Showing posts sorted by date for query DRUGS. Sort by relevance Show all posts

Thursday, March 19, 2026

The scientist who warned that profit, not science, decides which drugs reach patients

Dr. Gabriella Gobbi, CINP president-elect and McGill neuropsychopharmacologist and psychiatrist, challenges the logic of drug discovery

Genomic Press

image:
Gabriella Gobbi, MD, PhD, McGill University, Canada.
view more
Credit: Gabriella Gobbi, MD, PhD

MONTREAL, Quebec, CANADA, 17 March 2026 – Dr. Gabriella Gobbi, Professor of Psychiatry at McGill University, Canada Research Chair (Tier 1) in Therapeutics for Mental Health, Staff Psychiatrist at the McGill University Health Center (MUHC), and Senior Scientist, Brain Repair and Integrative Neuroscience Program at the Research Institute of the MUHC, and President-Elect of the Collegium Internationale of Neuropsychopharmacology (CINP), has issued an unambiguous challenge to the global drug-development system, warning that promising treatments for mental illness are failing to reach patients not because the science is flawed but because venture capital and profit motive govern which compounds advance through clinical trials. Her warning appears in a new Genomic Press Interview published in Brain Medicine.

"My greatest fear concerns the future of psychopharmacology and drug discovery," Dr. Gobbi states in the interview, "not because the science is failing, but because a greedy system oversees innovation today." She describes a landscape in which public funding can sustain early academic research, but the more expensive steps, from toxicology to first-in-human trials, depend on private investment that is guided by margin expectations rather than medical need. "We may lose good, non-expensive treatments because a greedy, capitalistic system controls which drug will finally be brought to market."

A Career Built on Bedside Questions

Dr. Gobbi grew up in a book-filled house in central Italy, the granddaughter of a man who died under Allied bombing in March 1945 after writing from a German prison to insist that his children receive the education he himself had been denied. That inheritance, part moral conviction and part intellectual hunger, runs as a thread through everything she has since done. At fourteen she put down comic books and picked up Freud. In high school she read about Rita Levi-Montalcini and the discovery of nerve growth factor, and understood that the brain was not fixed but plastic, a revelation that pointed her toward medicine. By twenty, during training in Rome, she had encountered translational research, the practice of moving continuously between laboratory bench and clinical ward, and found that she could not relinquish either world.

The path to independence was neither smooth nor linear. In Italy during the 1990s, academic positions were controlled by senior professors acting as gatekeepers, and Dr. Gobbi spent time working at a private psychiatric hospital in a small central-Italian town, applying to PhD programs and genuinely unsure whether she would ever gain entry to research. The turning point arrived on the evening of January 29, 1996, in the form of a telephone call. She was invited to sit a PhD entrance examination in Cagliari, in Sardinia, the following morning. She boarded a plane at eleven that night. At eight the next morning she sat the exam, and she won. That examination opened the door to work with Professor Gianluigi Gessa, a neuroscientist known for landmark contributions to the neurobiology of dopamine and addiction. Two years later, at a Biological Psychiatry meeting in Nice, a chance conversation with Professor Pierre Blier led to an invitation to join his laboratory at McGill. That single year in Montreal became more than two decades.

From Cannabis and Anhedonia to Melatonin and Psychedelics

The clinical observation that drives her best-known research line is almost painfully simple. In the early 2000s, she kept seeing adolescents and young adults who smoked cannabis and who, in the years that followed, developed depression marked by profound anhedonia. The bedside pattern became a bench question. In 2007 her laboratory reported one of the first links between cannabinoids, serotonin systems, and depression-related phenotypes. In 2010, animal-model studies demonstrated that adolescent cannabis exposure could increase vulnerability to later depressive-like outcomes. By 2019, supporting evidence had emerged in human cohorts. This body of work has now accumulated more than 1,700 citations and contributed directly to public-health decisions in Quebec. Dr. Gobbi also testified as an expert witness before the Canadian Senate and the Ministries of Health and Justice in Quebec on cannabis policy, contributing to legislation raising the legal age for cannabis access and to the regulation of cannabis advertising.

A second major research program, running in parallel since 2006, has focused on the melatonin MT2 receptor, a target that was poorly understood when her group began. Her laboratory contributed to defining MT2 receptor localization and elucidated its specific role in restorative NREM sleep and neuropathic pain. An MT2-selective partial agonist, a first-in-class candidate, is now moving from early discovery toward clinical development. "I have learned that in science, the projects that take the longest are often those that yield the most meaningful results," she observes in the interview. Her laboratory began investigating psychedelics in 2013, before the contemporary wave of clinical trials brought the field to prominence, characterizing the anxiolytic and prosocial effects of LSD in preclinical models and beginning to identify underlying molecular mechanisms including mTORC1 signaling. That work is now extending to psilocybin, DMT, and 5-MeO-DMT, while new clinical studies aim to identify objective neurophysiological biomarkers of psychedelic action in humans.

