Genetic Discovery Could Lead to Development of New Bipolar Meds

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Abnormal variations in the gene PDE10A19 might impact signaling of a messaging pathway responsible for learning, memory.
Abnormal variations in the gene PDE10A19 might impact signaling of a messaging pathway responsible for learning, memory.

In a discovery that could have implications for the development of new drug therapies, researchers at the The Scripps Research Institute (TSRI) have identified genetic variations that make an individual more susceptible to bipolar disorder. They say the discovery could provide new targets for medications to treat the illness.

Ron Davis, PhD, chair of TSRI's Department of Neuroscience, and colleagues honed in on a gene, PDE10A, which has been associated with a greater likelihood of developing bipolar disorder. PDE10A produces proteins that play a part in regulating intracellular levels of a messaging pathway called cAMP (cyclic adenosine monophosphate), which has a role in processes including learning and memory.

The team examined brain tissue both from patients with bipolar disorder and those without the illness. Their research indicates that abnormal variations in PDE10A19 might impact signaling of cAMP by engaging with another protein, restricting that protein's activity and its signaling. The study was published in the journal Translational Psychiatry.

“The PDE10A19 protein is interesting because we previously didn't know it even existed in the human brain and because it's found only in other primates — not mice or rats,” research assistant Courtney MacMullen, PhD, said in a statement. “Once we understand how this protein helps neurons remain healthy, we might be able to develop medications to treat neurons when they function abnormally, such as in patients with bipolar disorder and schizophrenia.”

 

Reference

MacMullen CM, et al. Novel, primate-specific PDE10A isoform highlights gene expression complexity in human striatum with implications on the molecular pathology of bipolar disorder. Transl Psychiatry. 2016; 6:e742.

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