Whether it’s large crowds or air travel, most of us avoid the source of our fears like the plague. We’ll pass up the chance to see our favorite musician play a packed concert venue or we’ll opt to drive cross-country rather than hop on a plane. But should we do the opposite? Fear experts Michael Telch, a psychologist at the University of Texas, and Kerry Ressler, a psychiatrist at Emory University, explain how facing our fears can retrain the brain.
Feeling panic is an adaptive response to danger. The related increase in breathing rate and blood flow provides what’s needed to fight off — or escape from — the threat. But feeling panic can be a problem when there is no threat. Heide Klumpp, associate professor of psychiatry at the University of Illinois at Chicago explains what can happen when an unexpected panic attack comes out of the blue.
Fear of heights, spiders, crowds, flying, and small spaces are just a few typical examples that cause anxiety for many people, but when do those feelings produce the extreme reactions that become a phobia? Barbara Rothbaum, professor of psychiatry and associate vice chair of clinical research at the Emory University, explains.
Published by the Society for Neuroscience and overseen by an editorial board of leading neuroscientists from around the world, BrainFacts.org shares the stories of scientific discovery and the knowledge they reveal.
Relaunched in the fall of 2017, the site affirms its continued commitment to neuroscience literacy and outreach to the public. The corresponding book has also seen a recent relaunch.
I had the pleasure and privilege of writing Chapter 15: Neurodegenerative Diseases.
Prions are a type of protein gone wrong. The complex three-dimensional structure of a prion’s progenitor protein has been altered, somehow causing it to no longer function as expected. Worse, the malformation of these progenitor proteins into prions causes them to aggregate into amyloid plaques that can result in a disease state. Prions are responsible for an odd sort of protein-caused infectious neurodegenerative diseases like Mad Cow disease and scrapie in livestock.
Neuroscientists at the Massachusetts Institute of Technology have provided evidence opposing the current model for how working memory operates at the cellular level. The current model says the cellular basis for working memory lies in consistent, sustained activity by brain cells, or neurons. Results from the MIT study, published in the March 17 issue of the scientific journal Neuron, shows the story is more complex, that brain cells involved in working-memory tasks are activated discretely and sporadically.
In the spring of 2004, Antonio Ulloa was visiting San Francisco, California, for the Cognitive Neuroscience Society meeting when he was beset with nausea and a feeling of intoxication. A postdoc at the National Institutes of Health’s (NIH’s) National Institute on Deafness and Other Communication Disorders at the time, he was at the conference to present his neuroimaging studies about short-term memory and to network and scout possible employers. He remembers presenting and participating at the conference but not much else from the trip other than lying in bed. Upon returning home to Washington, D.C., he was diagnosed with testicular cancer.