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Category: genetics – Page 12

Tracing brain chemistry across humanity’s family tree

The evolutionary success of our species may have hinged on minute changes to our brain biochemistry after we diverged from the lineage leading to Neanderthals and Denisovans about half a million years ago.

Two of these tiny changes that set modern humans apart from Neanderthals and Denisovans affect the stability and genetic expression of the adenylosuccinate lyase, or ADSL. This enzyme is involved in the biosynthesis of purine, one of the fundamental building blocks of DNA, RNA, and other important biomolecules.

In a study published in PNAS, researchers from the Okinawa Institute of Science and Technology (OIST), Japan and the Max Planck Institute for Evolutionary Anthropology, Germany have discovered that these changes may play an important role in our behavior, contributing new pieces to the great puzzle of who we humans are and where we come from.

Rationale engineering generates a compact new tool for gene therapy

Scientists at the McGovern Institute for Brain Research at MIT and the Broad Institute of MIT and Harvard have re-engineered a compact RNA-guided enzyme they found in bacteria into an efficient, programmable editor of human DNA.

The protein they created, called NovaIscB, can be adapted to make precise changes to the genetic code, modulate the activity of specific genes, or carry out other editing tasks. Because its small size simplifies delivery to cells, NovaIscB’s developers say it is a promising candidate for developing gene therapies to treat or prevent disease.

The study was led by Feng Zhang, the James and Patricia Poitras Professor of Neuroscience at MIT who is also an investigator at the McGovern Institute and the Howard Hughes Medical Institute, and a core member of the Broad Institute. Zhang and his team reported their open-access work this month in the journal Nature Biotechnology.

Researchers at MIT and the Broad Institute, led by Professor Feng Zhang, redesign a compact RNA-guided enzyme from bacteria, making it an efficient editor of human DNA.

Protein condensate sequesters synaptic vesicles at the release site

Message transfer from brain cell to brain cell is key to information processing, learning and forming memories. The bubbles, synaptic vesicles, are housed within the synapse — the connection point where brain cells communicate. In typical synapses within the brains of mammals, 300 synaptic vesicles are clustered together in the intersection between any two brain cells, but only a few of these vesicles are used for such message transfer, researchers say. Pinpointing how a synapse knows which vesicles to use has long been a target of research by those who study the biology and chemistry of thought.

In an effort to better understand the operation of these synaptic vesicles, the team designed a study that first focused on endocytosis, a process in which brain cells recycle synaptic vesicles after they are used for neuronal communication.

Already aware of intersectin’s general role in endocytosis and neuronal communication, the scientists genetically engineered mice to lack the gene that codes for intersectin. However, and somewhat to their surprise, the lead says removing the protein did not appear to halt endocytosis in brain cells.

The research team refocused their experiments, taking a closer look at the synaptic vesicles themselves.

Using a high-resolution fluorescence microscope to observe where intersectin is in a synapse, the researchers found it in between vesicles that are used for neuronal communication and those that are not, as if they are physically separating the two.

To further understand the role of intersectin at this location, they used an electron microscope to visualize synaptic vesicles in action across one billionth of a meter. In all the nerve cells from mice lacking this protein, the scientists say synaptic vesicles close to the membrane were absent from the release zone of the synapse, the place where the bubbles would discharge to nearby neurons.

“This suggested that intersectin regulates release, rather than recycling, of these vesicles at this location of the synapse,” says the author.

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Can Dietary Sodium Reduce Grey Hair?

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Scientists Use Engineered Cells to Combat Aging in Primates

As we age, our bodies gradually lose their ability to repair and regenerate. Stem cells diminish, making it increasingly difficult for tissues to heal and maintain balance. This reduction in stem cells is a hallmark of aging and a key driver of age-related diseases. Scientists have long debated whether this decline is the root cause of aging or a side effect. Efforts to use stem cell transplants to reverse aging have faced many challenges, such as ensuring the cells survive and integrate into the body without causing serious side effects, like tumors.

In a recent study published in Cell, researchers from the Chinese Academy of Sciences and Capital Medical University introduced a new type of human stem cell called senescence-resistant mesenchymal progenitor cells (SRCs) by reprogramming the genetic pathways associated with longevity. These cells, which resist aging and stress without developing tumors, were tested on elderly crab-eating macaques, which share physiological similarities with humans in their 60s and 70s.

The research team conducted a 44-week experiment on these macaques. The macaques received biweekly intravenous injections of SRCs, with a dosage of 2×106 cells per kilogram of body weight. The researchers found no adverse effects among the macaques. Detailed assessments confirmed that the transplanted cells did not cause tissue damage or tumors.

