Johns Hopkins has filed a patent on techniques to measure electrical currents from GluDs, with funding support from NIH, Searle, and the Diana Helis Henry Medical Research Foundation; key contributors include Haobo Wang, Fairine Ahmed, Jeffrey Khau, and Anish Kumar Mondal.

In cerebellar ataxia, GluDs may become overactive without electrical signaling, implying therapies to block excessive GluD activity could improve movement and balance.

Dr. Edward Twomey notes that GluDs are active and represent a promising therapeutic channel, challenging the view of them as dormant.

The Nature study used cryo-electron microscopy to show GluDs contain a central ion channel that interacts with neurotransmitters, clarifying their role in neuron communication and offering a mechanism to modulate brain activity.

Cryo-EM findings reveal GluDs’ central ion channel can regulate neurotransmitter signaling and synapse formation, providing a path to therapeutic modulation.

A Johns Hopkins Medicine study shows delta-type ionotropic glutamate receptors (GluDs) are active regulators of neuronal communication and present GluDs as a promising drug target for psychiatric and movement disorders.

Researchers identify GluDs as a drug target capable of modulating brain protein activity relevant to psychiatric and movement disorders.

The study was funded by the NIH, the Searle Scholars Program, and the Diana Helis Henry Medical Research Foundation.

Published in Nature, the findings highlight the potential to translate these insights into new therapies for anxiety, schizophrenia, cerebellar ataxia, and related conditions.

In schizophrenia, GluDs are underactive, suggesting that future therapies should aim to enhance GluD activity to restore neural function.

The researchers plan to collaborate with pharmaceutical companies to advance GluD-based therapies and are examining GluD mutations linked to schizophrenia, anxiety, and other disorders to design more precise treatments.

Targeting GluDs could influence aging and memory by regulating synapse function, potentially mitigating memory decline.