The Hidden Tax on Women in Science

Dr. Gobbi does not confine her scrutiny to drug-development economics. She speaks with notable directness about gender inequality in academic science, describing both overt harassment and a quieter structural erosion: unequal access to administrative support, diversion toward low-visibility service work, and a conference-invitation culture that disadvantages researchers who carry disproportionate caregiving burdens. "This is the cause that fires me up the most," she states, "changing the structure of our scientific culture so excellence is recognized without imposing an additional, hidden tax on women." In her current role as President-Elect of the CINP, the organization whose presidency she will hold as its first woman in the organization's 70-year history, she has heard such accounts repeatedly from accomplished women who have been isolated, evaluated inconsistently, or simply not invited to the table.

The Letter and the Paddleboard

There is a letter from Dr. Gobbi's mother, written before her death from glioblastoma in 2000, that she names as her most treasured possession. It is the kind of detail that resists elaboration, so this account will leave it alone. What she says about happiness is perhaps more useful to science journalism: her happiest moments have occurred in those rare instants in research when data suddenly align and something obscure becomes clear, "the feeling that nature has briefly lifted a corner of the veil, and that an experiment is no longer just results on a page but a story that finally makes sense." When she disconnects entirely, in summer, she paddles on the Adriatic Sea. In Quebec she skis in spring, when the light softens. Winter skiing here, she notes in the interview, is simply too cold.

Asked what she would change about herself, Dr. Gobbi does not cite a scientific limitation. She wishes she had sought mentorship and leadership education earlier. She began her career as an assistant professor without a mentor and without foundational training in management, grant-writing, or conflict resolution. The regret is characteristic: it is not personal but structural, a comment about what academic systems fail to provide rather than about what she personally lacks. Her life philosophy, offered at the interview's close, is unadorned: "Do your best, stay true to what matters, and trust what comes."

Dr. Gabriella Gobbi's Genomic Press interview is part of a larger series called Innovators and Ideas that highlights the people behind today's most influential scientific breakthroughs. Each interview in the series offers a blend of cutting-edge research and personal reflections, providing readers with a comprehensive view of the scientists shaping the future. By combining a focus on professional achievements with personal insights, this interview style invites a richer narrative that both engages and educates readers. This format provides an ideal starting point for profiles that explore the scientist's impact on the field, while also touching on broader human themes. More information on the research leaders and rising stars featured in our Innovators and Ideas – Genomic Press Interview series can be found on our interview website: https://interviews.genomicpress.com/.

The Genomic Press Interview in Brain Medicine titled “Gabriella Gobbi: Embracing psychiatry from bench to bedside,” is freely available via Open Access, starting on 17 March 2026 in Brain Medicine at the following hyperlink: https://doi.org/10.61373/bm026k.0015.

About Brain Medicine: Brain Medicine (ISSN: 2997-2639, online and 2997-2647, print) is a peer-reviewed medical research journal published by Genomic Press, New York. Brain Medicine is a new home for the cross-disciplinary pathway from innovation in fundamental neuroscience to translational initiatives in brain medicine. The journal’s scope includes the underlying science, causes, outcomes, treatments, and societal impact of brain disorders, across all clinical disciplines and their interface.

Visit the Genomic Press Virtual Library: https://issues.genomicpress.com/bookcase/gtvov/

Our media website is at: https://media.genomicpress.com/

Our full website is at: https://genomicpress.com/

Journal

Brain Medicine

DOI

10.61373/bm026k.0015

Method of Research

News article

Subject of Research

People

Article Title

Gabriella Gobbi: Embracing psychiatry from bench to bedside

Article Publication Date

17-Mar-2026

Gabriella Gobbi: Embracing psychiatry from bench to bedside

Gabriella Gobbi paddling on the Adriatic Sea at dawn.

Credit

Gabriella Gobbi

Cannabis use disorder among young people linked to diagnosis of psychiatric disorders

Analysis of nearly 700,000 health records reveals age-related association between cannabis use disorder and subsequent psychiatric disorders diagnoses

Johns Hopkins Bloomberg School of Public Health

A new study led by Johns Hopkins researchers found that young people with cannabis use disorder were more likely than young people with other substance use disorders to later be diagnosed with a psychiatric disorder. In contrast, adults with cannabis use disorder were significantly less likely to develop psychiatric disorders, compared to adults with other substance use disorders.

