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First blood test to personalize antidepressant treatment 

Developed by NeuroKaire, the blood-based test creates neurons from patient samples and analyzes their response to antidepressants to guide prescribing decisions.
Written byBree Foster, PhD
| 5 min read
A neuron, lit up, against a blue background.

A blood test that uses patient-derived neurons to predict antidepressant response.

credit: istock.com/DamienGeso

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For patients seeking help for depression, starting treatment often marks the beginning of a long guessing game. More than half won’t respond to the first medication they try, and many will continue switching drugs without finding meaningful relief. That prolonged uncertainty has fueled growing calls for more personalized treatment strategies — ones that can shorten the path to effective care and reduce unnecessary suffering.

In almost every other area of medicine, you can biopsy the affected tissue. In cancer, that's the standard of care. But for brain disorders, we’ve had to infer everything indirectly — from genetics, from imaging, from peripheral blood. And that just hasn’t been enough.

—Talia Cohen Solal, NeuroKaire

The core problem, according to Talia Cohen Solal, is surprisingly simple: psychiatry has never had direct access to the brain.

“In almost every other area of medicine, you can biopsy the affected tissue,” Cohen Solal told DDN. “In cancer, that's the standard of care. But for brain disorders, we’ve had to infer everything indirectly — from genetics, from imaging, from peripheral blood. And that just hasn’t been enough.”

Cohen Solal is the cofounder and CEO of NeuroKaire, a company attempting to bring biology-based decision-making into psychiatric care. Its first clinical offering, BrightKaire, is a blood-based test designed to predict how an individual patient with major depressive disorder will respond to different antidepressants — before treatment begins.

From academic frustration to clinical ambition

Originally trained as a neuroscientist, Cohen Solal spent roughly a decade in academia, studying the biological underpinnings of mental illness at Oxford University, University College London, and later Columbia University. But she grew increasingly frustrated by the gap between scientific insight and patient impact.

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“I realized I wasn’t satisfied,” she said. “Psychiatric illness affects people early in life, affects families, caregivers, careers — and yet we didn’t have tools that could actually change outcomes in a meaningful way.”

In 2018, she co-founded NeuroKaire with neuroscientist Daphna Laifenfeld. Their shared vision was to build a scalable, clinically usable test that could replace guesswork in psychiatry with direct biological evidence.

Why now?

The idea of tailoring psychiatric treatment to biology is not new. Over the past two decades, researchers have explored genetics, peripheral blood biomarkers, electroencephalograms (EEGs), magnetic resonance imaging and positron emission tomography (PET) scans. But none have delivered reliable, patient-specific predictions of antidepressant response.

According to Cohen Solal, the missing piece was access to neurons themselves. “Until stem-cell-derived human neurons became viable at scale, there simply wasn’t a way to ask: what does this drug do to this patient’s brain cells?” she said.

Advances in induced pluripotent stem cell (iPSC) technology — combined with automation, imaging, and AI — made that question answerable for the first time. Just as importantly, the mental health landscape has changed: stigma has eased, investment has increased, and the unmet clinical need has become impossible to ignore.

“The problem has gotten bigger, the technology has matured, and we finally had the opportunity to put all the pieces together,” Cohen Solal said.

A “brain in a dish,” derived from blood

BrightKaire begins with a standard blood draw. From that sample, NeuroKaire reprograms blood cells into iPSCs using established Yamanaka-factor methods, then differentiates them into cortical neurons. Those neurons are then exposed to a wide panel of antidepressants. Using immunohistochemistry and confocal microscopy, the company examines structural and synaptic features associated with neuroplasticity, including the number of synaptic connections, their size, and how extensively they overlap.

“In depression, there's generally a reduction in motivation and reward volition and underlying that is reduced synaptic connectivity and reduced dendritic branching,” she said. “We see that from PET studies post-mortem, as well as preclinical animal studies. What we’re looking for is rescue — an increase in connectivity and circuit complexity when neurons are exposed to an effective drug.”

Together, these measurements provide a multidimensional picture of how each drug affects neuronal plasticity. Based on that signal, the drugs are ranked for each patient, with those showing the strongest restoration of connectivity placed at the top of the report and those with the weakest effects placed at the bottom.

Where AI fits — and where it doesn’t

AI plays a critical role in extracting and segmenting microscopic features at scale, drawing on thousands of images per patient to generate robust, biologically grounded data. BrightKaire then combines these quantified imaging features with genetic and clinical information to generate a report predicting how an individual is likely to respond to different antidepressants.

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However, while AI is central to the platform, Cohen Solal is careful to draw boundaries around its role. “Importantly, the neuroplasticity score itself is not generated by AI, which helps avoid issues such as overfitting. As a result, when evaluating prediction accuracy, the system is not trained on prior samples. Instead, it simply tests whether higher plasticity scores are associated with better clinical response outcomes.”

This approach was validated using longitudinal clinical datasets in which patients were followed for up to 12 weeks per medication, with outcomes tracked over periods of up to one year. These cohorts enabled the team to clearly distinguish between robust responders and non-responders in real-world treatment settings, rather than relying on short-term or proxy measures of improvement. Predictions from the platform were then evaluated against these independently defined clinical outcomes to assess whether higher neuroplasticity scores consistently correlated with better treatment response.

Cutting the treatment timeline

NeuroKaire estimates that BrightKaire can reduce the antidepressant selection process from more than a year to roughly two months. The company currently delivers results within eight weeks, with a six-week protocol in development — an unusually fast turnaround for iPSC-derived neuron work.

That difference can mean not losing your job, not losing your relationships, not losing critical time. Even when people eventually find the right drug, they’ve often already lost so much.

—Talia Cohen Solal, NeuroKaire

“That difference can mean not losing your job, not losing your relationships, not losing critical time,” Cohen Solal said. “Even when people eventually find the right drug, they’ve often already lost so much.”

BrightKaire is now available across 49 out of 50 US states through partnerships with national lab networks, enabling blood draws at sites such as Quest Diagnostics, as well as through at-home, clinician-assisted, or in-clinic collection options.

A broader vision for precision psychiatry

While depression is NeuroKaire’s first indication, it is not the last. The company plans to launch studies in ADHD next year and is exploring adaptations for other neuropsychiatric conditions, including schizophrenia, anxiety, and Alzheimer’s disease.

In parallel, NeuroKaire is working with pharmaceutical companies to apply its platform to drug development — helping identify responder populations earlier and prevent promising therapies from failing late-stage trials due to patient heterogeneity.

“There are drugs that make biological sense and help a subset of patients, but never reach the market,” Cohen Solal said. “By introducing secondary biomarkers into clinical studies, we can help identify the right patient populations earlier — either rescuing assets that might otherwise be abandoned or preventing late-stage failures in the first place. The goal is to embed precision medicine throughout the development pipeline, so that therapies reach the patients who will truly benefit from them, rather than ending up shelved after billions in investment.”

For Cohen Solal, the goal is nothing less than a shift in how psychiatry is practiced. “For decades, we’ve said a new era is coming,” she said. “This time, the biology, the technology, and the clinical need are finally aligned.”

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About the Author

  • Photo of Bree Foster

    Bree Foster is a science writer at Drug Discovery News with over 2 years of experience at Technology Networks, Drug Discovery News, and other scientific marketing agencies. She holds a PhD in comparative and functional genomics from the University of Liverpool and enjoys crafting compelling stories for science.

    View Full Profile

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