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Ribonucleic acid (RNA) is a molecule which is present in cells and made of genetic material to help build proteins necessary for cell function. RNA provides a template for the construction of proteins and is essential for cell and organism life. Immune cells rely on these proteins, including CD8⁺ or cytotoxic T cells which are responsible for killing invading pathogens. Importantly, cytotoxic T cells are a major component of the memory immune response. A pool of T cells specifically designed to recognize an invader is stored for future invasion of that particular pathogen. For example, once these cells are exposed to an invading antigen or protein, the immune system will expand T cells specific to that antigen and remember the antigen next time it enters the body. Vaccines work in a similar way by introducing a foreign antigen to the body, so the immune system is ready if the pathogen ever enters your body in the future. Only a small set of T cells that expand survive and it is unclear how this process occurs.

Recently a team of researchers at the University of Massachusetts Amherst (UMass) demonstrated that a single strand of RNA governs a T cells ability to recognize and kill tumors. The single strand of RNA is known as let-7 and is a microRNA, which is responsible for gene expression regulation. The recent discovery may improve vaccine development and cellular memory to enhance immunotherapy against cancers. Immunotherapy is a general term referring to cancer therapies that try to activate the immune system to kill the tumor compared to other drugs that try to directly kill the tumor with chemicals, such as chemotherapy.

The report published in Nature Communications identified that the microRNA, let-7, may enhance memory of T cells. Researchers led by Dr. Leonid Pobezinsky, Associate Professor of Veterinary and Animal Sciences at UMass, further built on our understanding of how T cells form immune memory. Pobezinsky and colleagues found that a small piece of microRNA that has been present throughout evolution is expressed in memory cells. Additionally, they found that more let-7 a cell has, the more likely that cell will recognize a cancer cell and kill it. The increased let-7 also indicates that the cell will turn into a memory cell after being exposed to an antigen. The regulation of enhanced memory T cells by let-7 is an integral process key to fight infections. This is a critical finding, especially because memory cells retain stem-like characteristics and can survive for decades.

Summary: Scientists made a novel discovery using zebrafish with a genetic mutation. These ‘deep-blind’ fish lack connections between the retina and brain yet retain functional brain circuits.

Remarkably, despite their inability to see, direct brain stimulation through optogenetics triggers normal visual behavior. This suggests that much of the zebrafish brain’s wiring is innate and doesn’t rely heavily on visual experience.

Hospital nurseries routinely place soft bands around the tiny wrists of newborns that hold important identifying information such as name, sex, mother, and birth date. Researchers at Rockefeller University are taking the same approach with newborn brain cells—but these neonates will keep their ID tags for life, so that scientists can track how they grow and mature, as a means for better understanding the brain’s aging process.

As described in a new paper in Cell, the new method developed by Rockefeller geneticist Junyue Cao and his colleagues is called TrackerSci (pronounced “sky”). This low-cost, high-throughput approach has already revealed that while newborn cells continue to be produced through life, the kinds of cells being produced greatly vary in different ages. This groundbreaking work, led by co-first authors Ziyu Lu and Melissa Zhang from Cao’s lab, promises to influence not only the study of the brain but also broader aspects of aging and disease across the human body.

“The cell is the basic functional unit of our body, so changes to the cell essentially underlie virtually every disease and the aging process,” says Cao, head of the Laboratory of Single-Cell Genomics and Population Dynamics. “If we can systematically characterize the different cells and their dynamics using this novel technique, we may get a panoramic view of the mechanisms of many diseases and the enigma of aging.”

