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The enzyme telomerase can prevent telomere attrition from happening by extending the length of telomeres. However, in most multicellular organisms, including humans, telomerase expression is switched off, except in germ cells, some types of stem cells, and certain white blood cells. While this might play a role in preventing cancer, as most cancerous cells must switch telomerase expression back on via mutations to enable runaway replication, numerous studies have shown that increasing telomerase through TERT delays aging and increases longevity of model organisms [1].

The small molecule that could

In the lab, this is usually done by introducing genetic vectors carrying a working copy of the gene that codes TERT. It’s this gene that is switched off in somatic cells. However, gene therapies are complex and expensive, and they are just entering the medical mainstream. What if we could do the same using a small molecule?

Transcription factors (TFs) are proteins that bind to specific DNA sequences, regulating the transcription of genetic information from DNA to messenger RNA (mRNA). These proteins play a pivotal role in the regulation of gene expression, which in turn impacts a wide range of biological processes and brain functions.

We present a developmental atlas that offers insight into sequential epigenetic changes underlying early human brain development modeled in organoids, which reconstructs the differentiation trajectories of all major CNS regions. It shows that epigenetic regulation via the installation of activating histone marks precedes activation of groups of neuronal genes.

Centenarians have become the fastest-growing demographic group in the world, with numbers approximately doubling every 10 years since the 1970s.

Many researchers have sought out the factors and contributors that determine a long and healthy life. The dissolution isn’t new either, with Plato and Aristotle writing about the ageing process over 2,300 years ago.

Understanding what is behind living a longer life involves unravelling the complex interplay of genetic predisposition and lifestyle factors and how they interact.

The cost of new gene-based sickle cell treatments isn’t the only barrier to access. Coming up with new ways to treat the whole disease—and person—could make treatment more equitable.

By Shobita Parthasarathy

Last fall, to great fanfare, US regulators approved two gene therapies for sickle cell disease, and the European Union and UK soon followed. Many people hope that these treatments will provide a “functional cure” for the genetic condition, which causes rigid, misshapen red blood cells that lead to anemia, episodes of extreme pain, blood vessel and organ damage, stroke risk and lower life expectancy. These sickle cell therapies also bring us closer to an age of “CRISPR medicine” in which new gene-editing tools could be used to fix a range of debilitating genetic diseases, including Duchenne muscular dystrophy and cancer.

“There is an urgent need for new methods for antibiotic discovery,” Dr. Luis Pedro Coelho, a computational biologist and author of a new study on the topic, said in a press release.

Coelho and team tapped into AI to speed up the whole process. Analyzing huge databases of genetic material from the environment, they uncovered nearly one million potential antibiotics.

The team synthesized 100 of these AI-discovered antibiotics in the lab. When tested against bacteria known to resist current drugs, they found 63 readily fought off infections inside a test tube. One worked especially well in a mouse model of skin disease, destroying a bacterial infection and allowing the skin to heal.

Groundbreaking maps reveal the complex gene regulation in brains with and without mental disorders, enhancing the understanding of mental illnesses and potential treatments.

A consortium of researchers has produced the largest and most advanced multidimensional maps of gene regulation networks in the brains of people with and without mental disorders. These maps detail the many regulatory elements that coordinate the brain’s biological pathways and cellular functions. The research, supported by the National Institutes of Health (NIH), used postmortem brain tissue from over 2,500 donors to map gene regulation networks across different stages of brain development and multiple brain-related disorders.

“These groundbreaking findings advance our understanding of where, how, and when genetic risk contributes to mental disorders such as schizophrenia, post-traumatic stress disorder, and depression,” said Joshua A. Gordon, M.D., Ph.D., director of NIH’s National Institute of Mental Health (NIMH). “Moreover, the critical resources, shared freely, will help researchers pinpoint genetic variants that are likely to play a causal role in mental illnesses and identify potential molecular targets for new therapeutics.”