BUFFALO, NY- March 5, 2024 – A new #research perspective was #published in Aging (listed by MEDLINE/PubMed as "Aging (Albany NY)" and "Aging-US" by Web of Science) Volume 16, Issue 4, entitled, “On standardization of controls in lifespan studies.”

In this new paper, researchers Olga Spiridonova, Dmitrii Kriukov, Nikolai Nemirovich-Danchenko, and Leonid Peshkin from Harvard Medical School's Department of Systems Biology discuss the burgeoning field of the search for interventions to slow down, and even reverse, aging. Currently available literature cites hundreds of supposedly beneficial pharmacological and genetic interventions in model organisms: mice, rats, flies, and worms, where research into physiology is routinely accompanied by lifespan data. However, when experimental animals from one article live as long as controls from another article, comparing the results of interventions across studies can yield misleading outcomes. 

“Theoretically, all lifespan data are ripe for re-analysis: we could contrast the molecular targets and pathways across studies and help focus the further search for interventions.” 

Alas, the results of most longevity studies are difficult to compare. This is in part because there are no clear, universally accepted standards for conducting such experiments or even for reporting such data. The situation is worsened by the fact that the authors often do not describe experimental conditions completely. As a result, works on longevity make up a set of precedents, each of which might be interesting in its own right, yet incoherent and incomparable at least for the reason that in a general context, it may indicate, for example, not prolonging the life of an average organism, but compensating for any genetic abnormalities of a particular sample or inappropriate living conditions. 

“Here we point out specific issues and propose solutions for quality control by checking both inter- and intra-study consistency of lifespan data.”

DOI - https://doi.org/10.18632/aging.205604

Corresponding author - Leonid Peshkin - pesha@hms.harvard.edu

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Keywords - aging, animal disease models, survival modeling, data standardization

About Aging-US

Launched in 2009, Aging-US publishes papers of general interest and biological significance in all fields of aging research and age-related diseases, including cancer—and now, with a special focus on COVID-19 vulnerability as an age-dependent syndrome. Topics in Aging-US go beyond traditional gerontology, including, but not limited to, cellular and molecular biology, human age-related diseases, pathology in model organisms, signal transduction pathways (e.g., p53, sirtuins, and PI-3K/AKT/mTOR, among others), and approaches to modulating these signaling pathways.

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Aging (Aging-US)

A Call for Standardization of Controls in Lifespan Studies

BUFFALO, NY- June 12, 2024 – A new review paper was published in Aging (listed by MEDLINE/PubMed as "Aging (Albany NY)" and "Aging-US" by Web of Science) Volume 16, Issue 10, entitled, “Peripheral vascular dysfunction and the aging brain.”

Aging is the greatest non-modifiable risk factor for most diseases, including cardiovascular diseases (CVD), which remain the leading cause of mortality worldwide. In their new review, researchers Devin Wahl and Zachary S. Clayton from Colorado State University and the University of Colorado note that robust evidence indicates that CVD are a strong determinant for reduced brain health and all-cause dementia with advancing age. 

“CVD are also closely linked with peripheral and cerebral vascular dysfunction, common contributors to the development and progression of all types of dementia, that are largely driven by excessive levels of oxidative stress (e.g., reactive oxygen species [ROS]).”

Emerging evidence suggests that several fundamental aging mechanisms (e.g., “hallmarks” of aging), including chronic low-grade inflammation, mitochondrial dysfunction, cellular senescence and deregulated nutrient sensing contribute to excessive ROS production and are common to both peripheral and cerebral vascular dysfunction. Therefore, targeting these mechanisms to reduce ROS-related oxidative stress and improve peripheral and/or cerebral vascular function may be a promising strategy to reduce dementia risk with aging. Investigating how certain lifestyle strategies (e.g., aerobic exercise and diet modulation) and/or select pharmacological agents (natural and synthetic) intersect with aging “hallmarks” to promote peripheral and/or cerebral vascular health represent a viable option for reducing dementia risk with aging. 

