Lifeboat Foundation

Genetic links hint at early migration from North America.

Chronic stress has long been associated with the pathogenesis of psychological disorders such as depression and anxiety. Recent studies have found chronic stress can cause neuroinflammation: activation of the resident immune cells in the brain, microglia, to produce inflammatory cytokines. Numerous studies have implicated the inflammatory cytokine, interleukin-1 (IL-1), a master regulator of immune cell recruitment and activity in the brain, as the key mediator of psychopathology. However, how IL-1 disrupts neural circuits to cause behavioral and emotional problems seen in psychological disorders has not been determined.

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The research team previously detailed how psychosocial stress results in peripheral immune activation, increased levels of circulating monocytes, and robust neuroimmunological responses in the brain. These responses include increases in IL-1 and other inflammatory cytokines, activation of brain glial cells and movements of peripheral immune cells to the brain, along with enhanced activity of specific neuronal pathways. The work makes it clear that inflammatory-related effects of stress are not just global effects, but are associated with increased IL-1 signaling within specific brain circuits.

The study shows for the first time that neuronal IL-1Rs in the hippocampus, a brain structure connected to learning and memory, is necessary and sufficient to mediate some of the behavioral deficits caused by chronic stress, pointing to a critical neuroimmune mechanism for the etiology of these types of disorders. Findings from the study augment the understanding of IL-1R signaling in physiological and behavioral responses to stress and also suggest that it may be possible to develop better medications to treat the consequences of chronic stress by limiting inflammatory signaling not just generally, which may not be beneficial in the long run, but to specific brain circuits.

Continue reading “Chronic stress? Limiting inflammatory signaling to specific brain circuits” »

The discovery of the Dead Sea Scrolls had an incomparable impact on the historical understanding of Judaism and Christianity. ‘Piecing together’ scroll fragments is like solving jigsaw puzzles with an unknown number of missing parts. Because most of the 2,000-year-old scrolls were written on processed animal skin, an international team of researchers used DNA sequencing to ‘fingerprint’ fragments based on their genetic signature.

An underlying assumption of research on aging holds that dietary restriction (and drugs that mimic its effects) will slow aging to extend both lifespan and healthspan jointly. While eating a Spartan diet has been shown to robustly extend lifespan and delay age-related diseases in many species, a genome-wide analysis of 160 genetically distinct strains of the fruit fly D. melanogaster shows that lifespan and healthspan are not linked under dietary restriction. Results are published in Current Biology.

Though on average lifespan was extended and healthspan was increased, researchers from the Kapahi lab at the Buck Institute say the devil is in the details. In the study researchers measured nutrient-dependent changes in lifespan and tracked age-related changes in physical activity to measure healthspan. While 97 percent of strains showed some lifespan or healthspan extension in response to dietary restriction, only 50 percent of strains showed a significantly positive response to dietary restriction for both. Thirteen percent of the strains were more vigorous, yet died sooner with dietary restriction; 5 percent lived longer, but spent more time in poor health. The remaining 32 percent of the strains showed no benefits or detriments to lifespan or healthspan, or negative responses to both.

“Dietary restriction works, but may not be the panacea for those wanting to extend healthspan, delay age-related diseases, and extend lifespan,” said Pankaj Kapahi, Ph.D., Buck professor and senior author on the paper. “Our study is surprising and gives a glimpse into what’s likely going to happen in humans, because we’re all different and will likely respond differently to the effects of dietary restriction. Furthermore, our results question the idea that lifespan extension will always be accompanied by improvement of healthspan.”

A team of scientists from Stanford University is working with researchers at the Molecular Foundry, a nanoscience user facility located at the Department of Energy’s Lawrence Berkeley National Laboratory (Berkeley Lab), to develop a gene-targeting, antiviral agent against COVID-19.

Last year, Stanley Qi, an assistant professor in the departments of bioengineering, and chemical and systems biology at Stanford University and his team had begun working on a technique called PAC-MAN—or Prophylactic Antiviral CRISPR in human cells —that uses the gene-editing tool CRISPR to fight influenza.

But that all changed in January, when news of the COVID-19 pandemic emerged. Qi and his team were suddenly confronted with a mysterious new virus for which no one had a clear solution. “So we thought, ‘Why don’t we try using our PAC-MAN technology to fight it?’” said Qi.

The cells fully integrated the genes that let squids turn translucent.

Microscopy and genetic studies yield a comprehensive map of the nerve cells found in the heart of a rat.

Understanding the prebiotic origins of the nucleic acids is a long-standing challenge. The latest experiments support the idea that the first nucleic acid encoded information using a mixed ‘alphabet’ of RNA and DNA subunits. RNA and DNA nucleosides might have emerged together on prebiotic Earth.

Once considered an unimportant curiosity, Z-DNA is now recognized to provide an on-the-fly mechanism to regulate how an RNA transcript is edited.

The Infant Gut Microbiome and Probiotics that Work.