Lifeboat Foundation: Safeguarding Humanity
Toggle light / dark theme

Blog

Category: neuroscience – Page 222

Acetamiprid-induced oxidative stress can harm DNA and tRNA, leading to health problems. A study conducted by Huixia Zhang at Macau University of Science and Technology in 2023 introduced a comprehensive approach to assessing acetamiprid-induced oxidative damage to tRNA in human cells through oxidized nucleotide and tRNA profiling. Acetamiprid, a modern insecticide, is known for causing oxidative stress and related toxicity. Despite its impact on oxidative stress, the effects of acetamiprid-induced oxidative stress on RNA, especially tRNA, remained unexplored until this study.

Acetamiprid was found to elevate reactive oxygen species (ROS) production in HepG2 and LO2 cells, contributing to mitochondrial damage, free radical generation, and antioxidant status depletion. Oxidative damage to DNA and RNA can harm organisms, with prior research addressing RNA damage in aging, neurodegenerative diseases, and mental illnesses. However, its role in acetamiprid-induced toxicities has not been investigated.

The study employed TMSD labeling-based LC-MS/MS to measure oxidized nucleotide levels in HepG2 and LO2 cells treated with two mM acetamiprid. It also examined the impact of acetamiprid on the 8-oxo-G content of tRNAs and created volcano plots to compare RNase T1 digestion products of tRNAs from untreated and acetamiprid-treated cells.

Read more | >

A team of scientists at the University of Wisconsin-Madison claim to have 3D-printed functional human brain tissue for the first time.

They hope their research could open the doors for the development of treatments for existing neurological disorders, including Alzheimer’s and Parkinson’s disease.

As detailed in a new paper published in the journal Cell Stem Cell, the team flipped the usual method of 3D-printing on its side, fabricating horizontal layers of brain cells encased in soft “bio-ink” gel.

Read more | >

Drugs known as antidepressants target the serotonin transporter in nerve cells and are among the most commonly prescribed medicines worldwide, but are sometimes associated with significant side effects. As part of a study, a research group led by Thomas Stockner from MedUni Vienna identified the basic principles of serotonin transport and thus created a possible basis for the development of novel drugs with improved selectivity and with fewer undesirable effects. The results were recently published in the renowned scientific journal “Nature Communications”

While the desired effects of drugs unfold through the interaction with the relevant target structures, the undesirable side effects are often due to a lack of selectivity and therefore due to interactions with other target structures. Accordingly, developing drugs that can differentiate between the various physiologically relevant targets (e.g. transporters and receptors) is one of the challenges for research. A team led by Ralph Gradisch under the supervision of Thomas Stockner from MedUni Vienna’s Center for Physiology and Pharmacology set out to find a way to increase selectivity for the serotonin transporter while reducing interaction with other targets at nerve cells in the brain.

Read more | >

Multiple sclerosis (MS) is a neurological disease that usually leads to permanent disabilities. It affects about 2.9 million people worldwide, and about 15,000 in Switzerland alone. One key feature of the disease is that it causes the patient’s own immune system to attack and destroy the myelin sheaths in the central nervous system.

These protective sheaths insulate the nerve fibers, much like the plastic coating around a copper wire. Myelin sheaths ensure that electrical impulses travel quickly and efficiently from nerve cell to nerve cell. If they are damaged or become thinner, this can lead to irreversible visual, speech and coordination disorders.

So far, however, it hasn’t been possible to visualize the myelin sheaths well enough to reliably diagnose and treat MS. Now researchers at ETH Zurich, led by Markus Weiger and Emily Baadsvik from the Institute for Biomedical Engineering, have developed a new magnetic resonance imaging (MRI) procedure that maps the condition of the myelin sheaths more accurately than was previously possible. The researchers successfully tested the procedure on healthy people for the first time.

Read more | >

Ball is not alone in calling for a drastic rethink of how scientists discuss biology. There has been a flurry of publications in this vein in the past year, written by me and others2–4. All outline reasons to redefine what genes do. All highlight the physiological processes by which organisms control their genomes. And all argue that agency and purpose are definitive characteristics of life that have been overlooked in conventional, gene-centric views of biology.

This burst of activity represents a frustrated thought that “it is time to become impatient with the old view”, as Ball says. Genetics alone cannot help us to understand and treat many of the diseases that cause the biggest health-care burdens, such as schizophrenia, cardiovascular diseases and cancer. These conditions are physiological at their core, the author points out — despite having genetic components, they are nonetheless caused by cellular processes going awry. Those holistic processes are what we must understand, if we are to find cures.

Ultimately, Ball concludes that “we are at the beginning of a profound rethinking of how life works”. In my view, beginning is the key word here. Scientists must take care not to substitute an old set of dogmas with a new one. It’s time to stop pretending that, give or take a few bits and pieces, we know how life works. Instead, we must let our ideas evolve as more discoveries are made in the coming decades. Sitting in uncertainty, while working to make those discoveries, will be biology’s great task for the twenty-first century.

Read more | >