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An international study led by the Institut de Neurociències at the UAB (INc-UAB) has shown that increasing levels of the Klotho protein in mice extends lifespan and improves both physical and cognitive health when aging.

As we grow older, it is natural to lose and , leading to greater frailty and a higher risk of falls and serious injuries. Cognitively, neurons progressively degenerate and lose connections, while diseases such as Alzheimer’s and Parkinson’s become more prevalent. In a society where the population is steadily aging, reducing these effects is one of the main challenges for research.

Now, in an article published in Molecular Therapy, an international research team led by Professor Miguel Chillón, ICREA researcher at the INc-UAB, has shown that increasing levels of the secreted form of the Klotho protein (s-KL) improves aging in mice.

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A new health-assessment method, called the Health Octo Tool, uses eight measures drawn from physical exams and routine lab tests to calculate a person’s biological age.

The tool may predict an individual’s risk of disability and death more accurately than existing health predictors.

The research team, led by Shabnam Salimi from the University of Washington School of Medicine, believes the tool could uncover new factors that shape the aging process and help design interventions to extend lifespan. Salimi is a physician-scientist and acting instructor in the Department of Anesthesiology & Pain Medicine.

In research published in New Phytologist, investigators reveal that tomato ripening is regulated by the same mechanism that contributes to humans’ and animals’ life-and health spans.

The mechanism, called autophagy, regulates cellular recycling and operates in all lifeforms apart from bacteria. This latest work shows that autophagy affects tomato fruit ripening by controlling the production of ethylene. Ethylene is the primary hormone that controls ripening in many fruits such as apples, bananas, mangoes, avocados, and tomatoes.

To assess the role of autophagy in ripening, the team of researchers from the Volcani Institute, in Israel, and the University of Tübingen, in Germany, generated tomato plants that allow a temporal genetic repression of autophagy, specifically in mature non-ripe fruits.

Recent discoveries of glymphatics and meningeal lymphatics have redefined our understanding of CNS immunosurveillance. Kim and Kipnis illustrate how the clearance of brain-derived antigens creates an “immune code” that, when presented by meningeal antigen-presenting cells, instructs T cells to safeguard neural homeostasis. They review how inflammation, aging, and neurodegeneration disrupt this finely tuned process and highlight emerging therapeutic opportunities.

From birth to the last moments of life, the human brain is known to change and evolve significantly, both in terms of its physical organization (i.e., structural connectivity) and the coordination between different brain regions (i.e., functional connectivity). Mapping and understanding the brain’s evolution over time is of crucial importance, as it could also shed light on differences in the brains of individuals who develop various mental health disorders or experience an aging-related cognitive decline.

Researchers at Beijing Normal University and other institutes in China recently carried out a large-scale study to gather new insights into how the brain’s of humans worldwide changes over the course of their lifespan. Their paper, published in Nature Neuroscience, unveils patterns in the evolution of the brain that could inform future research focusing on a wide range of neuropsychiatric and cognitive disorders.

“Functional connectivity of the changes through life,” wrote Lianglong Sun, Tengda Zhao and their colleagues in their paper. “We assemble task-free functional and structural magnetic resonance imaging data from 33,250 individuals at 32 weeks of postmenstrual age to 80 years from 132 global sites.”

The strong links between changes in astrocyte structure and function in the context of neurodevelopment and disease have been supported by studies examining astrocyte cytoskeletal markers such as glial fibrillary acidic protein (GFAP) in disease models and postmortem human brain tissue, where increases or decreases in its expression in various brain nuclei are often linked with neurocognitive and psychiatric disorders. Hence, changes in GFAP expression are often the first-line test for astrocyte involvement in disease and support a role for astrocyte dysfunction in major depression, schizophrenia, alcohol and substance use disorders, anorexia nervosa, and bipolar disorder (719), where changes in astrocyte structure, density, complexity, and/or blood vessel association are linked with disrupted astrocyte function. Although reactive astrogliosis remains the single most studied astrocytic response involving morphological adaptations and changes in GFAP expression (20, 21), in recent years, astrocyte morphological plasticity has been shown to be more nuanced. GFAP expression is dynamic across the circadian cycle (2224) and increases with physical exercise and environmental enrichment (25, 26). Moreover, in aging, astrocytes increase or decrease their GFAP expression in different brain regions (27, 28), suggesting heterogeneity in astrocyte form and function.

We previously found a notable relationship between astrocyte structure and vulnerability to substance use disorders, with astrocytes in the nucleus accumbens (NAc) altering their association with different neural subcircuits to drive or suppress drug-seeking behavior depending on heroin availability (2931). The NAc is critical for regulating behavioral outputs in response to rewards, including substances of abuse and natural reinforcers, such as food or sucrose. The NAc is composed of core and shell subregions that are themselves heterogeneous structures with regard to synaptic input and output connectivity and function (3236). Heterogeneity has been observed in astrocyte morphology within the NAc core (3, 30, 37), but studies have not yet examined how astrocyte structure and function differ across NAc subregions at baseline or in response to operant conditioning with natural or pathological reinforcers.

To address this gap, we developed an automated pipeline for single-cell morphological analysis of astrocytes that integrates state-of-the-art deep learning models for astrocyte detection and segmentation, together with highly sensitive geometrical tools for precise quantitation of single-cell morphological characteristics. We introduce the rigorous notion of morphological distance (MD) to measure alterations in astrocyte morphology and compare astrocyte subpopulations according to their structural characteristics. By applying this pipeline in combination with supervised machine learning, we found that single-astrocyte morphological characteristics were predictive not only of anatomical location within the NAc at baseline but also of the availability of heroin or sucrose at the moment of image capture. This geometrically sensitive approach yields substantially more detailed information about astrocyte structure than previously applied manual or semiautomated approaches and serves as a rigorous quantitative assay for identifying brain nuclei where astrocytes undergo plasticity in the context of disease. We found that astrocyte structural plasticity across the NAc was disrupted in animals that had been exposed to heroin but not sucrose, consistent with a largely protective role for NAc astrocytes in maintaining synaptic homeostasis and behavioral flexibility. We also found that astrocyte structural plasticity in the dorsomedial portion of the NAc shell was uniquely engaged during the initiation of opioid but not sucrose seeking, suggesting the involvement of this structure in drug relapse.

The researchers discovered that AP2A1 seemed to be responsible for switching cells between their “young” and “old” states—senescent cells were rejuvenated by the suppression of the protein, and younger cells aged by its overexpression.

The scientists also found that the AP2A1 was frequently in close proximity to another protein: integrin β1, which aids cells in binding to the collagen scaffold that envelops them. Both proteins, the researchers described, travel along stress fibers within cells.

The number of people suffering from osteoarthritis is expected to top 1 billion by 2050. The biggest risk factor for the prevalent, often painful, chronic joint disease is aging. And like aging, there is currently no way to stop it.

A discovery by scientists at Henry Ford Health + Michigan State University Health Sciences could pave the way for new breakthroughs in detecting and treating the disease. Their findings were recently published in Nature Communications.

“Our hope is that this discovery will one day allow doctors to catch the disease earlier and intervene before significant joint damage occurs,” said Shabana Amanda Ali, Ph.D., a Henry Ford Health assistant scientist and senior author of the paper. “Osteoarthritis is so complex and so heterogeneous that even with decades of research there hasn’t been a single therapeutic.”