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Category: genetics – Page 118

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.

Young blood, old brains.

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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Researchers at Baylor College of Medicine have developed a new compound called d16 that can reduce tumor growth and overcome therapeutic resistance in mutant p53-bearing cancers in the lab. The findings, published in the journal Cancer Research Communications, a journal of the American Association for Cancer Research, open opportunities for new combination therapies for these difficult-to-treat cancers.

“One of the most common alterations in many human cancers is mutations in p53, a gene that normally provides one of the most powerful shields against tumor growth,” said first author, Dr. Helena Folly-Kossi, a postdoctoral associate in Dr. Weei-Chin Lin’s lab at Baylor. “Mutations that alter the normal function of p53 can promote tumor growth, cancer progression and resistance to therapy, which are associated with poor prognosis. It is important to understand how p53 mutations help cancer grow to develop therapies to counteract their effects.”

Studying how to target p53 mutations that promote cancer growth has been difficult. “One of the challenges has been to develop drugs that act on mutant p53 directly. Some of these drugs are under development, but they appear to be toxic,” said Lin, professor of medicine-hematology and oncology and of molecular and cellular biology. He also is a member of Baylor’s Dan L Duncan Comprehensive Cancer Center and the corresponding author of the work.

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The animal looked and barked like a dog—albeit one with long, pointed, foxlike ears—but it also climbed bushes, a behavior more typical of the local Pampas fox, and it refused common dog food, preferring to eat rats.

Caretakers began to wonder if it might be a hybrid—a mixture of domestic dog and some local wild canid. They contacted geneticists Thales Renato Ochotorena de Freitas from the Universidade Federal do Rio Grande do Sul and Rafael Kretschmer from the Universidade Federal de Pelotas who, last month, published a study confirming the animal was the world’s first documented fox-dog. The finding excited and intrigued experts in animal genetics.

“What a strange hybrid beast!” wrote Roland Kays, a biologist with North Carolina State University and the North Carolina Museum of Natural Sciences, on X (formerly Twitter), alongside a photo of the creature and link to the study.

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A genetically engineered marine microorganism is shown to break down polyethylene terephthalate (PET) in saltwater. This plastic, used in everything from water bottles to clothing, is a significant contributor to microplastic pollution in oceans.

“This is exciting because we need to address plastic pollution in marine environments,” says Nathan Crook, corresponding author of a paper on the work and an assistant professor of chemical and biomolecular engineering at North Carolina State University.

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And the answers point to a profound reality: We have far more in common with our extinct cousins than we ever thought.

Neanderthals within us

Until recently, the genetic legacy from ancient humans was invisible because scientists were limited to what they could glean from the shape and size of bones. But there has been a steady stream of discoveries from ancient DNA, an area of study pioneered by Nobel Prize winner Svante Paabo who first pieced together a Neanderthal genome.

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A new artificial intelligence program is helping scientists speedily sift through thousands of data sets and millions of papers to home in on genes that underly disease, drastically condensing a search process that once took months.

Using computer software, scientists can scan entire genomes, or an organism’s full set of DNA, of mice that model human diseases. The goal: to identify genetic mutations that cause those diseases and open new doors for scientists to better harness genetics to develop disease treatments, said Gary Peltz, MD, PhD, professor of anesthesiology, perioperative and pain medicine at Stanford Medicine.

But to do that, scientists must search through massive sets of genomic data, which yields more false positives than researchers care to admit. It’s also time intensive. Peltz wanted to make the genetic discovery process easier, faster and more accurate.

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The genetic code of a rare form of kidney cancer, called reninoma, has been studied for the first time. In a paper, published in Nature Communications, researchers at the Wellcome Sanger Institute, Great Ormond Street Hospital and The Royal Free Hospital also revealed a new drug target that could serve as an alternative treatment if surgery is not recommended.

There are around 100 cases of reninoma reported to date worldwide, and it is among the rarest of tumors in humans. Although it can usually be cured with surgery, it can cause severe hypertension or it can spread and develop into metastases. There are no existing medical treatments for reninoma and management involves surgery alone. Until now, it had been unknown what genetic error causes reninoma.

In the new study, a collaboration between the Wellcome Sanger Institute and Great Ormond Street Hospital and The Royal Free Hospital, researchers found that there is a specific error in the genetic code of a known cancer gene, NOTCH1, that is behind the development of this rare cancer.

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