When is the Brain “Mature”?

In the New York state budget just passed by Albany, legislators will raise the age to be tried as an adult from 16 to 18 years. New York was one of only two states left in the US that prosecuted youth as adults when they turned 16–now North Carolina stands on its own.

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In the US, law and policy have struggled to determine an accurate age to judge people mature and accountable, but new scientific findings regarding the brain, adolescence, and neurodevelopment counter the idea that we can pinpoint one age for everyone.

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New Paper: Incorporating Sex Influences into Today’s Brain Research

Historically, most medical research has used male subjects (human and animal) and tissues, but recently there has been a notable increase in the acceptance of the need to incorporate sex influences into brain research. in 2014, the National Institutes of Health (NIH) mandated that all future biomedical research funded by the agency include sex differences.

But two years after the NIH passed its mandate, the research community continues to debate how best to address sex as a biological variable.

Why not just introduce female subjects to the studies, you might wonder, but it’s not that simple, as Jill Goldstein, director of research at the Connors Center for Women’s Health and Gender Biology at Brigham and Women’s Hospital explains in our new briefing paper:

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Meditation in Education

Can something as simple as designated quiet time for 15 minutes twice a day help struggling students perform better in school? After adopting this approach for three years, one school in a troubled area of San Francisco saw suspension rates drop by 79 percent, attendance rise 98 percent, and grade point averages increase.

Yesterday’s New York Times reported on this school and other studies in the Bay Area, which also showed encouraging results. While these types of studies are still in their infancy, schools around the country are jumping on the meditation train in search of a cost-effective ways to nurture healthier and more focused students.

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Image: Shutterstock

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Putting Genetic Studies into Perspective

The genetics field has grown dramatically in recent years as we look to our DNA to explain our health and predict future diseases and disorders. At-home genetic testing kits are readily available and relatively affordable these days, though the tests may not live up to the hype and raise some ethical questions.

Beyond pursuing answers about our health, researchers, funders, and the public have grown increasingly interested in behavioral genetics, as we seek insight into cognition, intelligence, and personality. But don’t be too quick to buy into simple causal explanations about why you may have certain traits. For example, scientists argued in a New York Magazine article last year that Catechol-O-methyl transference may cause certain people to handle stress better than others. In our new briefing paper, “How Should We Be Thinking About Genetic Studies?” a number of experts note that the science is not that clear-cut:

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The How of Tau

The debate over whether the tau protein’s corruption is a cause or effect of the Alzheimer’s disease process is now all but over. In fact, its corruption seems to be a driver of disease not only in Alzheimer’s, but in more than half a dozen other tau-linked maladies.

The Dana Foundation’s latest briefing paper, “The How of Tau,” looks at how tau dysfunction kills and how scientists are working to stop it.

Since the early 1990s, autopsy studies have found that the spread of tau NFTs [neurofibrillary tangles and threads] through memory-related brain areas tracks the progress of Alzheimer’s dementia—and does so better than the spread of Aβ [amyloid beta] plaques. About fifteen years ago scientists also linked a familial form of the dementia syndrome known as frontotemporal dementia with parkinsonism to a set of tau mutations—whose effects turned out to be very similar to what is seen in Alzheimer’s. “Some of the mutations impair the binding of tau to microtubules, while others cause tau to aggregate more readily,” says John Q. Trojanowski, [M.D., Ph.D., a Dana Alliance for Brain Initiatives member who co-directs the Center for Neurodegenerative Disease Research at the University of Pennsylvania.]

Throughout the 2000s, scientists found more and more evidence that tau dysfunction kills and Aβ doesn’t—or rather that Aβ contributes to Alzheimer’s only indirectly, by causing tau dysfunction. The more conclusive findings have come only in the past few years. In 2011, for example, researchers in the Harvard Medical School laboratory of Dennis Selkoe, M.D. (also a Dana Alliance member) reported that small aggregates (“oligomers”) of Aβ, isolated from Alzheimer’s brains, triggered the hyperphosphorylation of tau as well as Alzheimer’s-like changes in neurons, including the loss of synapses, even at very low concentrations. This toxic effect was tau-dependent: no tau, no toxicity.

Read the full paper here.

–Ann L. Whitman

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