For generations, obsessive-compulsive disorder and chronic tic disorders have been managed at the surface — their inner biological architecture remaining largely hidden. A study published in Nature Neuroscience has now identified 36 genes that substantially raise the risk of these conditions, revealing shared brain pathways and offering pharmaceutical researchers more than 30 concrete targets for intervention. The discovery marks a quiet but profound shift: from treating what people suffer to understanding why their brains are suffering.
Researchers identify 36 genes linked to OCD and tic disorders, opening new treatment pathways
Now you've got over 30 targets, and that opens up new possibilities.
Mark
So they found 36 genes linked to OCD and tic disorders. Does that mean if you have one of these genes, you'll definitely develop the condition?
Mimi
Not at all. Having a gene that raises risk is different from having the condition itself. These genes increase susceptibility, but they're not destiny. The researchers are saying these 36 genes substantially raise the risk—meaning they're important contributors, but other factors matter too.
Luke
Right, and I want to flag something: they analysed DNA from nearly 4,000 people. That's a solid sample, but we should know whether that's representative globally, or if it's mostly from one population. The source doesn't specify, and that matters for how broadly these findings apply.
Mark
Why does it matter that the genes are shared between OCD and tic disorders?
Mimi
It suggests these aren't completely separate diseases. They may involve overlapping brain pathways. That's why the researchers emphasize networks rather than individual genes—the same biological systems seem to be involved in both conditions.
Luke
That's interesting, but the source says the genes "appear to involve many of the same brain pathways." That's an observation from the data, not a proven mechanism. We don't yet know exactly how these pathways malfunction or why some people with the genes develop symptoms and others don't.
Mark
The researcher mentioned "over 30 targets" for drug development. Is that a lot?
Mimi
It's a dramatic shift. Before, they had only a couple of strong genetic targets. Now pharmaceutical companies have 30-plus potential entry points. That's the difference between having almost nowhere to start and having a real map.
Luke
True, but having 30 targets doesn't automatically mean 30 new drugs. It means 30 potential directions to explore. Drug development is slow and expensive. The source doesn't tell us how close any of these are to becoming actual treatments.
Mark
What about the connection to autism and schizophrenia?
Mimi
Several of the genes they identified had already been linked to those conditions. It reinforces the idea that psychiatric disorders may share common biological roots—that they're not entirely separate diseases but variations on related brain disruptions.
Luke
That's a reasonable inference, but it's still inference. The source says it "reinforces increasing evidence," which means this is one piece of a larger pattern researchers are noticing. It's not proof that OCD, tics, autism, and schizophrenia are fundamentally the same condition.
Il Polso
- OCD and chronic tic disorders have long resisted effective drug treatment, leaving millions with little more than symptom suppression and limited relief.
- A landmark genetic study of nearly 4,000 patients has uncovered 36 genes driving these conditions — shattering the previous landscape where only a handful of genetic targets were known.
- Crucially, many of these genes are shared between OCD and tic disorders, suggesting the two conditions are biologically entangled through overlapping neural pathways.
- The genes operate not alone but in networks, and researchers say targeting those entire networks could make it far easier to design therapies that address root causes rather than symptoms.
- Connections to autism and schizophrenia were also found among the identified genes, deepening the case that multiple psychiatric conditions may spring from related disruptions in how the brain develops and communicates.
For generations, obsessive-compulsive disorder and chronic tic disorders have been managed at the surface — their inner biological architecture remaining largely hidden. A study published in Nature Neuroscience has now identified 36 genes that substantially raise the risk of these conditions, revealing shared brain pathways and offering pharmaceutical researchers more than 30 concrete targets for intervention. The discovery marks a quiet but profound shift: from treating what people suffer to understanding why their brains are suffering.
A research team has identified 36 genes that substantially increase the risk of obsessive-compulsive disorder and chronic tic disorders — a finding that could fundamentally change how these conditions are treated. Published in Nature Neuroscience, the study drew on DNA from nearly 4,000 patients and broke open a genetic landscape that had long remained opaque.
OCD is characterised by persistent intrusive thoughts and compulsive behaviours, while chronic tic disorders — including Tourette syndrome — involve sudden, repeated movements or vocalisations that sufferers struggle to control. Until now, only a small number of genes had been associated with either condition, leaving pharmaceutical developers with few entry points. "Now you've got over 30 targets," said Jay Tischfield of Rutgers University, "and that opens up new possibilities for treatment development."