The study found that the relative risk of young people age 17 and under with cannabis use disorder was 52% higher for schizophrenia, 30% higher for recurrent major depression, and 21% higher for anxiety disorders, compared to young people with other substance use disorders. Adults with cannabis use disorder had lower relative risks for being diagnosed with a psychiatric disorder.

The findings highlight the question of whether excessive cannabis use, perhaps more than other substances, might alter brain development of young people, predisposing them to developing a psychiatric disorder.

The study was published online March 5 in the American Journal of Psychiatry.

“Is cannabis use a unique risk factor compared to the use of other substances such as alcohol, opioids, or cocaine? That’s the question we addressed in this study, and our findings suggest that that relative risk depends on the user’s age,” says study co-author Johannes Thrul, PhD, associate professor in the Department of Mental Health at the Bloomberg School.

Products made from the Cannabis sativa plant have been used recreationally in the U.S. since at least the 1800s. Their popularity increased during alcohol prohibition in the 1920s and the counterculture movement in the 1960s. Today, cannabis use by adults age 21 and older is legal in 24 U.S. states and the District of Columbia. Surveys suggest daily use of cannabis is higher than alcohol consumption.

“Much of our interest in this came from the recent legalization of recreational cannabis in Maryland, in 2023, and other states,” says Ryan Nicholson, MD, resident at Johns Hopkins University School of Medicine. “We wanted to understand cannabis-related psychotic disorders clinicians are seeing in the context of other substance-related psychotic disorders."

The link between cannabis and psychosis first appeared in medical literature in the early twentieth century. In 1987, a study of more than 45,000 Swedish army recruits found that the use of cannabis at the time of conscription was associated with large increases in the risk of subsequent schizophrenia, especially when the cannabis use was heavy. Other studies since then have found similar associations.

For the study, the researchers analyzed nearly 700,000 U.S. medical records from a large commercial database. They identified patients who had been diagnosed with cannabis use disorder—a condition that implies relatively heavy cannabis use—but had not been diagnosed with other psychiatric disorders. They then matched these patients on measures such as age, sex, ethnicity, and income level, with patients who had been diagnosed with other, non-cannabis substance use disorders and did not have other psychiatric conditions. The researchers compared the rates of subsequent schizophrenia and other psychiatric diagnoses in these two patient groups—adults age 18 and older (691,806 patients) and one for those age 17 and under (49,586 patients).

The median age among patients with cannabis use disorder was 16 versus 15 among patients with other substance use disorders. About 10% of patients in the cohort of all substance use disorders were under age 12. The authors note that this aligns with reports from adult patients being treated for substance use disorder: 10.2% reported starting substance use at age 11 or younger.

Adults in the cannabis use disorder group had a 19% lower risk (0.34% vs. 0.42%) of subsequent schizophrenia compared to the group with other substance use disorders. Risks of subsequent psychosis, recurrent major depression, and suicide attempts were also lower in the cannabis-use group.

The results are consistent with the idea that heavy cannabis use predisposes young people to subsequent schizophrenia and some other psychiatric disorders that they might not develop otherwise. Thrul notes that this acceleration effect could make these illnesses seem less likely at later ages, thus appearing to lower the risk in adults, at least in relation to other recreational drugs.

Thrul cautions, however, that the causation might point in the other direction, with individuals who are innately more likely to develop certain psychiatric disorders to also have a greater tendency to self-medicate with cannabis, even before their mental health issues have become evident.

“There are still many unknowns on that question, but I would never recommend that teenagers use cannabis, especially not the high-potency cannabis products that are on the market now,” he says.

One of the paper’s limitations is that the database the researchers used relied on International Classification of Diseases ICD-10 coding by other physicians, so the researchers may not know the exact patient history that led to the diagnosis.

“Association of Cannabis Versus Other Substance Use Disorders with Psychiatric Conditions: A Propensity-Matched Retrospective Cohort Analysis” was co-authored by Ryan Nicholson, Una Choi, Ramin Mojtabai and Johannes Thrul.

# # #

Three anesthesia drugs all have the same effect in the brain, MIT researchers find

Discovering this common mechanism could lead to a universal anesthesia-delivery system to monitor patients more effectively

Massachusetts Institute of Technology

CAMBRIDGE, MA -- When patients undergo general anesthesia, doctors can choose among several drugs. Although each of these drugs acts on neurons in different ways, they all lead to the same result: a disruption of the brain’s balance between stability and excitability, according to a new MIT study.

This disruption causes neural activity to become increasingly unstable, until the brain loses consciousness, the researchers found. The discovery of this common mechanism could make it easier to develop new technologies for monitoring patients while they are undergoing anesthesia.

