How Do Tics Develop in Tourette Syndrome?

Tourette syndrome is a brain dysfunction that leads to involuntary motor tics, such as sniffing, blinking, or clapping. In about 10 percent of cases, it also leads to the spontaneous utterance of taboo words or phrases, known as coprolalia. Until recently, these tics were believed to be the result of a dysfunction primarily in a brain structure known as the basal ganglia—a brain region associated with voluntary motor control, which primarily uses the neurotransmitter gamma-aminobutyric acid (GABA) to function. Recent studies of rat, monkey, and even human brains, however, has suggested that the tics stem from a more complex, system-level dysfunction that involves the cerebellum, the thalamus, and the cortex, which are all connected.

To better explore these brain regions and their influence on Tourette syndrome, Daniele Caligiore, a researcher at the Institute of Cognitive Sciences and Technologies of the Italian National Research Council in Italy, and his colleagues created a computer-simulated model of the neural activity of a brain with Tourette syndrome. The results are published in PLOS Computational Biology.

“The model presented here is a first step of a research agenda aiming at building virtual patients, allowing us to test potential therapies by using computer simulations,” Caligiore tells mental_floss. This method can be performed at low cost, without ethical implications, and, he hopes, help develop “more effective therapeutic protocols, and suggest promising therapeutic interventions.”

Using a computer programming language called Python, Caligiore’s team built an artificial neural network model. In it, each neuron has a behavior that is regulated by mathematical equations. He explains, “Once built, the model works like a computer program—you can run it and observe its behavior.”

Caligiore reproduced the brain activity from monkey studies, published in the Journal of Neuroscience, in which an agent called bicuculline was microinjected into a region of the brain called the sensorimotor striatum that is involved in motor function. The researchers found that this microinjection of bicuculline inhibits GABA, which causes an abnormal release of the neurotransmitter dopamine.

“This excess [dopamine] might cause an abnormal functioning of the basal ganglia-thalamo-cortical circuit, leading to the production of tics,” Caligiore says. The abnormal dopamine release is one necessary condition for a tic, but it's not the only one, he says. “To have a motor tic you need both abnormal dopamine and a background activity in the motor cortex (due to the neural noise) above a threshold.”

In other words, “it is not just a matter of dopamine or just a matter of abnormal cortical activity," he explains. "It is a necessary combination of both.”

Caligiore’s team also found that the cerebellum appeared to influence tic production as well. Their model shows that during a tic, there is abnormal activity in a region of the basal ganglia called the subthalamic nucleus (STN). The STN connects with the cerebellum. “This is a possible reason [for a tic] because there is an abnormal tic-related activity in the cerebellum as well.”

What the computer model shows is that motor tics in Tourette syndrome “are generated by a brain system-level dysfunction, rather than by a single area malfunctioning as traditionally thought.” Studying this interaction between regions “could substantially change our perspective about how these areas interact with each other and with the cortex,” he adds.

Moreover, Caligiore’s team’s computer model is a noninvasive, ethical, and low-cost way to study these brain systems—and it certainly could be the first important step to identify new target areas for future therapies.

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More Studies See Links Between Alzheimer's and Herpes
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Although it was discovered in 1906, Alzheimer’s disease didn’t receive significant research attention until the 1970s. In 1984, scientists identified the plaque-like buildup of amyloid beta proteins in brain tissue that causes nerve damage and can lead to symptoms like memory loss, personality changes, and physical debility.

Now, researchers are learning why amyloid beta tends to collect in brain tissue like barnacles on a ship. It might not be rallying expressly to cause damage, but to protect the brain from another invader: the herpes simplex virus.

As The Atlantic recently noted, a number of studies have strengthened the notion that amyloid beta activity is working in response to herpes, the virus that travels along nerve pathways and typically causes cold sores around the mouth (HSV-1) or genitals (HSV-2). In a study involving mice, those engineered to produce more amyloid beta were more resistant to the herpes virus than those who were not.

But when too much amyloid beta is produced to combat the virus, the proteins can affect the brain’s neurons. And while herpes tends to target specific pathways in the body that result in external sores, it’s possible that the virus might act differently in an older population that is susceptible to more widespread infection. Roughly half of adults under age 50 in the U.S. are infected with HSV-1 and 12 percent with HSV-2, which suggests that a large swath of the population could be vulnerable to Alzheimer's disease. Two other strains of the virus, HHV-6A and HHV-7, have also been found to be more common in the brains of deceased Alzheimer’s patients than in the general population.

More research will be needed to further understand the possible relationship between the two. If more findings support the theory, then it’s possible that antiviral drugs or vaccines targeting herpes might also reduce the chances of amyloid beta buildup.

[h/t Atlantic]

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Heatwaves Can Affect Your Ability to Think Clearly and Make Decisions
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Dehydration and body odor aren't the only things to hate about oppressive heat. According to new research reported by The Guardian, living through a heatwave without relief hampers your ability to think quickly and clearly.

For their study, published recently in PLOS Medicine, researchers at the Harvard T.H. Chan School of Public Health tested the mental performance of 44 students during a heatwave in Boston in 2016. Roughly half the students were living in newer dorm buildings with central AC, with the other half living in older dorms without it.

Over 12 days, researchers had participants take cognition tests on their phones immediately after waking up. The students living without AC took about 13 percent longer to respond to the questions and their answers were about 13 percent less accurate.

The results indicate that even if high temperatures don't pose an immediate threat to someone's health, they can impair them in other ways. “Most of the research on the health effects of heat has been done in vulnerable populations, such as the elderly, creating the perception that the general population is not at risk from heat waves,” Jose Guillermo Cedeño-Laurent, research fellow at Harvard Chan School and lead author of the study, said in a statement. “Knowing what the risks are across different populations is critical considering that in many cities, such as Boston, the number of heat waves is projected to increase due to climate change.”

Summers are gradually becoming hotter and longer in Boston—a trend that can be observed throughout most of the rest of the world thanks to the rising temperatures caused by human activity. In regions with historically cold winters, like New England, many buildings, including Harvard's oldest dorms, are built to retain heat, which can extend the negative effects of a heat wave even as the weather outside starts to cool. If temperatures continue to rise, we'll have to make a greater effort to keep people cool indoors, where American adults spend 90 percent of their time.

Our thinking isn't the only thing that suffers in the stifling heat. A study published last year found that hot weather does indeed make you crankier—which may not be as bad as bombing a test, but it's not exactly not fun for the people around you.

[h/t The Guardian]

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