A map of DNA methylation changes in human organs could help researchers to discover more targets for anti-ageing therapies.

With aging, somatic mutations accumulate in cellular DNA; however, whether they drive age-related functional decline is incompletely understood. Here the authors show that these mutations can weaken muscle repair and reduce strength after injury, suggesting they play a role in age-related physical decline in mouse muscle.
Alzheimer’s disease (AD) is a debilitating neurodegenerative disorder that causes progressive memory loss and a decline in mental (i.e., cognitive) abilities. Statistics suggest that between 500,000 and 900,000 people are diagnosed with this disease every year, while several hundreds of thousands experience dementia or other aging-related cognitive decline.
While there are some available treatments designed to delay cognitive decline in individuals with mild or moderate AD symptoms, a cure for the disease has not yet been identified. A better understanding of the neural, genetic, cellular and molecular processes that contribute to the disease’s progression, as well as to neurodegeneration in general, could thus be highly valuable, as it could inform the future development of alternative treatments.
Past neuroscience research has identified the key role of microglia in AD. These are specialized immune cells that monitor the environment in the brain, clearing out damaged cells, debris and pathogens. The dysregulation of these cells has been linked to neurodegeneration and to the progression of AD.
MIT researchers have developed a technique that enables real-time, 3D monitoring of corrosion, cracking, and other material failure processes inside a nuclear reactor environment.
This could allow engineers and scientists to design safer nuclear reactors that also deliver higher performance for applications like electricity generation and naval vessel propulsion.
During their experiments, the researchers utilized extremely powerful X-rays to mimic the behavior of neutrons interacting with a material inside a nuclear reactor.
A new survey-based study suggests that the “unhappiness hump”—a widely documented rise in worry, stress, and depression with age that peaks in midlife and then declines—may have disappeared, perhaps due to declining mental health among younger people. David Blanchflower of Dartmouth College, U.S., and colleagues present these findings in the open-access journal PLOS One.
Since 2008, a U-shaped trend in well-being with age, in which well-being tends to decline from childhood until around age 50 before rebounding in old age, has been observed in developed and developing countries worldwide. Data have also revealed a corresponding “ill-being” or unhappiness hump.
Recent data point to a worldwide decline in well-being among younger people, but most studies have not directly addressed potential implications for the unhappiness hump. To help clarify, Blanchflower and colleagues first analyzed data from U.S. and U.K. surveys that included questions about participants’ mental health.
Researchers from University of California San Diego Sanford Stem Cell Institute have developed a novel method to stimulate and mature human brain organoids using graphene, a one-atom-thick sheet of carbon. Published in Nature Communications, the study introduces Graphene-Mediated Optical Stimulation (GraMOS), a safe, non-genetic, biocompatible, non-damaging way to influence neural activity over days to weeks. The approach accelerates brain organoid development — especially important for modeling age-related conditions like Alzheimer’s disease — and even allows them to control robotic devices in real time.
“This is a game-changer for brain research,” said Alysson Muotri, Ph.D., corresponding author, professor of pediatrics, and director of the UC San Diego Sanford Stem Cell Institute Integrated Space Stem Cell Orbital Research Center. “We can now speed up brain organoid maturation without altering their genetic code, opening doors for disease research, brain–machine interfaces and other systems combining living brain cells with technology.”