NEW BRUNSWICK — Rutgers University published a study in Molecular Psychiatry on July 14, 2026, identifying widespread synaptic loss in the brains of people with schizophrenia. The findings reveal distinct patterns of neural degradation not visible through conventional imaging and offer a potential roadmap for new therapeutic approaches.

The study used positron emission tomography (PET) imaging to measure synaptic connections in the human brain, a technique that allows researchers to visualize and quantify synaptic density in living subjects. This method provided a more detailed view of brain connectivity than standard structural MRI scans, which primarily detect changes in brain volume. The research included 122 individuals, 29 of whom had been diagnosed with schizophrenia, enabling direct comparison with healthy controls.

People with schizophrenia showed a widespread lowering of synaptic connections across multiple brain regions compared to healthy individuals. The synaptic loss was particularly pronounced in areas associated with frontal and temporal functions, as well as regions involved in memory and emotional processing., the left side of the brain was substantially more affected by synaptic loss than the right side, suggesting an asymmetrical progression of the disease’s neural impact.

The pattern of synaptic loss was distinct from brain volume alterations detected by standard MRI scans, indicating that synaptic degradation occurs independently of gross anatomical changes. Brain regions with the greatest synaptic loss were found to be rich in receptors for serotonin, gamma-aminobutyric acid (GABA), and glutamate—neurotransmitters long implicated in mood regulation, inhibition, and excitatory signaling. This finding aligns with existing pharmacological approaches to schizophrenia, which often target these same neurotransmitter systems.

Computer simulations conducted as part of the study identified a region in the left frontal lobe as a likely starting point for the spread of synaptic loss throughout the brain. This computational modeling suggests that schizophrenia may follow a predictable neurobiological trajectory, beginning in a specific cortical hub and propagating to connected regions. Such insights could refine early detection strategies and inform the timing of interventions.

The study was led by senior authors Avram Holmes and Rajiv Radhakrishnan. Holmes is an associate professor of psychiatry at Robert Wood Johnson Medical School and a core faculty member of the Center for Advanced Human Brain Imaging Research within the Rutgers Brain Health Institute. Radhakrishnan is an associate professor of psychiatry and radiology and biomedical imaging at Yale University. Sidhant Chopra, the first author of the study, is a McKenzie Research Fellow at Orygen, Australia's center of Excellence in Youth Mental Health, and the University of Melbourne.

“This detailed mapping of synaptic vulnerability could eventually help identify where and how to intervene to preserve or restore brain function, such as emerging therapies to prevent and regrow synapses,” Holmes said.

Schizophrenia affects approximately 1% of the global population and remains one of the most disabling psychiatric disorders, with limited treatment options that often address symptoms rather than underlying biology. The study’s use of PET imaging to directly observe synaptic density marks a methodological advance over prior reliance on postmortem tissue or indirect proxies. By demonstrating that synaptic loss follows a specific spatial and neurochemical pattern, the research provides a biological basis for developing targeted treatments aimed at synaptic preservation or regeneration.

Molecular Psychiatry, the journal in which the study appears, is a peer-reviewed scientific publication focused on the intersection of neuroscience and mental health. Rutgers University, a multi-campus public research university in New Jersey, has prioritized brain health research through institutes like the Rutgers Brain Health Institute, where this work originated.