“Therefore, the primary purpose of this review is to explore mechanistic links among peripheral vascular dysfunction, cerebral vascular dysfunction, and reduced brain health with aging. Such insight and assessments of non-invasive measures of peripheral and cerebral vascular health with aging might provide a new approach for assessing dementia risk in older adults.”

DOI - https://doi.org/10.18632/aging.205877

Corresponding authors - Devin Wahl - devin.wahl@colostate.edu, and Zachary S. Clayton - zachary.clayton@colorado.edu

Video short - https://www.youtube.com/watch?v=0gx9DklNZVM

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Keywords - aging, peripheral vascular health, cerebrovascular health, cognitive function, dementia

About Aging-US

Aging publishes research papers in all fields of aging research, including but not limited to aging processes (from yeast to mammals), cellular senescence, age-related diseases (such as cancer and Alzheimer’s disease) and their prevention and treatment, anti-aging strategies and drug development, and, importantly, the role of signal transduction pathways in aging (such as mTOR) and potential approaches to modulate these signaling pathways to extend lifespan.

The journal aims to promote 1) treatment of age-related diseases by slowing down aging, 2) validation of anti-aging drugs by treating age-related diseases, and 3) prevention of cancer by inhibiting aging. (Cancer and COVID-19 are age-related diseases.)

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The Aging Brain and Peripheral Vascular Dysfunction

Werner syndrome (WS) is a rare genetic disorder marked by the premature onset of features typically associated with normal aging. This autosomal recessive condition manifests in individuals who generally develop normally until adolescence. As the syndrome progresses, affected individuals are predisposed to age-related diseases much earlier in life. These conditions include cataracts, type 2 diabetes, atherosclerosis, osteoporosis, and various cancers. The underlying cause of Werner syndrome is believed to be mutations in the WRN gene, which encodes a RecQ helicase crucial for DNA repair and replication.

Despite the accelerated aging, cognitive function remains unaffected in individuals with WS, providing a unique model for studying the mechanisms of aging and exploring potential therapeutic interventions. Although extensive research has been conducted, the precise mechanisms underlying these effects remain elusive.

On May 24, 2024, researchers Lucie Aumailley, Marie Julie Dubois, André Marette, and Michel Lebel from Université Laval published research paper chosen as the cover of Aging’s Volume 16, Issue 10, entitled, “Integrated liver and serum proteomics uncover sexual dimorphism and alteration of several immune response proteins in an aging Werner syndrome mouse model.” Recognizing the limitations of traditional investigative approaches, Aumailley et al. utilized advanced proteomics in their study. Proteomics allows the simultaneous identification and quantification of hundreds of proteins, providing a comprehensive analysis of liver and serum proteome profiles from wild-type and WRN mutant mice at different ages to uncover biological processes influenced by age and genotype.

Full blog - https://aging-us.org/2024/06/werner-syndrome-and-the-power-of-proteomics/

Paper DOI - https://doi.org/10.18632/aging.205866

Corresponding author - Michel Lebel - michel.lebel@crchudequebec.ulaval.ca

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Keywords - aging, proteomics, Werner syndrome, fatty liver, sexual dimorphism, immunoglobulins

About Aging-US

Aging publishes research papers in all fields of aging research, including but not limited to aging processes (from yeast to mammals), cellular senescence, age-related diseases (such as cancer and Alzheimer’s disease) and their prevention and treatment, anti-aging strategies and drug development, and, importantly, the role of signal transduction pathways in aging (such as mTOR) and potential approaches to modulate these signaling pathways to extend lifespan.

The journal aims to promote 1) treatment of age-related diseases by slowing down aging, 2) validation of anti-aging drugs by treating age-related diseases, and 3) prevention of cancer by inhibiting aging. (Cancer and COVID-19 are age-related diseases.)

Please visit our website at https://www.Aging-US.com​​ and connect with us:

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Werner Syndrome and the Power of Proteomics

A traditional, twice-monthly, peer-reviewed, open-access journal covering all areas of research on aging and age-related diseases, including cancer and now, with a special focus on COVID-19 vulnerability as an age-dependent syndrome.

Read about the Aging (Aging-US) Scientific Integrity Process: https://aging-us.com/scientific-integrity

A Call for Standardization of Controls in Lifespan Studies

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