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.