainstream neurology has no specific treatment for the thing that may be most responsible for her decline.

That gap — between what I could diagnose and what I could actually offer — is what led me to write BrainFlow, and ultimately, to develop Neurovasa.

For decades, dementia research has centered on amyloid and tau — the proteins behind Alzheimer's disease. That research matters. But it has, I'd argue, pulled attention away from something equally important and far more modifiable: the health of the blood vessels that keep brain tissue alive in the first place. The brain has no fuel reserve. It survives entirely on continuous blood flow, supplied by a network of vessels so fine that red blood cells pass through them single file. When that network falters — through hypertension, diabetes, inflammation, or simply age — the consequences are subtle at first, then not.

This is not a fringe idea. It is supported by a substantial and growing body of research on cerebral blood flow, vasomotor reactivity, and small vessel disease — and it is also where I have chosen to spend my own research time, not just my reading time.

I am currently a co-investigator on multiple sclerosis clinical trials evaluating next-generation disease-modifying therapies, and I direct a Normal Pressure Hydrocephalus clinic in collaboration with neurosurgical colleagues. But the work closest to the science behind Neurovasa is a study I designed using transcranial Doppler ultrasound to identify patients with impaired cerebral vasomotor reactivity — essentially, vessels that have lost their ability to dilate and respond to the brain's demands — and to test whether that impairment is modifiable.

The initial phase of that work demonstrated improvement in cognition with a structured exercise intervention. I am now designing a randomized trial extending that work, including a study examining whether daily low-dose tadalafil — a medication that acts on the same nitric oxide signaling pathway involved in vascular dilation — can improve cerebral vasomotor reactivity in patients with mild cognitive impairment. This work builds on findings from European stroke researchers and reflects exactly the question I think the field hasn't taken seriously enough: not just whether vessels are involved in cognitive decline, but whether improving vessel function can change its course.

I share this not because Neurovasa is a drug — it isn't, and I want to be clear about that distinction — but because the same biology motivates both. The pathway that interests me as a researcher is the same pathway I considered when formulating this supplement: supporting the body's own capacity for healthy vascular function, through ingredients with published evidence in that domain.

Neurovasa is not a replacement for medical care, and it is not a treatment for dementia, MCI, or any diagnosed condition. It's a supplement, formulated around the same vascular framework I write about in BrainFlow and study in my research: ingredients selected for their evidence in supporting healthy circulation, endothelial function, and the day-to-day biology that keeps brain tissue well supplied.

I built it because patients kept asking me the same question, year after year: I understand the problem now — what can I actually do? I wanted to be able to offer something grounded in the same science I'd trust enough to study myself.

I've spent time living and working in Denmark, Sicily, Russia, and Brazil, mostly on health research, and I speak Danish, Russian, Spanish, and French with varying degrees of rust. I also play saxophone, badly enough to keep it humbling and well enough to enjoy it. I mention this only because I think it matters: the person formulating Neurovasa is the same person who sits in clinic, reads MRIs, designs trials, and — like anyone managing their own brain health — is just trying to stay sharp for the long run, too.

Disclaimer: These statements have not been evaluated by the Food and Drug Administration. This product is not intended to diagnose, treat, cure, or prevent any disease.