The researchers discovered that SRCs triggered a multi-system rejuvenation, reversing key markers of aging across 10 major physiological systems and 61 different tissue types. The treated macaques exhibited improved cognitive function, and tissue analyses indicated a reduction in age-related degenerative conditions such as brain atrophy, osteoporosis, fibrosis, and lipid buildup. 👍

Estimating Polar Bear (Ursus maritimus) Age Based on an Epigenetic DNA Methylation Clock

We developed a robust epigenetic clock to estimate age from two wild polar bear subpopulations using blood samples. There was a correlation between epigenetic (DNAm) and chronological age throughout the polar bear lifespan. Polar bears in the wild have a lifespan of approximately 25 years (Rode and Stirling 2018), thus the clock estimates age to ±3% of the polar bear lifespan, although we caution that age estimates may be less accurate for older individuals. Advantages to this method include obtaining more accurate age estimates compared to cementum annuli-derived ages and leveraging samples likely already routinely collected (e.g., blood, tissue) during capture, as opposed to pulling teeth. Further, archived samples or previously extracted DNA may be used for DNAm analysis, extending the value of existing samples and saving money on DNA extraction costs. Our results complement other polar bear clocks (Newediuk et al. 2024, 2025) and provide additional support for the use of DNAm methods to estimate the age of wild mammals (De Paoli-Iseppi et al. 2017).

Our DNAm method estimates polar bear age with a MAE of 0.75 years. In contrast, accuracy of cementum annuli for aging polar bears to within 1 year of actual age has ranged from 32% to 75% (Calvert and Ramsay 1998 ; Christensen-Dalsgaard et al. 2010 ; Hensel and Sorensen 1980). Cementum annuli age estimates are less accurate when made by less experienced observers (Christensen-Dalsgaard et al. 2010 ; Hensel and Sorensen 1980 ; McLaughlin et al. 1990) and can vary between laboratories by 10 years (Christensen-Dalsgaard et al. 2010). For example, in one lab, multiple female polar bears were aged at ~10 years, while a second laboratory aged them at 20 years old (Christensen-Dalsgaard et al. 2010). Our method removes these sources of error. We do, however, acknowledge a potential source of technical error, given that all but three of the tooth-aged samples were run on one plate, and the majority of our known age samples were run on another plate.

ER-100: The “Miracle Cure” For Aging? | Aubrey de Grey

The ER-100 drug candidate reverses aging in mice, and David Sinclair says human trials start soon. Is this a magic pill for aging? Dr. Aubrey de Grey discusses the latest advances in life-extension research.

Our story begins on X, where user “rand_longevity” wrote, “Aging will be reversible in humans within 8 years”, to which Dr. David Sinclair replied, “8 years? After successful non-human primate trials, human age reversal trials are set to begin in 6 months”, later naming the ER-100 drug candidate.

Life Biosciences ER-100 drug candidate leverages partial epigenetic programming using 3 of the 4 Yamanaka factors to promote cellular rejuvenation to a younger state without the loss of cell identity. They believe this will help prevent or reverse age-related diseases at a root level — but they’re not the only organization pursuing life-extension research.

Dr. de Grey’s own research has focused primarily on accumulated side effects from metabolism, embodied in the title of his 1999 book, “The Mitochondrial Free Radical Theory of Aging”.

Dr. de Grey is well-known as one of the top gerontology and life-extension scientists in the world, and his own work has also been successful in extending the lifespan of lab animals. In this program, he discusses his work and some of the key elements of living a longer, healthier life.

DISCLAIMER: This program is a discussion is about ongoing scientific research, and is NOT providing medical advice. Please consult your doctor before starting any supplements, beginning an exercise routine, or undertaking lifestyle changes.

Continue reading “ER-100: The “Miracle Cure” For Aging? | Aubrey de Grey” | >

Sugar layer on beta cells prevents immune system from causing type 1 diabetes

Scientific breakthroughs in one disease don’t always shed light on treating other diseases. But that’s been the surprising journey of one Mayo Clinic research team. After identifying a sugar molecule that cancer cells use on their surfaces to hide from the immune system, the researchers have found the same molecule may eventually help in the treatment of type 1 diabetes, once known as juvenile diabetes.

Type 1 diabetes is a chronic autoimmune condition in which the immune system errantly attacks that produce insulin. The disease is caused by genetic and other factors and affects an estimated 1.3 million people in the U.S.

In their studies, the Mayo Clinic researchers took a cancer mechanism and turned it on its head. Cancer cells use a variety of methods to evade , including coating themselves in a known as sialic acid. The researchers found in a preclinical model of type 1 diabetes that it’s possible to dress up beta cells with the same sugar molecule, enabling the immune system to tolerate the cells.

Scientists shrink the genetic code of E. coli to contain only 57 of its usual 64 codons

The DNA of nearly all life on Earth contains many redundancies, and scientists have long wondered whether these redundancies served a purpose or if they were just leftovers from evolutionary processes. Both DNA and RNA contain codons, which are sequences of three nucleotides that either provide information about how to form a protein with a specific amino acid or tell the cell to stop (a stop signal) during protein synthesis.

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