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Early adult binge drinking has lasting impact on aging brain in mice

In a new work, a team from the University of Pennsylvania tracked the impact of alcohol consumption from the age of 20 on brain health and came to disappointing conclusions.


UNIVERSITY PARK, Pa. — Binge drinking in early adults can lead to long-lasting and potentially permanent dysregulation in the brain, according to a new study in mice, led by researchers at Penn State. They found that neurons, cells that transmit information in the brain via electrical and chemical signals, showed changes following binge drinking were similar in many ways to those seen with cognitive decline.

These findings, published in the journal Neurobiology of Aging, reveal that binge drinking early in life may have lasting impacts that are predictive of future health issues, like Alzheimer’s disease and related dementias, the researchers said. The work could inform the development of therapeutics to help combat these changes — particularly in aging populations who may have given up alcohol decades earlier, according to Nikki Crowley, director of the Penn State Neuroscience Institute at University Park, Huck Early Career Chair in Neurobiology and Neural Engineering, assistant professor of biology in the Eberly College of Science, and the leader of the research team.

“We know from previous studies that there are immediate effects of binge drinking on the brain, but we didn’t have any sense of if these changes were long-lasting, or reversible over time,” said Crowley, who is also an assistant professor of biomedical engineering and of pharmacology. “We were interested in understanding if binge drinking during early adulthood may have lasting consequences that are not revealed until later in life — even if drinking had stopped for a very long period of time. This allows us to consider the effects of alcohol on an individual’s holistic health, in terms of their entire life history.”

Bright Nights, Dark Days, And Low Greenspace Exposure Are Associated With Poor Health

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RNA editing is the next frontier in gene therapy—here’s what you need to know

The United States Food and Drug Administration has just approved the first-ever clinical trial that uses CRISPR-Cas13 RNA editing. Its aim is to treat an eye disease called wet age-related macular degeneration that causes vision loss in millions of older people worldwide.

This trial marks a new frontier in —the process of treating or curing medical conditions by changing a person’s genes.

What makes it special is the fact the therapy targets RNA, instead of DNA. So, what does that mean, and why should we be excited?

MIT Longevity, AI, and Cognitive Research Hackathon: Michael Lustgarten, PhD @ekkolapto3

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Scientists discover ‘toolkit’ to fix DNA breaks associated with aging, cancer and motor neuron disease

A new “toolkit” to repair damaged DNA that can lead to aging, cancer and motor neuron disease (MND) has been discovered by scientists at the Universities of Sheffield and Oxford.

Published in Nature Communications, the research shows that a protein called TEX264, together with other enzymes, is able to recognize and “eat” toxic proteins that can stick to DNA and cause it to become damaged. An accumulation of broken, damaged DNA can cause cellular aging, cancer and neurological diseases such as MND.

Until now, ways of repairing this sort of DNA damage have been poorly understood, but scientists hope to exploit this novel repair toolkit of proteins to protect us from aging, cancer and neurological disease.

Frontiers: As we age, our immune system’s ability to effectively respond to pathogens declines, a phenomenon known as immunosenescence

This age-related deterioration affects both innate and adaptive immunity, compromising immune function and leading to chronic inflammation that accelerates aging. Immunosenescence is characterized by alterations in immune cell populations and impaired functionality, resulting in increased susceptibility to infections, diminished vaccine efficacy, and higher prevalence of age-related diseases. Chronic low-grade inflammation further exacerbates these issues, contributing to a decline in overall health and resilience. This review delves into the characteristics of immunosenescence and examines the various intrinsic and extrinsic factors contributing to immune aging and how the hallmarks of aging and cell fates can play a crucial role in this process. Additionally, it discusses the impact of sex, age, social determinants, and gut microbiota health on immune aging, illustrating the complex interplay of these factors in altering immune function. Furthermore, the concept of immune resilience is explored, focusing on the metrics for assessing immune health and identifying strategies to enhance immune function. These strategies include lifestyle interventions such as diet, regular physical activity, stress management, and the use of gerotherapeutics and other approaches. Understanding and mitigating the effects of immunosenescence are crucial for developing interventions that support robust immune responses in aged individuals.

The immune system plays a crucial role in protecting our bodies from harmful pathogens. It is divided into two segments: innate immunity and adaptive immunity. The innate immune system acts as an immediate but non-specific first responder to defend against pathogens, composed of phagocytic and natural killer cells. Besides innate immune cells, another important component of the innate system includes physical barriers like skin and mucous membranes. Meanwhile, adaptive immunity is more specialized and requires time to mount a high-affinity and specific response, relying on anticipatory receptors that recognize pathogen-specific antigens. The adaptive immune response is centered around B and T lymphocytes, which are produced in the bone marrow and thymus, respectively (Farber, 2020; Lam et al., 2024). With age, the ability of our immune system to mount productive and timely responses to pathogens diminishes.