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Now, scientists at the Salk Institute for Biological Studies in La Jolla, Calif., have pinpointed a gene linked to these disorders that seems to be crucial for normal brain structure in prenatal development. The findings, which appear in an open-access article in the Jan. 14 issue of Cell Reports, shed new light on the mechanistic workings of a gene called MDGA1, previously implicated in autism, schizophrenia and bipolar disorder.

An exciting new test might help us save antibiotics. Needing only a drop of blood, researchers at Duke have developed a rapid assay that can tell viral infections-which generally can't be treated-from bacterial ones that may benefit from antibiotics. While I don't usually write about drugs or products in development, this test piqued my interest and left me excited about its potential to help contain antibiotic overuse.

A new study by Duke University researchers helps clarify the matter by showing how a sugar habit changes specific brain circuits, and how those changes produce cravings that reinforce the habit. The research team began by getting a group of healthy mice hooked on sugar. Similar to classic studies on drug addiction, the mice in this study were trained to press a tiny lever to receive doses of sweets. Once the mice were hooked, they continued pressing the lever even when the sweets were removed. So that was step one, establishing a behavioral pattern to get the goods.

But this tiny sample turned out to hold tremendous scientific value. It was from a person fortunate to survive the deadly Ebola virus outbreak of 2014. Walker and her colleagues wanted to know if they could identify some special antibodies in that person's blood. If this person had special Ebola-neutralizing antibodies, that might help explain why that person lived. The antibodies might also help provide a template for future development of a vaccine. Or, they could be the basis for genetically engineered copies that could be manufactured at large scale, stockpiled and used to rescue people newly infected in an outbreak.

The study is the first to examine all of the gene networks affected by fructose that result in changes to brain function and metabolism-more than 20,000 genes in total. Although the study was conducted using rats, the researchers report that the majority of the sequenced genes are comparable to those in humans, including more than 200 genes in the hippocampus, a brain area crucial to memory, and 700 in the hypothalamus, the seat of the brain's metabolic control center.

Overview of genetic engineering and business assessment of scientific feasibility.  Good overview of past gene therapy attempts.

The conclusion is that the high-fat diet triggered chronic inflammation, which in turn triggered an autoimmune response in the mice's central nervous systems. Normally this response protects the brain from invaders like bacteria, but a high-saturated fat diet knocks the process off track, resulting in damage to synapses in the brain - specifically in the hippocampus. Since the hippocampus is a brain area central to memory and learning, the eventual outcome is impaired brain function. In short, the high-fat diet caused brain damage.

Scientists may debate the accuracy of this equivalency, but most people agree that humans live many times longer than their furry friends. And, as it happens, these friends have features that uniquely qualify them to help us speed biomedical research.