||NCI scientists have shown that smoking affects the way genes are expressed—leading to alterations in cell division and regulation of immune response.
Smoking and Gene Expression
It’s well known that smoking plays a role in lung cancer development. Now, NCI scientists have shown that smoking also affects the way genes are expressed—leading to alterations
in cell division and regulation
of immune response. In fact, according to the study, published
in the Feb. 20 issue of PLoS One, some of the changes in gene expression persisted in people who had quit smoking many years earlier. These findings are significant,
researchers said, because even though we’re well aware that smoking is a leading cause of lung cancer worldwide, scientists
still don’t have a full mechanistic
understanding of the effects of smoking on the cells of the lung. Gaining a better understanding of the genetic alterations that occur with smoking could provide insight into the development of cellular targets for treating—and even preventing—lung cancer.
Insights into Cognitive Decline in Diabetes
Why does diabetes impair cognitive health in humans? A new study conducted by NIA and published in the Feb. 17 issue of Nature Neuroscience has identified one potential mechanism underlying this problem. Researchers found that in diabetic rodents, increased levels of a stress hormone produced by the adrenal gland disrupted the healthy functioning of the hippocampus—
the region of the brain responsible
for learning and short-term memory. In addition, when levels of the hormone corticosterone—
also known as cortisol in humans—returned to normal, the hippocampus recovered
its ability to build new cells and regained the plasticity needed to compensate for injury and disease and adjust to change. Studies like this could provide a better understanding of the complex interplay between the nervous system, hormones and cognitive health and could eventually point to approaches for preventing
and treating cognitive decline in diabetes,
Deciphering How Memories Last
More about mice and memory: NIMH-supported
researchers have developed a way to pinpoint the cellular components that sustain a specific
memory in genetically engineered mice. For a memory to last long-term, the neural connections
holding it have to be strengthened by incorporating new proteins triggered by learning.
Until now, however, it’s been a mystery as to how these new proteins end up becoming
part of the specific connections in neuronal extensions that encode the memory. Researchers
followed such migrating proteins and found the neural connections, or synapses, that hold a specific fear memory; in the process they found that these synapses have molecular tags that help them capture the proteins. This newfound ability to link a learning experience in a mouse to consequent changes in the inner workings of its neurons—reported in the Feb. 22 issue of Science—will help scientists gain a better overall understanding of how memory works.
Stopping Staph Virulence
An international team of researchers supported
by NIGMS, NIAID and NICHD has blocked staph infections in mice using a drug previously
tested in clinical trials as a cholesterol-lowering
agent. The finding, reported in the Feb. 15 online edition of Science, could provide a new direction for therapies to fight against a bacterium
that’s becoming increasingly resistant to antibiotics. The key to the research? Color. Staphylococcus aureus, or staph, has a golden pigment that acts as an antioxidant to block the reactive oxygen molecules the immune system
uses to kill bacteria. Researchers speculated
that blocking pigment formation in staph could restore the immune system’s ability to impede infection. Thanks to the work of several researchers, one drug compound that blocked pigment production was found to reduce the bacterial population in mice with staph by 98 percent. Researchers said the next step will be to explore whether this could work in humans.—