Early-life stress (ELS) is one of the strongest lifetime risk factors for depression, anxiety, suicide, and other psychiatric disorders, particularly after facing additional stressful events later in life. Human and animal studies demonstrate that ELS sensitizes individuals to subsequent stress. However, the neurobiological basis of such stress sensitization remains largely unexplored. We hypothesized that ELS-induced stress sensitization would be detectable at the level of neuronal ensembles, such that cells activated by ELS would be more reactive to adult stress. To test this, we leveraged transgenic mice to genetically tag, track, and manipulate experience-activated neurons. We found that in both male and female mice, ELS-activated neurons within the nucleus accumbens (NAc), and to a lesser extent the medial prefrontal cortex, were preferentially reactivated by adult stress. To test whether reactivation of ELS-activated ensembles in the NAc contributes to stress hypersensitivity, we expressed hM4Dis receptor in control or ELS-activated neurons of pups and chemogenetically inhibited their activity during experience of adult stress. Inhibition of ELS-activated NAc neurons, but not control-tagged neurons, ameliorated social avoidance behavior following chronic social defeat stress in males. These data provide evidence that ELS-induced stress hypersensitivity is encoded at the level of corticolimbic neuronal ensembles.

SIGNIFICANCE STATEMENT Early-life stress enhances sensitivity to stress later in life, yet the mechanisms of such stress sensitization are largely unknown. Here, we show that neuronal ensembles in corticolimbic brain regions remain hypersensitive to stress across the life span, and quieting these ensembles during experience of adult stress rescues stress hypersensitivity.

Once we fully we understand intelligence it could be essentially increased to nearly infinite levels once everything is quantified like this article talks about 😗😁.

Modern humans have a gene mutation that boosts the growth of neurons in the brain neocortex, a brain region associated with higher intelligence.

By Michael Le Page

Continue reading “A single gene mutation may have made us smarter than Neanderthals” »

Mothers who eat apples and herbs in early pregnancy could be protecting the brain health of their children and grandchildren, a Monash University study using genetic models has found.

The discovery is part of a project that found a mother’s diet can affect not just her child’s brain but also those of her grandchildren.

Published in Nature CellBiology, the Monash Biomedicine Discovery Institute study found that certain foods could help protect against the deterioration of brain function.

Continue reading “A mother’s diet can protect her grandchildren’s brains: genetic model study” »

A protein involved in wound healing can improve learning and memory in ageing mice1.

Platelet factor 4 (PF4) has long been known for its role in promoting blood clotting and sealing broken blood vessels. Now, researchers are wondering whether this signalling molecule could be used to treat age-related cognitive disorders such as Alzheimer’s disease.

“The therapeutic possibilities are very exciting,” says geneticist and anti-ageing scientist David Sinclair at Harvard University in Boston, Massachusetts, who was not involved in the research. The study was published on 16 August in Nature.

Continue reading “Older mouse brains rejuvenated by protein found in young blood” »

This is a significant development that brings hope to the one billion individuals with obesity worldwide. Researchers led by Director C. Justin LEE from the Center for Cognition and Sociality (CCS) within the Institute for Basic Science (IBS) have discovered new insights into the regulation of fat metabolism. The focus of their study lies within the star-shaped non-neuronal cells in the brain, known as ‘astrocytes’. Furthermore, the group announced successful animal experiments using the newly developed drug ‘KDS2010’, which allowed the mice to successfully achieve weight loss without resorting to dietary restrictions.

The complex balance between food intake and energy expenditure is overseen by the hypothalamus in the brain. While it has been known that the neurons in the lateral hypothalamus are connected to fat tissue and are involved in fat metabolism, their exact role in fat metabolism regulation has remained a mystery. The researchers discovered a cluster of neurons in the hypothalamus that specifically express the receptor for the inhibitory neurotransmitter ‘GABA (Gamma-Aminobutyric Acid)’. This cluster has been found to be associated with the α5 subunit of the GABAA receptor and was hence named the GABRA5 cluster.

In a diet-induced obese mouse model, the researchers observed significant slowing in the pacemaker firing of the GABRA5 neurons. Researchers continued with the study by attempting to inhibit the activity of these GABRA5 neurons using chemogenetic methods. This in turn caused a reduction in heat production (energy consumption) in the brown fat tissue, leading to fat accumulation and weight gain. On the other hand, when the GABRA5 neurons in the hypothalamus were activated, the mice were able to achieve a successful weight reduction. This suggests that the GABRA5 neurons may act as a switch for weight regulation.

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Continue reading “Fish Oil Supplementation: No Impact On NAD” »