SNAPSHOT NARRATIVES

Bridge over Meuse River, showing damage left by Germans in their retreat, 11/13/1918

Series: Photographs of American Military Activities, ca. 1918 - ca. 1981. Record Group 111: Records of the Office of the Chief Signal Officer, 1860 - 1985.

Uncover more World War I Centennial Resources at the National Archives.

Ever get chills listening to a particularly moving piece of music? You can thank the salience network of the brain for that emotional joint. Surprisingly, this region also remains an island of remembrance that is spared from the ravages of Alzheimer’s disease. Researchers at the University of Utah Health are looking to this region of the brain to develop music-based treatments to help alleviate anxiety in patients with dementia. Their research appeared in the April online issue of The Journal of Prevention of Alzheimer’s Disease.

“People with dementia are confronted by a world that is unfamiliar to them, which causes disorientation and anxiety” said Jeff Anderson, MD, PhD, associate professor in Radiology at U of U Health and contributing author on the study.“We believe music will tap into the salience network of the brain that is still relatively functioning.”

Previous work demonstrated the effect of a personalized music program on mood for dementia patients. This study set out to examine a mechanism that activates the attentional network in the salience region of the brain. The results offer a new way to approach anxiety, depression and agitation in patients with dementia. Activation of neighboring regions of the brain may also offer opportunities to delay the continued decline caused by the disease.

For three weeks, the researchers helped participants select meaningful songs and trained the patient and caregiver on how to use a portable media player loaded with the self-selected collection of music.

“When you put headphones on dementia patients and play familiar music, they come alive,” said Jace King, a graduate student in the Brain Network Lab and first author on the paper. “Music is like an anchor, grounding the patient back in reality.”

Using a functional MRI, the researchers scanned the patients to image the regions of the brain that lit up when they listened to 20-second clips of music versus silence. The researchers played eight clips of music from the patient’s music collection, eight clips of the same music played in reverse and eight blocks of silence. The researchers compared the images from each scan.

The researchers found that music activates the brain, causing whole regions to communicate. By listening to the personal soundtrack, the visual network, the salience network, the executive network and the cerebellar and corticocerebellar network pairs all showed significantly higher functional connectivity.

“This is objective evidence from brain imaging that shows personally meaningful music is an alternative route for communicating with patients who have Alzheimer’s disease,” said Norman Foster, MD, Director of the Center for Alzheimer’s Care at U of U Health and senior author on the paper. “Language and visual memory pathways are damaged early as the disease progresses, but personalized music programs can activate the brain, especially for patients who are losing contact with their environment.”

However, these results are by no means conclusive. The researchers note the small sample size (17 participants) for this study. In addition, the study only included a single imaging session for each patient. It is remains unclear whether the effects identified in this study persist beyond a brief period of stimulation or whether other areas of memory or mood are enhanced by changes in neural activation and connectivity for the long term.

An international team of researchers led by a Case Western Reserve University School of Medicine scientist has uncovered a novel mechanism in which a protein—neuregulin 3—controls how key neurotransmitters are released in the brain during schizophrenia. The protein is elevated in people with schizophrenia and other severe mental illnesses, but the study is the first to investigate how it causes such severe mental illness.

In a study published in the Proceedings of the National Academy of Sciences, neuroscientists from around the globe used genetic, electrophysiological, biochemical, and molecular techniques to uncover the function of neuregulin 3. They discovered it suppresses a protein complex required for proper neuron communication. The research team included 15 neuroscientists from across Case Western Reserve University School of Medicine, Louis Stokes Cleveland Veterans Affairs Medical Center, Augusta University of Georgia, plus Nanchang University and Guangzhou Medical University of China.

Certain variations in the gene encoding neuregulin 3 are considered risk factors for schizophrenia. The new study helps explain why neuregulin 3 is central to the disease. “We have identified a novel function of a schizophrenia susceptibility gene, neuregulin 3, which provides insight into cellular mechanisms of this devastating disorder and could lead to new therapeutic targets,” said senior author Lin Mei, PhD. Mei is professor and chair of the department of neurosciences at Case Western Reserve University School of Medicine. By understanding how neuregulin 3 acts in the brain, researchers could conceivably design drugs to restore its function during schizophrenia.

Schizophrenia affects nearly 1 in 100 American adults and is poorly understood, says Mei. It is difficult to tease apart the many interrelated proteins and neurotransmitters behind the disease. Mei’s study outlines a previously unknown mechanism found in neurons affected by schizophrenia.

In the new study, researchers mutated the gene encoding neuregulin 3 in mice—but only in certain populations of neurons. When they mutated neuregulin 3 in neurons that help activate the brain—called pyramidal neurons—the genetically modified mice displayed behavior consistent with schizophrenia. They had healthy hearing and reflexes, but were unusually active. They had trouble remembering and navigating mazes. In social interactions, the mice shied away from strangers. The experiments not only supported a role for neuregulin 3 in schizophrenia, but also helped define types of neurons involved. By studying brain samples from the mice, the researchers learned how neuregulin 3 works at the cellular level. They found it inhibits assembly of a complex of proteins at synapses, the place where adjacent nerve cells communicate. Neurons need the complex, called SNARE, to transmit certain neurotransmitters between each other. In particular, SNARE complex helps neurons transmit glutamate—the most common “excitatory” neurotransmitter in the brain. Glutamate helps activate neurons and is essential for learning. Glutamate imbalances can cause schizophrenic symptoms.

