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Seemingly countless self-help books and seminars tell you to tap into the right side of your brain to stimulate creativity. But forget the “right-brain” myth—a new study suggests it’s how well the two brain hemispheres communicate that sets highly creative people apart.

For the study, statisticians David Dunson of Duke University and Daniele Durante of the University of Padova analyzed the network of white matter connections among 68 separate brain regions in healthy college-age volunteers.

The brain’s white matter lies underneath the outer grey matter. It is composed of bundles of wires, or axons, which connect billions of neurons and carry electrical signals between them.

😗😁 Year 2022


Quantum processes are helpful to know about when we hear a gimcrack new theory that dismisses or explains away human consciousness. We know it can’t just be that simple.

You may also wish to read: Researchers: The brain’s claustrum acts as a router for thoughts Francis Crick thought the claustrum might be the “seat of consciousness,” an inherently materialist concept. The researchers think he was wrong. Of course, seeing the claustrum as a router is more consistent with the immaterial nature of consciousness than seeing it as a seat.

Glioblastoma is a fast-growing and aggressive brain tumor. As one of the most common malignant brain tumors, life expectancy after diagnosis is between 14 and 16 months. Roughly 1% of patients survive more than ten years with the longest patients living over 20 years. Symptoms include headaches, double vision, vomiting, loss of appetite, changes in mood and personality, inability to accurately think and learn, seizures, and difficulty speaking. Unfortunately, there is no cure, and treatment options include radiation and chemotherapy with limited efficacy. Glioblastoma is difficult to treat due to its location in the brain, its resistance to common treatment, the brains limited ability to heal itself, disrupted blood supply, blood vessel leakage, seizures, and neurotoxicity from treatments. Due to limited treatment and the life expectancy of this devastating disease, researchers at the SALK Institute in La Jolla, California have set out to find better ways to treat glioblastoma and prolong survival in patients.

Immune checkpoint inhibitors (ICIs) are a form of immunotherapy that block receptors on immune cells which activate them to kill tumor cells. The ICI using by the SALK group is known as anti-CTLA-4, which binds to the CTLA-4 protein on the T immune cells responsible for killing infected cells. This therapy was generated by Dr. James Allison at the MD Anderson Comprehensive Cancer Center in Houston, Texas. For his work, he was awarded the Nobel Prize in Physiology or Medicine in 2018. While this therapy proved effective in other cancers such as melanoma, it was unclear its effect in glioblastoma. The researchers at SALK recently published their findings on the effect of anti-CTLA-4 on glioblastoma.

The study published in Immunity by Dr. Susan Kaech and colleagues at SALK demonstrated prolonged survival of mice with glioblastoma after treatment with anti-CTLA-4. They also discovered that the treatment was largely dependent on CD4+ T cells, which aid in activating other cells, and not CD8+ T cells, which directly kill the tumor. More specifically, CD4+ T cells were found to infiltrate the brain and trigger other immune cells, like microglia to destroy cancerous cells. In Kaech’s work, the lab significantly shrunk the glioblastoma in mice and in some cases completely eradicated it.

Can you recognize someone you haven’t seen in years, but forget what you had for breakfast yesterday? Our brains constantly rearrange their circuitry to remember familiar faces or learn new skills, but the molecular basis of this process isn’t well understood. Today, scientists report that sulfate groups on complex sugar molecules called glycosaminoglycans (GAGs) affect “plasticity” in the brains of mice. Determining how GAGs function could help us understand how memory and learning work in humans, and provide ways to repair neural connectivity after injuries.

The researchers will present their results today at the fall meeting of the American Chemical Society (ACS).

The sugars that sweeten fruits, candies or cakes are actually just a few simple varieties of the many types of sugars that exist. When strung together, they can make a wide array of complex sugars. GAGs are formed by then attaching other chemical structures, including sulfate groups.

Exactly how, and how much, the unconscious processing of information influences our behavior has always been one of the most controversial questions in psychology. In the early 20th century, Sigmund Freud popularized the idea that our behaviors are driven by thoughts, feelings, and memories hidden deep within the unconscious mind — an idea that became hugely popular, but that was eventually dismissed as unscientific.

Modern neuroscience tells us that we are completely unaware of most brain activity, but that unconscious processing does indeed influence behavior; nevertheless, certain effects, such as unconscious semantic “priming,” have been called into question, leading some to conclude that the extent of unconscious processing is limited.

A recent brain scanning study now shows that unconsciously processed visual information is distributed to a wider network of brain regions involved in higher-order cognitive tasks. The results contribute to the debate over the extent to which unconscious information processing influence the brain and behavior and led the authors of the study to revise one of the leading theories of consciousness.

A study that peered into live mouse brains suggests for nearly 70 years we’ve been targeting the wrong neurons in our design of antipsychotic drugs.

Untangling the vast web of brain cells and determining how drugs work upon them is a tough task. Using a miniature microscope and fluorescent tags, a team of researchers led by Northwestern University neuroscientist Seongsik Yun discovered that effective antipsychotic drugs cling to a different type of brain cell than scientists originally thought.

Just like research suggesting depression might not be a chemical imbalance in serotonin levels, our understanding of schizophrenia treatments may need a rethink if widely-used antipsychotics are targeting different neurons than expected.

Psychedelics are known for inducing altered states of consciousness in humans by fundamentally changing our normal pattern of sensory perception, thought and emotion. Research into the therapeutic potential of psychedelics has increased significantly in the last decade.

While this research is important, I have always been more intrigued by the idea that psychedelics can be used as a tool to study the neural basis of human consciousness in laboratory animals. We ultimately share the same basic neural hardware with other mammals, and possibly some basic aspects of consciousness, too. So by examining what happens in the brain when there’s a psychedelically induced change in conscious experience, we can perhaps glean insights into what consciousness is in the first place.

We still don’t know a lot about how the networks of cells in the brain enable conscious experience. The dominating view is that consciousness somehow emerges as a collective phenomenon when the dispersed information processing of individual neurons (brain cells) is integrated as the cells interact.

A team of scientists took a bunch of macaque monkeys, made them into alcoholics, and then successfully weaned them off the sauce after injecting their brains with a special gene — an experiment, detailed in a new paper published in Nature Medicine, that could potentially provide a compelling new treatment for addiction.

“Drinking went down to almost zero,” Oregon Health and Science University professor and co-author Kathleen Grant told The Guardian. “For months on end, these animals would choose to drink water and just avoid drinking alcohol altogether.”

The researchers set out with the premise that continued alcohol use causes changes to neurons and hampers the dopamine “reward circuitry” in the brain.