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July 27, 2018

Teen Crash Risk Highest During First 3 Months After Getting Driverís License

Teenage drivers are 8 times more likely to be involved in a collision or near miss during the first 3 months after getting a driver’s license, compared to the previous 3 months on a learner’s permit, suggests a study led by NICHD. Teens are also 4 times more likely to engage in risky behaviors such as rapid acceleration, sudden braking and hard turns during this period. In contrast, teens on a learner’s permit drove more safely, with their crash/near crash and risky driving rates similar to those of adults. The study appears in the Journal of Adolescent Health.

“Given the abrupt increase in driving risks when teenagers start to drive independently, our findings suggest that they may benefit from a more gradual decrease in adult supervision during the first few months of driving alone,” said NICHD senior investigator Dr. Bruce Simons-Morton, one of the authors of the study.

The study is one of the first to follow the same individuals over time, from the beginning of the learner period through the first year of independent driving, while continuously collecting information using software and cameras installed in the participants’ vehicles.

The study also evaluated parents’ driving in the same vehicles, over the same time, on similar roads and under similar driving conditions as their children. Near-crash events were those requiring a last-moment maneuver to avoid a crash, while crashes were physical contact between the driver’s vehicle and another object.

The study enrolled 90 teenagers and 131 parents in Virginia and the data collection system was developed by the Virginia Tech Transportation Institute, Blacksburg.

New Evidence That Viruses May Play a Role in Alzheimer’s

People with EoE experience difficulty swallowing and nutritional problems because an accumulation of immune cells scars the esophagus.
Viral species may have a role in Alzheimer’s disease biology.


Analysis of large data sets from post-mortem brain samples of people with and without Alzheimer’s disease has revealed new evidence that viral species, particularly herpesviruses, may have a role in Alzheimer’s disease biology.

Researchers funded by NIA made the discovery by harnessing data from brain banks and cohort studies participating in the Accelerating Medicines Partnership-Alzheimer’s Disease consortium. Reporting in the June 21 issue of Neuron, the authors emphasize that their findings do not prove that the viruses cause the onset or progression of Alzheimer’s. Rather, the findings show viral DNA sequences and activation of biological networks—the interrelated systems of DNA, RNA, proteins and metabolites—may interact with molecular, genetic and clinical aspects of Alzheimer’s.

“The hypothesis that viruses play a part in brain disease is not new, but this is the first study to provide strong evidence based on unbiased approaches and large data sets that lends support to this line of inquiry,” said NIA director Dr. Richard Hodes. “This research reinforces the complexity of Alzheimer’s disease, creates opportunities to explore Alzheimer’s more thoroughly and highlights the importance of sharing data freely and widely with the research community.”

Novel Drug Therapy Partially Restores Hearing in Mice

People with EoE experience difficulty swallowing and nutritional problems because an accumulation of immune cells scars the esophagus.
A new treatment strategy for deafness offers hope.


A small-molecule drug is one of the first to preserve hearing in a mouse model of an inherited form of progressive human deafness, report investigators at the University of Iowa, Iowa City, and NIDCD. The study, which appears online in Cell, sheds light on the molecular mechanism that underlies a form of deafness (DFNA27) and suggests a new treatment strategy.

“We were able to partially restore hearing, especially at lower frequencies, and save some sensory hair cells,” said Dr. Thomas B. Friedman, chief of NIDCD’s Laboratory of Human Molecular Genetics and a coauthor of the study. “If additional studies show that small-molecule-based drugs are effective in treating DFNA27 deafness in people, it’s possible that using similar approaches might work for other inherited forms of progressive hearing loss.”

The seed for the advance was planted a decade ago, when NIDCD researchers led by Friedman and Dr. Robert J. Morell, another coauthor of the current study, analyzed the genomes of members of an extended family, dubbed LMG2. Deafness is genetically dominant in the LMG2 family, meaning that a child needs to inherit only one copy of the defective gene from a parent to have progressive hearing loss.

The investigators localized the deafness-causing mutation to a region on chromosome 4 called DFNA27, which includes a dozen or so genes. The precise location of the mutation eluded the NIDCD team, however.

A crucial clue to explain the DFNA27 form of progressive deafness arose from later studies of the mouse RE1 silencing transcription factor, or Rest, gene conducted by researchers at the University of Iowa. Dr. Botond Banfi and Dr. Yoko Nakano, lead authors of the current study, discovered that mouse Rest is regulated through an unusual mechanism in the sensory cells of the inner ear and this regulation is critical for hearing in mice. Because the human counterpart of the mouse Rest gene is located in the DFNA27 region, the Iowa and NIDCD researchers teamed up to reexamine the mystery of DFNA27 progressive deafness.

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