Scientists uncover why certain animals live far longer than expected. New research reveals mechanisms that could reshape how we understand human aging.
In a preprint published in bioRxiv, Prof. Vadim Gladyshev and a team of researchers have used an artificial intelligence-based system to discover a wide variety of potential interventions, including a drug that significantly improves biomarkers of frailty in mice.
Repurposing previous data
Previous research efforts have created a massive dataset in the form of the Gene Expression Omnibus (GEO), which contains the results of a great many experiments related to potentially disease-modifying drugs, many of which are tissue-specific [1]. These researchers refer to this dataset as a “massive missed opportunity” in aging research, because the vast majority of the experiments in the GEO were unrelated to aging and their data was never investigated in that context.
Life’s instructions are written in DNA, but it is the enzyme RNA polymerase II (Pol II) that reads the script, transcribing RNA in eukaryotic cells and eventually giving rise to proteins. Scientists know that Pol II must advance down the gene in perfect sync with other biological processes; aberrations in the movement of this enzyme have been linked to cancer and aging. But technical hurdles prevented them from precisely determining how this important molecular machine moves along DNA, and what governs its pauses and accelerations.
A new study fills in many of those knowledge gaps. In a paper published in Nature Structural & Molecular Biology, researchers used a single-molecule platform to watch individual mammalian transcription complexes in action. The result is a clear view of how this molecular engine accelerates, pauses, and shifts gears as it transcribes genetic information.
“What’s really striking is how this machine functions almost like a finely tuned automobile,” says Shixin Liu, head of the Laboratory of Nanoscale Biophysics and Biochemistry. “It has the equivalent of multiple gears, or speed modes, each controlled by the binding of different regulatory proteins. We figured out, for the first time, how each gear is controlled.”
Taking a photo of a friend? You’ve probably got their face centered and focused. Driving down a highway? Eyes on the road.
But for millions of adults with age-related macular degeneration, that crucial, central field of sight is blurred beyond recognition. Current treatments can only slow its progression or augment vision, but the blur will usually continue to worsen.
A recent clinical trial of a treatment based on stem cell transplants has found the procedure may be able to safely reverse the cumulative damage to the hard-working macula – that part of the retina responsible for all you see directly in front of you.
Biomedical researchers at Texas A&M University may have discovered a way to stop or even reverse the decline of cellular energy production—a finding that could have revolutionary effects across medicine.
Dr. Akhilesh K. Gaharwar and Ph.D. student John Soukar, along with their fellow researchers from the Department of Biomedical Engineering, have developed a new method to give damaged cells new mitochondria, returning energy output to its previous levels and dramatically increasing cell health.
Mitochondrial decline is linked to aging, heart disease and neurodegenerative disorders. Enhancing the body’s natural ability to replace worn-out mitochondria could fight all of them.