We all have the capacity to respond to threats, but why do some of us hold onto our fears more than others? Francis. S. Lee, of the Psychiatry Department, Weill Cornell Medicine and his work is focused on uncovering and explaining the mechanisms of how we learn, forget, or remember our fears. During his research, Lee has discovered that times are changing and so is the view in which people have the mechanisms of the brain that cause anxieties, how they should best be treated, and what point.
There’s a heightened level of brain plasticity when we’re at a young age that’s an essential period when the brain is able to adjust and learn more rapidly. For example, Lee explains, “If you have what they call a lazy eye when you’re young, you can patch one eye, and your visual cortex will adjust and coordinate vision again. But after about eight to ten years of age, it becomes more difficult because you’ve passed the critical period.”
In 2010, Lee and colleagues conducted a study that looked into when we learn to become fearful of things. By accident, what the team discovered was that there is a critical period for fear learning. “During adolescence, the whole fear system goes offline, which made no sense to us six years ago, and now we’re slowly putting it together. But it suggest that brain development is not a linear process. It seems to go through waves of growth and then rearrangement and growth again. We were able to find a period in adolescent mice models, where that regulate fear in a very different way,” says Lee.
Because of these differences in regulation, an adolescent experiencing trauma may remember it much more vividly than a child or adult. The fear will be learned and ingrained in their memory. However, because the young are adaptable and able to learn quickly, intervention early on may be the key to regulating fears. Much of Lee’ inspiration for his work comes from the fact that the statistics for anxiety in American teens is so shocking, with roughly a quarter of them having some form of diagnosable anxiety disorder. And, what’s worse it that we’re treating them with therapies that have been designed for adults.
During part of his research, Lee and former colleague at the Sackler Institute for Developmental Psychobiology B.J. Casey came together to demonstrate the circuit in which the protein BDNF (brain-derived neurotropic factor) is found to heighten anxiety and fear responses. The pair also has a patent relating to a BDNF single nucleotide polymorphism (SNP) and fear regulation. “Eventually we are hoping to use the polymorphism as a biomarker to determine how patients will respond to certain treatments,” says Lee. If this particular polymorphism can be screened doctors may have a better understanding of a person’s patterns of fear learning, which could be used to help those suffering from anxiety disorders or post-traumatic stress disorder (PTSD).
Lee has also discovered another polymorphism in the endocannabinoid system and says, “If they have this cannabinoid polymorphism, it makes the animals less anxious and makes them extinguish fear and get rid of fear much more quickly.” Statistics confirm that around 30 percent of the population has the BDNF polymorphism, while 30 percent has the cannabinoid one. A small percentage of people have both. “We’re in the midst of a variety of studies to untangle the mechanisms, but ultimately we’d like to get a repertoire of anxiety genes that can help us understand anxiety and develop treatments based on genotypes,” says Lee.
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