Excess Protein during Brain Development may cause Schizophrenia

Bonnie Firestein, a professor at Rutgers in cell biology and neuroscience explains that too much protein expressed by the NOS1AP gene is associated with schizophrenia. In her research she found that the excess protein resulted in dendrites that were stunted in growth in rats.

Firestein and her colleagues found that too much of the NOS1AP protein didn't allow the dendrites to branch out like they should and they stayed contained in the neocortex which is the part of the brain that is responsible for higher functioning skills. In the control group where there was a regular amount of NOS1AP the connection between the cells properly develop and allowed for proper communication between the different areas of the brain. In the experimental group they brain cells didn't have the dendrites branched out enough to make the proper connections. Of course this is not the pinpoint and exact cause of schizophrenia but it is definitely associated with an increased risk for it.

This is definitely an important finding because with this information we could possibly find ways to detect and treat schizophrenia earlier. 1% of the entire population is affected with schizophrenia and for people that are first relatives of them the chances increase to 10% for having schizophrenia. Being able to find new and better treatments and medications would be extremely beneficial.

Article: http://www.sciencedaily.com/releases/2014/11/141124081034.htm

One Gene Mutation = Uncontrollable Obesity

In America, it seems like a major issue that is plaguing us with worry is obesity. Some of the lucky ones with a faster metabolism, allowing digestion to occur more quickly, results in a more or less slimmer figure. But has anyone ever given thought that it might be the other way around also?

Baoji Xu, Ph.D. has. As an associate professor of pharmacology and physiology at Georgetown University Medical Center, Xu has been researching a single gene mutation that occurs within the brain-derived neurotrophic factor gene (Bdnf). With this mutation, the brain does not receive the chemical signals needed, by leptin and insulin, to turn on the mechanism that suppresses the desire to keep eating, and then tells the body that it is now full. Without these signals transmitted, individuals will just keep eating until they become obese and beyond. The can never fully feel satisfied.

Until this study, it was known that the Bdnf gene has some correlation with controlling body weight. After this study, published on the Nature’s Medicine website, now we know why. Bdnf synthesis is stimulated with leptin and insulin in the dendrites on neuroglia to get their chemical message across the synapses to adjacent neurons. With the mutation of the Bdnf gene, the chemical signals cannot be passed on through the neurons, and one’s hunger will never be suppressed.