A particularly striking finding is that many of the 36 genes appear in both OCD and tic disorders, pointing to shared biological pathways. Equally important is how these genes behave: not in isolation, but as interconnected networks. Tischfield noted that targeting whole networks — rather than single genes — could make it considerably easier to design new therapies, representing a shift in the logic of psychiatric drug development.
Several of the identified genes had previously been linked to autism and schizophrenia, reinforcing growing evidence that distinct psychiatric conditions may share common roots in how the brain develops and communicates. At the cellular level, the genes appear to influence neurotransmitter signalling — the chemical messaging that shapes how information moves through neural circuits.
The broader implication is a transition from managing what patients experience to intervening in what is biologically occurring. With a clearer map of the genes and networks involved, researchers can now pursue treatments aimed at halting disease progression rather than merely softening its effects.
A team of researchers has identified 36 genes that substantially increase the risk of obsessive-compulsive disorder and chronic tic disorders, a finding that could reshape how the pharmaceutical industry approaches treatment for these conditions. The study, published September 1 in Nature Neuroscience, analysed DNA from nearly 4,000 people diagnosed with OCD or chronic tic disorders—conditions that have long resisted effective pharmaceutical intervention.
OCD manifests as persistent intrusive thoughts paired with repetitive behaviours that sufferers feel compelled to perform. Chronic tic disorders, which include Tourette syndrome, involve sudden, repeated movements or vocalisations that people struggle to control. Until now, the genetic landscape underlying these conditions remained largely opaque. "In the past, we knew about a couple of strong genes, so there were few opportunities for the pharmaceutical industry to develop drugs," said Jay Tischfield, an emeritus distinguished professor at Rutgers School of Arts and Sciences. "Now you've got over 30 targets, and that opens up new possibilities for treatment development."
What makes this discovery particularly significant is that many of the newly identified genes appear in both OCD and chronic tic disorders. This overlap suggests the two conditions may operate through similar brain pathways at the biological level. The genes do not function in isolation; instead, they work as interconnected networks. "These genes don't act individually," Tischfield explained. "They act in networks. And now you can target whole networks, which will make it easier to design new therapies." This shift from single-gene targets to network-based approaches represents a fundamental change in how researchers might design interventions.
The researchers also discovered that several of the identified genes had previously been linked to autism and schizophrenia. This finding adds weight to a growing body of evidence suggesting that multiple psychiatric conditions may stem from related disruptions in how the brain develops and communicates. At the cellular level, the genes appear to influence neurotransmitter signalling—the chemical messages that travel between nerve cells and shape how information flows through neural circuits.
The practical implications are substantial. Rather than developing drugs that merely suppress symptoms, researchers can now target the underlying biological mechanisms driving these disorders. By understanding which genes and networks are involved, pharmaceutical developers gain a clearer map of where intervention might prevent or halt disease progression. The study represents a transition from treating what people experience to addressing what is happening inside their brains.
In a separate but related development, researchers have also made progress on fatty liver disease, a condition affecting hundreds of millions of people worldwide. Scientists discovered that a protein called EFHD1, located in the mitochondria—the energy-producing structures within liver cells—appears to trigger the damage seen in some patients. When researchers blocked this protein in mice on high-fat diets, measures of inflammation and liver scarring dropped by 30 to 60 percent. Mice engineered to lack EFHD1 showed normal metabolism and weight gain, suggesting that drugs targeting this protein might avoid significant side effects. The research team at University of Utah Health is currently working to develop such a treatment.
Both discoveries share a common thread: they move beyond symptom management toward understanding and targeting the biological systems that drive disease. For OCD and tic disorders, the identification of 36 genes and their interconnected networks provides pharmaceutical companies with concrete targets for drug development. For fatty liver disease, blocking a single protein shows promise in preventing the cascade of cellular damage that leads to scarring and organ failure. The next phase will be translating these genetic and molecular insights into therapies that can reach patients.
Citazioni salienti
In the past, we knew about a couple of strong genes, so there were few opportunities for the pharmaceutical industry to develop drugs. Now you've got over 30 targets, and that opens up new possibilities for treatment development.— Jay Tischfield, emeritus distinguished professor at Rutgers School of Arts and Sciences
These genes don't act individually. They act in networks. And now you can target whole networks, which will make it easier to design new therapies.— Jay Tischfield
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