People with severe mental illnesses like schizophrenia, bipolar disorder, and major depression, tend to have higher levels of neuregulin 3. The researchers mimicked protein levels found in the brains of schizophrenics by elevating neuregulin 3 in cultured neurons, and found higher levels of neuregulin 3 suppresses glutamate release. Cells with high levels of neuregulin 3 couldn’t form SNARE complexes properly. Too much of the inhibitory protein prevented the complex from forming, and suppressed glutamate levels in the brain cells. The researchers concluded that neuregulin 3 is critical to proper glutamate transmission in the brain.

According to Mei, the findings are particularly intriguing because they show neuregulin 3 works differently than other proteins in its family. Neuregulin 1, for example, activates an entirely different set of proteins in other types of neurons. The mechanism Mei’s team discovered for neuregulin 3 is even distinct from other roles previously described for the protein.

Said Mei, “In cancer biology, neuregulin 3 stimulates another risk gene of schizophrenia called ErbB4. Yet, unexpectedly, we found that neuregulin 3 in the brain may not act by activating ErbB4. Rather, it regulates glutamate release, and this novel function does not require ErbB4.”

(Figure 1 from paper: Social network. The social network of an entire cohort of first-year graduate students was reconstructed based on a survey completed by all students in the cohort (N = 279; 100% response rate). Nodes indicate students; lines indicate mutually reported social ties between them. A subset of students (orange circles; N = 42) participated in the fMRI study. Image by Carolyn Parkinson)

Your Brain Reveals Who Your Friends Are

You may perceive the world the way your friends do, according to a Dartmouth study finding that friends have similar neural responses to real-world stimuli and these similarities can be used to predict who your friends are.

The researchers found that you can predict who people are friends with just by looking at how their brains respond to video clips. Friends had the most similar neural activity patterns, followed by friends-of-friends who, in turn, had more similar neural activity than people three degrees removed (friends-of-friends-of-friends).

Published in Nature Communications, the study is the first of its kind to examine the connections between the neural activity of people within a real-world social network, as they responded to real-world stimuli, which in this case was watching the same set of videos.

“Neural responses to dynamic, naturalistic stimuli, like videos, can give us a window into people’s unconstrained, spontaneous thought processes as they unfold. Our results suggest that friends process the world around them in exceptionally similar ways,” says lead author Carolyn Parkinson, who was a postdoctoral fellow in psychological and brain sciences at Dartmouth at the time of the study and is currently an assistant professor of psychology and director of the Computational Social Neuroscience Lab at the University of California, Los Angeles.

The study analyzed the friendships or social ties within a cohort of nearly 280 graduate students. The researchers estimated the social distance between pairs of individuals based on mutually reported social ties. Forty-two of the students were asked to watch a range of videos while their neural activity was recorded in a functional magnetic resonance imaging (fMRI) scanner. The videos spanned a range of topics and genres, including politics, science, comedy and music videos, for which a range of responses was expected. Each participant watched the same videos in the same order, with the same instructions. The researchers then compared the neural responses pairwise across the set of students to determine if pairs of students who were friends had more similar brain activity than pairs further removed from each other in their social network.

The findings revealed that neural response similarity was strongest among friends, and this pattern appeared to manifest across brain regions involved in emotional responding, directing one’s attention and high-level reasoning. Even when the researchers controlled for variables, including left-handed- or right-handedness, age, gender, ethnicity, and nationality, the similarity in neural activity among friends was still evident. The team also found that fMRI response similarities could be used to predict not only if a pair were friends but also the social distance between the two.

“We are a social species and live our lives connected to everybody else. If we want to understand how the human brain works, then we need to understand how brains work in combination— how minds shape each other,” explains senior author Thalia Wheatley, an associate professor of psychological and brain sciences at Dartmouth, and principal investigator of the Dartmouth Social Systems Laboratory.

For the study, the researchers were building on their earlier work, which found that as soon as you see someone you know, your brain immediately tells you how important or influential they are and the position they hold in your social network.

Broadway’s Original Mansplainer

Hilton Als looks at class, colonialism, and self-creation in “My Fair Lady.”

In George Bernard Shaw’s play, there were too many entrances and exits, musings and changes of mind. In the film, and thus in the musical, the lines between men and women, privilege and class degradation, humor and drama are more clearly drawn. Part of the pleasure of watching this staging—and it is a pleasure, if not entirely satisfying, but then what is?—is observing not how Eliza becomes more herself as the show goes on but how she learns to express that self, strong, indomitable, softened by dreams and wishes, in the language of the class that helps her cross over.

Colonialism works in many ways. We don’t know how long Eliza has been a Covent Garden flower seller when we meet her, but those filthy cobblestones and the close, damp air have become part of her being. She’s on her own, though she has a father, Alfred P. Doolittle, a loafer and a drinker who hits her up for cash when he runs into her. Eliza doesn’t have class aspirations—at first—but she does have comfort aspirations, which are tied to her desire to do better for herself.

Treaty of Fort Laramie, 4/29/1868

Treaty with the Sioux-Brule, Oglala, Miniconjou, Yanktonai, Hunkpapa, Blackfeet, Cuthead, Two Kettle, San Arcs, and Santee-and Arapaho, 4/29/1868 Series: Indian Treaties, 1722 - 1869. Record Group 11: General Records of the United States Government, 1778 - 2006

In this treaty, signed 150 years ago on April 29, 1868, between the U.S. Government and the Sioux Nation at Fort Laramie, Dakota Territory (now Wyoming), the United States recognized the Black Hills as part of the Great Sioux Reservation, set aside for exclusive use by the Sioux people. However the discovery of gold in the Black Hills and further encroachment by white settlers led to increased tensions and renewed hostilities.  The United States would continue its battle against the Sioux in the Black Hills until the government confiscated the land in 1877. To this day, ownership of the Black Hills remains the subject of a legal dispute between the U.S. Government and the Sioux.

See all pages of the treaty in the @usnatarchives online catalog.