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Summary: Researchers have identified a genetic mechanism that regulates behavioral adaptations to emotional experiences by forming R-loops, unique RNA: DNA structures that activate target genes. The study focused on NPAS4, a gene implicated in stress and drug addiction, showing how blocking R-loops prevents maladaptive behaviors like cocaine seeking and stress-induced anhedonia in mice.
This mechanism demonstrates how emotional experiences influence brain circuits by altering gene expression through enhancer RNA. The findings could pave the way for RNA-based therapies to treat psychiatric disorders linked to stress and substance use.
In this study, the authors present magnetoelectric nanodiscs that enable minimally invasive, remote magnetic neuromodulation with subsecond precision to drive reward and motor behaviours in genetically intact mice.
New research reshapes our understanding of the universal genetic code, revealing surprising insights into early life’s amino acid evolution.
Microorganisms produce a wide variety of natural products that can be used as active ingredients to treat diseases such as infections or cancer. The blueprints for these molecules can be found in the microbes’ genes, but often remain inactive under laboratory conditions.
A team of researchers at the Helmholtz Institute for Pharmaceutical Research Saarland (HIPS) has now developed a genetic method that leverages a natural bacterial mechanism for the transfer of genetic material and uses it for the production of new active ingredients. The team has published its results in the journal Science.
In contrast to humans, bacteria have the remarkable ability to exchange genetic material with one another. A well-known example with far-reaching consequences is the transfer of antibiotic resistance genes between bacterial pathogens. This gene transfer allows them to adapt quickly to different environmental conditions and is a major driver of the spread of antibiotic resistance.
The Tbx1 gene influences brain volume and social behavior in autism and schizophrenia, with its deficiency linked to amygdala shrinkage and impaired social incentive evaluation.
A study published in Molecular Psychiatry has linked changes in brain volume to differences in social behavior associated with psychiatric conditions like autism spectrum disorder and schizophrenia.
The research, led by Noboru Hiroi, Ph.D., a professor in the Department of Pharmacology at the Joe R. and Teresa Lozano Long School of Medicine at The University of Texas Health Science Center at San Antonio (UT Health San Antonio), revealed that a deficiency in a specific gene was connected to social behavior differences in mice. These behavioral differences are similar to those often observed in psychiatric disorders.
Researchers have developed a method using viruses to track neuronal development in frogs, shedding light on the evolution of vertebrate nervous systems and offering comparative insights with mammals.
Although viruses are typically associated with illnesses, not all viruses are harmful or cause disease. Some are instrumental in therapeutic treatments and vaccinations. In scientific research, viruses are often used to infect certain cells, genetically modify them, or visualize neurons in the organism’s central nervous system (CNS)—the command center made up of the brain, spinal cord, and nerves.
The highlighting process has now been successfully applied to amphibians, which are crucial for understanding the brain and spinal cord of tetrapods—four-limbed animals, including humans. This has been shown in a new study by an international EDGE consortium jointly led by the Sweeney Lab at the Institute of Science and Technology Austria (ISTA) and the Tosches Lab at Columbia University.
The study offers new genetic insights into dietary preferences and suggests the potential to target SI as a means to selectively decrease sucrose consumption on a population scale.
The study was led by Dr. Peter Aldiss, now a group leader in the School of Medicine at the University of Nottingham, alongside Assistant Professor Mette K Andersen, at the Novo Nordisk Foundation Centre for Basic Metabolic Research in Copenhagen and Professor Mauro D’Amato at CIC bioGUNE in Spain and LUM University in Italy. It also involves scientists internationally from Copenhagen, Greenland, Italy, and Spain as part of the ‘Sucrase-isomaltase working group’
Dr. Marta di Forti: “Our study indicates that daily users of high potency cannabis are at increased risk of developing psychosis independently from their polygenic risk score for schizophrenia.”
Is there a connection between cannabis use and developing psychosis? This is what a recent study published in Psychological Medicine hopes to address as an international team of researchers investigated how frequent cannabis use combined with a genetic predisposition for schizophrenia could lead to developing psychosis later in life. This study holds the potential to help researchers, medical professionals, and the public better understand how to identify the signs of psychosis in cannabis users and take necessary steps to address them as soon as possible.
For the study, the researchers conducted an observational study by obtaining data records of almost 150,000 individuals registered in United Kingdom and European Union medical databanks, one of which was the European Network of National Schizophrenia Networks Studying Gene-Environment Interactions (EU-GEI), to examine records regarding patients who self-reported use and psychosis diagnoses. In the end, the researchers discovered a connection between individuals who self-reported lifetime frequent cannabis use and psychosis diagnoses, specifically regarding high potency cannabis which contains 10 percent or greater Delta-9 tetrahydrocannabinol (THC).
“These are important findings at a time of increasing use and potency of cannabis worldwide,” said Dr. Marta di Forti, who is a Professor of Drug use, Genetics, and Psychosis at King’s College London and a co-author on the study. “Our study indicates that daily users of high potency cannabis are at increased risk of developing psychosis independently from their polygenic risk score for schizophrenia. Nevertheless, the polygenic risk score for schizophrenia might, in the near future, become useful to identify those at risk for psychosis among less frequent users to enable early preventative measures to be put in place.”
Large-scale protein and gene profiling have massively expanded the landscape of cancer-associated proteins and gene mutations, but it has been difficult to discern whether they play an active role in the disease or are innocent bystanders. In a study published in Nature Cancer, researchers at Baylor College of Medicine revealed a powerful and unbiased machine learning-based approach called FunMap for assessing the role of cancer-associated mutations and understudied proteins, with broad implications for advancing cancer biology and informing therapeutic strategies.
“Gaining functional information on the genes and proteins associated with cancer is an important step toward better understanding the disease and identifying potential therapeutic targets,” said corresponding author Dr. Bing Zhang, professor of molecular and human genetics and part of the Lester and Sue Smith Breast Center at Baylor.
“Our approach to gain functional insights into these genes and proteins involved using machine learning to develop a network mapping their functional relationships,” said Zhang, member of Baylor’s Dan L Duncan Comprehensive Cancer Center and a McNair Scholar. “It’s like, I may not know anything about you, but if I know your LinkedIn connections, I can infer what you do.”
