Researchers from the Broad Institute and the Massachusetts Institute of Technology have identified a similar pattern of gene activity changes in brain tissue from people with schizophrenia and in older adults. The findings appeared in Nature, a leading scientific journal, underscoring a shared biological thread in cognitive decline seen with schizophrenia and aging.
In a large-scale analysis, neuroscientists measured gene expression across more than a million brain cells from 191 donated brains. The analysis revealed that both schizophrenia patients and older individuals show a reduction in the activity of genes that support communication between nerve cells. The affected cell types are synapses and astrocytes, crucial players in brain signaling and support.
Astrocytes are star-shaped glial cells that help sustain the brain’s internal environment, supply neurons with oxygen and nutrients, regulate ion balance, and shield brain tissue from harmful substances. Synapses are the contact points where signals pass from one neuron to another or from a neuron to a different cell. They are central to forming memories and enabling learning.
The team described these changes as the Synaptic Neuron and Astrocyte Program, highlighting a coordinated shift in the cellular activities that underlie neural communication. The lead author, Amy Ling, noted that while neurons and synapses have long been linked to schizophrenia risk, astrocytes appear to play a meaningful role as well, pointing to a broader network of cellular interactions involved in the disorder.
Experts suggest that similar brain changes may be present in other psychiatric conditions such as bipolar disorder and major depression, indicating a potential common pathway for cognitive impairment across multiple illnesses. Earlier work has already challenged the idea that brain toxicity in diseases like Alzheimer’s disease is driven solely by toxic protein buildup, opening the door to new models of brain aging and disease that emphasize diverse cellular processes.
These insights carry implications for future research and treatment strategies. By mapping how synaptic communication and astrocyte support alter in schizophrenia and aging, scientists may identify targets that help preserve cognitive function, improve neuron-to-neuron signaling, or bolster the brain’s resilience to age-related decline. The study adds to a growing body of work that views mental health and neurodegenerative conditions through the lens of cellular networks rather than single culprits, offering a more integrated view of brain health across the lifespan.
Continued investigation will help determine how these changes arise, whether they respond to existing therapies, and how interventions might promote healthier synaptic and glial function. As researchers expand their analyses to diverse populations and additional brain regions, they anticipate a more complete picture of how aging intersects with psychiatric risk, ultimately guiding precision approaches to prevention and care for cognitive disorders in North America and beyond. These developments align with ongoing efforts to translate cellular and molecular discoveries into practical strategies for maintaining brain health across communities in the United States and Canada, supported by a growing emphasis on early detection and targeted intervention.
Additional findings from this line of research reinforce the importance of a holistic view of brain biology, one that accounts for the interconnected roles of neurons, synapses, and supporting glial cells in health and disease. By continuing to map these networks, scientists aim to unravel the complex biology that underpins cognitive function and its decline, with the goal of reducing the burden of mental illness and age-related cognitive impairment across populations.