Despite being present in some of our most beloved artists, including Carrie Fisher, Catherine Zeta Jones, Demi Lovato, and Jean-Claude Van Damme, bipolar disorder carries a stigma that forces many people to go undiagnosed.
Often characterized by dramatic shifts in mood, energy and activity levels, which ultimately affect one’s habits and relationships, the causes of bipolar disorder have remained partially unknown — until now.
Researcher from the Ulsan National Institute of Science and Technology in Ulsan, South Korea, have been working on a particular protein phospholipase called PLCγ1, and published their findings in Molecular Psychiatry. While previous research showed it to be connected to bipolar disorder, scientists are just beginning to discover how.
To find the link between PLCγ1 and bipolar disorder, researchers took genetically designed mice — all with PLCγ1 deficiency in their forebrain — and studied what happened to their synapses, a process that directs electric signals between one brain cell to another.
The PLCγ1-deficient mice lacked the ability for their synapses to change shape, function and strength over time. Because of this effect, scientists found another protein missing: the brain-derived neurotrophic factor, which is supposed to be present to regulate these kinds of functions.
BDNF deficiency leads to an imbalance between excitatory and inhibitory transmission between brain cells’ synapses. But after administering treatment to the mice, scientists found a reduction of bipolar symptoms, regulating their brain activity to more normal levels.
So what's the discovery?
Bipolar disorder is a result of a neurchemical chain reaction due to the lack of PLCγ1, which is also due to a lack of BDNF. As a result, there is an imbalance of excitatory and inhibitory synapses, which in a healthy person is supposed to be well-balanced for proper neurotransmission.
“PLCγ1 protein plays a major role in the onset of bipolar disorder," Pann-Ghill Suh, a professor of life sciences at UNIST, said. “Our findings, therefore, provide evidence that PLCγ1 is critical for synaptic function and plasticity and that the loss of PLCγ1 from the forebrain results in manic-like behavior."
This breakthrough is going to be huge for future treatment options, as well as medical research.