Lifeboat Foundation: Safeguarding Humanity
Toggle light / dark theme

Blog

Category: life extension – Page 65

How Decision-Making Improves with Age

Summary: Adolescents are known for making less optimal, noisy decisions, but a recent study reveals that these tendencies decrease with age and are linked to improvements in complex decision-making skills. Researchers found that decision noise, or variability in choices, mediates age-related gains in goal-directed behaviors and adaptability.

Adolescents may rely on less efficient strategies due to limited cognitive resources, which makes them more susceptible to emotional and motivational influences. These findings shed light on the computational mechanisms behind developmental shifts in decision-making and open avenues for understanding neurodevelopmental disorders.

Quantifying Brain Aging in Diabetes Type 2 Patients

Researchers from Johns Hopkins University have recently discovered several prominent biomarkers that allow for the early diagnosis of dementia and/or mild cognitive impairment (MCI). In a recently published article, evidence has been presented that patients with diabetes type 2 exhibited more changes to their brains than healthy controls, including the shrinking of certain brain areas. These changes occurred earlier in life, and some of the patients developed MCI sooner than others.

The Older Controls at Risk for Dementia (BIOCARD) study is a long-term trial which has been conducted for the past 27 years with the goal of determining how medical conditions and other factors might be impacting cognitive function and perhaps even affecting the biological age of the brain as a whole. BIOCARD was originally a National Institutes of Health initiative, which began in 1995 and later continued at Johns Hopkins University from 2015 to 2023. The cohort consisted of 185 participants, with an average age of 55 years and normal cognitive function.

The trial subjects received routine brain scans and cerebrospinal fluid (CSF) tests for 20 years, in order to measure changes in brain structures and levels of proteins associated with Alzheimer’s disease. Scientists have been increasingly using CSF to attempt to uncover early signs of neurodegenerative disease, since it is a minimally-invasive procedure which is inexpensive and widely available.

Human skin rejuvenation via mRNA

Aging is characterized by a gradual decline in function, partly due to accumulated molecular damage. Human skin undergoes both chronological aging and environmental degradation, particularly UV-induced photoaging. Detrimental structural and physiological changes caused by aging include epidermal thinning due to stem cell depletion and dermal atrophy associated with decreased collagen production. Here, we present a comprehensive single-cell atlas of skin aging, analyzing samples from young, middle-aged, and elderly individuals, including both sun-exposed and sun-protected areas. This atlas reveals age-related cellular composition and function changes across various skin cell types, including epidermal stem cells, fibroblasts, hair follicles, and endothelial cells. Using our atlas, we have identified basal stem cells as a highly variable population across aging, more so than other skin cell populations such as fibroblasts. In basal stem cells, we identified ATF3 as a novel regulator of skin aging. ATF3 is a transcriptional factor for genes involved in the aging process, with its expression reduced by 20% during aging. Based on this discovery, we have developed an innovative mRNA-based treatment to mitigate the effects of skin aging. Cell senescence decreased 25% in skin cells treated with ATF3 mRNA, and we observed an over 20% increase in proliferation in treated basal stem cells. Importantly, we also found crosstalk between keratinocytes and fibroblasts as a critical component of therapeutic interventions, with ATF3 rescue of basal cells significantly enhancing fibroblast collagen production by approximately 200%. We conclude that ATF3-targeted mRNA treatment effectively reverses the effects of skin aging by modulating specific cellular mechanisms, offering a novel, targeted approach to human skin rejuvenation.

The authors have declared no competing interest.

Indicators of an aging brain: A 20-year study

Johns Hopkins University-led researchers, working with the Biomarkers for Older Controls at Risk for Dementia (BIOCARD) cohort, have found that certain factors are linked to faster brain shrinkage and quicker progression from normal thinking abilities to mild cognitive impairment (MCI). People with type 2 diabetes and low levels of specific proteins in their cerebrospinal fluid showed more rapid brain changes and developed MCI sooner than others.

