Dec 12, 2018
In genetically engineered mice lacking the protein called importin alpha-5 (right), a molecule called MeCP2 (red), known to affect anxiety behaviors, stayed on the outside the nuclei (blue) of brain neurons, instead of getting inside the nuclei, as it does in regular mice (left). Images obtained with a confocal microscope and displayed using computational reconstruction. [Weizmann Institute of Science]
Scientists at the Weizmann Institute of Science have identified a molecular pathway in the brain that can be targeted to reduce anxiety. Their studies showed how symptoms of anxiety were reduced in mice engineered to lack a single protein, while normal animals treated using an existing multiple sclerosis drug that impacts on the same pathway remained similarly calm in stressful situations. Describing the research in Cell Reports, the researchers suggested that their findings could pave the way to the development of effective new treatments for anxiety that have fewer side effects than existing drugs.
“Our findings have opened up a new direction for research into the mechanisms of anxiety,” said Nicolas Panayotis, Ph.D., at the Weizmann Institute’s department of biomolecular sciences. “If we understand exactly how the circuitry that we’ve discovered controls anxiety, this may help develop new drugs, or direct the use of existing ones, to alleviate its symptoms.” The studies are described in a paper titled, “Importin α5 Regulates Anxiety through MeCP2 and Sphingosine Kinase 1.”
Severe anxiety and stress-related disorders are estimated to affect up to one in three people in their lifetime. Several hormones and neurotransmitters have been implicated in anxiety, but intracellular transport systems haven’t been studied in this context, the authors wrote. Current drugs may also have limited utility, and cause unwanted side effects. “Current therapies for anxiety disorders either directly affect neurotransmitter receptor systems or modulate neurotransmitter levels or availability, but their long-term use is limited by problematic side effects and suboptimal efficacy,” the authors wrote.
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