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MORGANTOWN, WV – Researchers at West Virginia University (WVU) have made a significant breakthrough in understanding and controlling zinc activity within the brain, potentially paving the way for new pharmaceutical treatments for neurological disorders. The study, led by Charles Anderson, assistant professor in the Department of Neuroscience and Rockefeller Neuroscience Institute with the WVU School of Medicine, reveals a method to precisely regulate zinc release to specific brain regions.
Zinc, an essential mineral, plays a critical role in brain function, influencing memory and mitigating symptoms of certain neurological conditions. However, achieving the correct zinc concentration at the right location has been a challenge.
“Zinc is like a volume knob in many parts of the brain,” explained Anderson. “You can turn it a little bit up and a little bit down. The idea was that if we could find the drugs that control that last little bit of volume, we can selectively change certain connections in the brain that have zinc and the receptors that zinc acts on.”
The research, published in The Journal of Neuroscience, focused on the zinc transporter protein ZIP12. The team successfully pinpointed its presence in a specific brain area and demonstrated its ability to influence synaptic activity – the communication between nerve cells.
“It’s basically a way to fine-tune synaptic transmission,” Anderson stated, highlighting the significance of this discovery in advancing the understanding of synaptic zinc’s role in both healthy and diseased states.
Previous studies have linked altered zinc levels and receptor sensitivity to neurological conditions such as autism, schizophrenia, and Alzheimer’s disease. “There are several neurological conditions associated with changes in these zinc transporter proteins,” Anderson noted. “For example, when we profile people who have schizophrenia versus healthy people, we find extra zinc transporters expressed in the brains of people with schizophrenia. If we could make a drug that reduces the function of that zinc transporter, that might help turn their system back down to the level of a healthy person.”
The researchers screened a class of molecular compounds that interact with the ZIP12 protein, enabling them to block or activate specific parts of the zinc transporter system. Philip Bender, a WVU alumnus and postdoctoral research fellow, conducted experiments on brain tissue using these compounds, measuring their impact on synaptic function.
“The major importance of this study is the identification of a family of compounds which could potentially lead to therapeutics for a wide range of disorders, as the transporters that were targeted have tissue-specific functions,” Bender said.
Anderson envisions this research providing a valuable toolbox for scientists studying the role of zinc transporter proteins in brain function. Future studies will explore zinc’s role in sensory processing, such as sound discrimination, which could have therapeutic implications for neurological conditions.
More information: Charles T. Anderson et al, The astrocytic zinc transporter ZIP12 is a synaptic protein that contributes to synaptic zinc levels in mouse auditory cortex., The Journal of Neuroscience (2025). DOI: 10.1523/JNEUROSCI.2067-24.2025
Journal information: Journal of Neuroscience
Disclaimer: This article is based on the information provided and should not be taken as medical advice. The findings discussed are preliminary and further research is needed to validate these results and translate them into clinical applications. The information provided does not constitute an endorsement of any specific treatments or therapies. Individuals with neurological conditions should consult with qualified healthcare professionals for diagnosis and treatment.
