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There was a crooked man: Scoliosis and the deep history of the brain’s inner sanctum

Lurking just beneath the surface of just about every common nursery rhyme is a complex record of times long gone. For example, the “crooked man” who “laid a crooked sixpence upon a crooked style” was none other than the great 17th-century Scot General Sir Alexander Leslie. The crooked stile was the uneasy border between Scotland and England established by the controversial covenant he signed. Quite similarly, many enigmatic structures that permanently persist or otherwise transiently appear and resorb in the development of the nervous systems of many creatures also encode a rich evolutionary past.

One such functioning relic is Reissner’s fiber, a glycoprotein sheet secreted by the subcommissural organ (SCO) that inexorably treadmills down the central canal of the spinal cord. Although the SCO was one of the first structures of the mammalian brain to differentiate, in humans, it begins regressing around age three or four and typically becomes vestigial by adulthood. The main component of Reissner’s fiber is a giant 5000-amino-acid vertebrate molecule called SCO-spondin. This protein contains axonal pathfinding domains critical to development of the posterior commissure, a transhemispheric highway that bears axons controlling the pupillary light reflex.

The other product of the SCO is a thyroid-hormone-transporting protein called transthyretin. Much like all the organified metals fixed by life, iodine has a unique story to tell in the evolution of the body plan. Recently, an intriguing connection between Reissner’s fiber and development of the spine that houses it has been discovered in the model organism, zebrafish. These fish, as recently observed for the serotonergic control of neurogenesis, have proven to be an exemplary model for studying all things neural. In the latest issue of Current Biology, author Nathalie Jurisch-Yaksi reviews a remarkable confluence of ideas that establish an indisputable role for Reissner’s membrane building a straight and strong spine.

Researchers uncover effects of negative stereotype exposure on the brain

The recent killings of unarmed individuals such as George Floyd, Breonna Taylor, Ahmaud Arbery and Tony McDade have sparked a national conversation about the treatment of Black people—and other minorities—in the United States.

“What we’re seeing today is a close examination of the hardships and indignities that people have faced for a very long time because of their race and ethnicity,” said Kyle Ratner, an assistant professor of psychological and at UC Santa Barbara. As a , he is interested in how social and give rise to intergroup bias and feelings of stigmatization.

According to Ratner, “It is clear that people who belong to historically marginalized groups in the United States contend with burdensome stressors on top of the everyday stressors that members of non-disadvantaged groups experience. For instance, there is the trauma of overt racism, stigmatizing portrayals in the media and popular culture, and systemic discrimination that leads to disadvantages in many domains of life, from employment and education to healthcare and housing to the legal system.”

How a protein’s small change leads to big trouble for cells

In molecular biology, chaperones are a class of proteins that help regulate how other proteins fold. Folding is an important step in the manufacturing process for proteins. When they don’t fold the way they’re supposed to, it can lead to the development of diseases such as cancer.

Researchers at the Sloan Kettering Institute have uncovered important findings about what causes chaperones to malfunction as well as a way to fix them when they go awry. The discovery points the way to a new approach for developing targeted drugs for cancer and other diseases, including Alzheimer’s disease.

“Our earlier work showed that defects in chaperones could lead to widespread changes in cells, but no one knew exactly how it happened,” says SKI scientist Gabriela Chiosis, senior author of a study published June 30 in Cell Reports. “This paper finally gets into the nuts and bolts of that biochemical mechanism. I think it’s a pretty big leap forward.”

Yale captures first ever video of brain clearing out dead neurons

In the average human body, tens of billions of cells die everyday. It’s a natural process, important for keeping the body healthy. Now, for the first time, researchers at Yale School of Medicine have directly imaged the death of neurons in mice, as well as how the body clears them out afterwards.

Although it might seem like brain cells are things you’d definitely want to keep around, it’s better to get rid of the ones that aren’t working. After all, a build-up of dead cells can damage the nervous system and has been implicated in neurodegenerative diseases.

To prevent this, the brain – and indeed the rest of the body – has a natural process that clears out dead cells. But scientists haven’t been sure about the exact mechanisms at work during this cellular “corpse removal” process.

Circular RNA found to make fruit flies live longer

Ribonucleic acid, or RNA, is part of our genetic code and present in every cell of our body. The best known form of RNA is a single linear strand, of which the function is well known and characterized. But there is also another type of RNA, so-called “circular RNA,” or circRNA, which forms a continuous loop that makes it more stable and less vulnerable to degradation. CircRNAs accumulate in the brain with age. Still, the biological functions of most circRNAs are not known and are a riddle for the scientific community. Now scientists from the Max Planck Institute for Biology of Aging have come one step closer to answer the question what these mysterious circRNAs do: one of them contributes to the aging process in fruit flies.

Carina Weigelt and other researchers in the group led by Linda Partridge, Director at the Max Planck Institute for Biology of Aging, used to investigate the role of the circRNAs in the aging process. “This is unique, because it is not very well understood what circRNAs do, especially not in an aging perspective. Nobody has looked at circRNAs in a longevity context before,” says Carina Weigelt who conducted the main part of the study. She continues: “Now we have identified a circRNA that can extend lifespan of fruit flies when we increase it, and it is regulated by signaling.”

The power struggle that resides within our brain

Our brain is divided. We just don’t know it. Or we do, but not in the way one thinks. To put it simply – a power struggle has been going on between the left side of our brain, or the analytical side, and the right side, the emotional side. It’s been going on for quite some time.

There have always been rumblings of the imbalance between the two for years, certainly covered off in a critical work of near genius by renowned psychiatrist and neuroscientist Dr. Iain McGilchrist, (iainmcgilchrist.com), author of the acclaimed The Master and his Emissary: the Divided Brain and the Making of the Western World.

Adult-born neurons grow more than their infancy-born counterparts

Summary: Neurons created as a result of adult neurogenesis mature for longer and grow larger than those created during infancy. Findings suggest adult-born neurons may have a more powerful function than those created during infancy and may play a critical role in neuroplasticity.

Source: SfN

Adult-born neurons keep growing and contributing to brain flexibility long after neurogenesis declines, according to research in rats published in Journal of Neuroscience.