“What’s exciting about that is the possibility of a universal anesthesia-delivery system that can measure this one signal and tell how unconscious you are, regardless of which drugs they’re using in the operating room,” says Earl Miller, the Picower Professor of Neuroscience and a member of MIT’s Picower Institute for Learning and Memory.

Miller, Edward Hood Taplin Professor of Medical Engineering and Computational Neuroscience Emery Brown, and their colleagues are now working on an automated control system for delivery of anesthesia drugs, which would measure the brain’s stability using EEG and then automatically adjust the drug dose. This could help doctors ensure that patients stay unconscious throughout surgery without becoming too deeply unconscious, which can have negative side effects following the procedure.

Miller and Ila Fiete, a professor of brain and cognitive sciences, the director of the K. Lisa Yang Integrative Computational Neuroscience Center (ICoN), and a member of MIT’s McGovern Institute for Brain Research, are the senior authors of the new study, which appears today in Cell Reports. MIT graduate student Adam Eisen is the paper’s lead author.

Destabilizing the brain

Exactly how anesthesia drugs cause the brain to lose consciousness has been a longstanding question in neuroscience. In 2024, a study from Miller’s and Fiete’s labs suggested that for propofol, the answer is that anesthesia works by disrupting the balance between stability and excitability in the brain.

When someone is awake, their brain is able to maintain this delicate balance, responding to sensory information or other input and then returning to a stable baseline.

“The nervous system has to operate on a knife’s edge in this narrow range of excitability,” Miller says. “It has to be excitable enough so different parts can influence one another, but if it gets too excited it goes off into chaotic activity.”

In that 2024 study, the researchers found that propofol knocks the brain out of this state, known as “dynamic stability.” As doses of the drug increased, the brain took longer and longer to return to its baseline state after responding to new input. This effect became increasingly pronounced until consciousness was lost.

For that study, the researchers devised a computational model that analyzes neural activity recorded from the brain. This technique allowed them to determine how the brain responds to perturbations such as an auditory tone or other sensory input, and how long it takes to return to its baseline stability.

In their new study, the researchers used the same technique to measure how the brain responds to not only propofol but two additional anesthesia drugs — ketamine and dexmedetomidine. Animals were given one of the three drugs while their brain activity was analyzed, including their response to auditory tones.

This study showed that the same destabilization induced by propofol also appears during administration of the other two drugs. This “universal signature” appears even though the three drugs have different molecular mechanisms: propofol binds to GABA receptors, inhibiting neurons that have those receptors; dexmedetomidine blocks the release of norepinephrine; and ketamine blocks NMDA receptors, suppressing neurons with those receptors.

Each of these pathways, the researchers hypothesize, affect the brain’s balance of stability and excitability in different ways, and each leads to an overall destabilization of this balance.

“All three of these drugs appear to do the exact same thing,” Miller says. “In fact, you could look at the destabilization measure we use and you can’t tell which drug is being applied.”

The researchers now plan to further investigate how each of these drugs may give rise to the same patterns of brain destabilization.

“The molecular mechanisms of ketamine and dexmedetomidine are a bit more involved than propofol mechanisms,” Eisen says. “A future direction is to do a meaningful model of what the biophysical effects of those are and see how that could lead to destabilization.”

Monitoring anesthesia

Now that the researchers have shown that three different anesthesia drugs produce similar destabilization patters in the brain, they believe that measuring those patterns could offer a valuable way to monitor patients during anesthesia. While anesthesia is overall a very safe procedure, it does carry some risks, especially for very young children and for people over 65.

For adults suffering from dementia, anesthesia can make the condition worse, and it can also exacerbate neuropsychiatric disorders such as depression. These risks are higher if patients go into a deeper state of unconsciousness known as burst suppression.

To help reduce those risks, Miller and Brown, who is also an anesthesiologist at MGH, are developing a prototype device that can measure patients’ EEG readings while under anesthesia and adjust their dose accordingly. Currently, doctors monitor patients’ heart rate, blood pressure, and other vital signs during surgery, but these don’t give as accurate a reading of how deeply the patient is unconscious.

“If you can limit people’s exposure to anesthesia, if you give just enough and no more, you can reduce risks across the board,” Miller says.

Working with researchers at Brown University, the MIT team is now planning to run a small clinical trial of their monitoring device with patients undergoing surgery.

###

The research was funded by the U.S. Office of Naval Research, the National Institute of Mental Health, the Simons Center for the Social Brain, the Freedom Together Foundation, the Picower Institute, the National Science Foundation Computer and Information Science and Engineering Directorate, the Simons Collaboration on the Global Brain, the McGovern Institute, and the National Institutes of Health.