Long-term studies tracking changes over many years are rare but valuable. Previous research mostly provided snapshots in time, which can’t show how individual brains change over the years. By following participants for up to 27 years (20-year median), this study offers new insights into how health conditions might speed up brain aging.

In a study, “Acceleration of Brain Atrophy and Progression From Normal Cognition to Mild Cognitive Impairment,” published in JAMA Network Open, researchers used the BIOCARD cohort to examine associated with the acceleration of brain atrophy and progression from normal cognition to MCI. An Invited Commentary is also available.

Dietary Restriction or Good Genes: New study tries to unpick which has a Greater Impact on Lifespan

As people who research aging like to quip, the best thing you can do to increase how long you live is to pick good parents. After all, it has long been recognized that longer-lived people tend to have longer-lived parents and grandparents, suggesting that genetics influence longevity.

Complicating the picture, however, is that we know that the sum of your lifestyle, specifically diet and exercise, also significantly influences your health into older age and how long you live. What contribution lifestyle versus genetics makes is an open question that a recent study in Nature has shed new light on.

Scientists have long known that reducing calorie intake can make animals live longer. In the 1930s, it was noted that rats fed reduced calories lived longer than rats who could eat as much as they wanted. Similarly, people who are more physically active tend to live longer. But specifically linking single genes to longevity was until recently a controversial one.

Aging drives a program of DNA methylation decay in plant organs

How organisms age is a question with broad implications for human health. In mammals, DNA methylation is a biomarker for biological age, which may predict age more accurately than date of birth. However, limitations in mammalian models make it difficult to identify mechanisms underpinning age-related DNA methylation changes. Here, we show that the short-lived model plant Arabidopsis thaliana exhibits a loss of epigenetic integrity during aging, causing heterochromatin DNA methylation decay and the expression of transposable elements. We show that the rate of epigenetic aging can be manipulated by extending or curtailing lifespan, and that shoot apical meristems are protected from this aging process. We demonstrate that a program of transcriptional repression suppresses DNA methylation maintenance pathways during aging, and that mutants of this mechanism display a complete absence of epigenetic decay. This presents a new paradigm in which a gene regulatory program sets the rate of epigenomic information loss during aging.

The authors have declared no competing interest.

Unexpected differences in genetically identical bacteria provide a new perspective on aging at the cellular level

Surprising findings on bacterial aging have emerged from a study carried out by a team of researchers led by the biologist Dr. Ulrich Steiner at Freie Universität Berlin. In a new paper published in Science Advances, the team demonstrated that even genetically identical bacterial cells living in the same environment react differently to the aging process and that changes occur at different rates within different regions of the cell.

Accumulation of advanced oxidation protein products promotes age-related decline of type H vessels in bone

Abstract. Type H vessels have been proven to couple angiogenesis and osteogenesis. The decline of type H vessels contributes to bone loss in the aging process. Aging is accompanied by the accumulation of advanced oxidation protein products (AOPPs). However, whether AOPP accumulation is involved in age-related decline of type H vessels is unclear. Here, we show that the increase of AOPP levels in plasma and bone were correlated with the decline of type H vessels and loss of bone mass in old mice. Exposure of microvascular endothelial cells to AOPPs significantly inhibited cell proliferation, migration, and tube formation, increased NADPH oxidase activity and excessive reactive oxygen species generation, upregulated the expression of vascular cell adhesion molecule-1 and intercellular cell adhesion molecule-1, and eventually impaired angiogenesis, which was alleviated by redox modulator N-acetylcysteine and NADPH oxidase inhibitor apocynin. Furthermore, reduced AOPP accumulation by NAC treatment was able to alleviate significantly the decline of type H vessels, bone mass loss and deterioration of bone microstructure in old mice. Collectively, these findings suggest that AOPPs accumulation contributes to the decline of type H vessels in the aging process, and illuminate a novel potential mechanism underlying age-related bone loss.