It’s possible that I shall make an ass of myself. But in that case one can always get out of it with a little dialectic. I have, of course, so worded my proposition as to be right either way (K.Marx, Letter to F.Engels on the Indian Mutiny)
Wednesday, January 10, 2024
Agility in cultural heritage management—Advancing competence within uncertainty as a sustainable and resilient adaptation to processes of dynamic change
The intense changes in our modern society and the associated challenges are constantly increasing, not least due to the meta-crisis of climate change. Yet our approach to cultural heritage is still strongly influenced by the narrative of preservation. The article aims to find solutions within the interplay of preservation and change. Based on the psychological impact on society resulting from the current challenges, it is argued that cultural heritage experts need competencies in dealing with uncertainty and tolerance of ambiguity in order to provide security of action. The article applies insights from multiple disciplines to urban environment studies and advocates for a systemic understanding of cultural heritage as a prerequisite for sustainable and resilient adaptation to current challenges. It also contributes to a body of knowledge on what skills cultural heritage professionals need to be competent and confident in their daily work. The case study provides some valuable examples from Regensburg of Germany by taking an integrated and holistic approach that views the city as a multi-layered system in cultural heritage management.
Agility in Cultural Heritage Management—Advancing Competence Within Uncertainty as a Sustainable and Resilient Adaptation to Processes of Dynamic Change
Scripps Research scientists give new insight into a molecular target of alcohol
By investigating a molecule in the brain tied to cellular communication, scientists uncover important information about the proteins that do—and do not—influence alcohol drinking behavior.
LA JOLLA, CA— Ethanol—the compound found in alcoholic beverages—interferes with the normal functioning of a long list of biological molecules, but how each of these interactions contributes to the behavioral effects of alcohol is not fully understood. A guiding, but elusive, goal of researchers is to identify the protein (or proteins) to which ethanol binds that makes some people vulnerable to excessive drinking. Solving this question would point the way to effective therapies for alcohol use disorder, which affects more than 10% of the U.S. adult population and is responsible for a myriad of health and societal issues.
Previous studies identified one such molecule, a protein widely expressed in the brain, called the BK channel. Ethanol can directly interact with a component of BK channels, known as the α subunit, to facilitate their opening. However, scientists at Scripps Research found that this interaction may not drive behaviors related to alcohol abuse as much as previously thought. Their study, appearing in the journal Molecular Psychiatry on December 22, 2023, demonstrates that preventing ethanol from interacting with the BK α subunit does not reduce or increase the motivation to consume alcohol in mice.
The relationship between the BK α subunit and ethanol had previously been explored in vitro, ex vivo and in live invertebrates. Previous studies suggested that the BK α subunit was involved in an animal’s response to alcohol exposure, but there was a gap in understanding its role in mammals, particularly for the control of alcohol drinking.
“Knowing what a molecule does from in vitro experiments really doesn’t tell you much about what the behavioral consequences of that action might be,” says senior author Candice Contet, PhD, associate professor in the Department of Molecular Medicine at Scripps Research. “Things get complicated in vivo, because there are many layers of modulation that may occur in a cell-type specific manner. Moreover, the initial effect often changes with repeated or prolonged exposure to alcohol. We thus sought to determine whether the ability of ethanol to alter BK channel activity was in any way influencing the motivation to drink alcohol.”
Tackling this question didn’t lend itself well to conventional pharmacological testing: blocking BK channels with a drug causes tremors, which then interfere with drinking behavior. However, Contet’s collaborator Alex Dopico, MD, PhD, of the University of Tennessee, had identified a residue in the mouse BK α subunit that is required for ethanol to activate BK channels but is dispensable for normal BK channel activity, as shown in frog eggs. In the new study, Contet and her colleagues leveraged this discovery to unlock the significance of ethanol’s interaction with BK channels for alcohol drinking in mice.
Accordingly, the team tested mice that had a mutation in this particular BK α subunit residue. First, they found that the mutation prevented alcohol from altering the firing properties of neurons in the medial habenula, a brain region with high levels of BK channels, thereby demonstrating that it also confers resistance to ethanol in mouse brain cells, not just in frog eggs. At the behavioral level, the mice harboring the mutation did not display any anomalies when compared to control littermates. Notably, they exhibited the standard signs of intoxication upon alcohol injection, such as loss of balance and hypothermia, and they consumed the same amount of alcohol when tested under various conditions of moderate or excessive drinking.
“The lack of effect of the mutation was surprising, especially in light of our previous results showing that other BK channel subunits, β1 and β4, influence alcohol intake escalation in the same model of alcohol dependence,” says Contet. “However, these negative results, which were replicated in multiple cohorts and both sexes, are just as important as positive ones, because they encourage the field to study other targets rather than focusing on the wrong culprit.”
While the study does not point to a critical role of the BK α subunit in the motivation to drink alcohol or several physiological responses related to ethanol intoxication and withdrawal, the group will continue to explore whether the molecular target plays a role in other aspects of alcohol use disorder.
“Ethanol is highly pleiotropic. Beyond its reinforcing effects, it alters the functioning of multiple organs and cell types,” Contet says. “It is likely that ethanol’s interaction with BK channels contribute to some of these effects, but we've only explored the tip of the iceberg so far; the next challenge will be to find the right experimental readout.”
In addition to Contet, authors of the study, “Ethanol’s interaction with BK channel α subunit residue K361 does not mediate behavioral responses to alcohol in mice,” include Agbonlahor Okhuarobo, Max Kreifeldt, Pauravi Gandhi, Catherine Lopez, Briana Martinez, Kiera Fleck, Michal Bajo, Pushpita Bhattacharyya, Marisa Roberto and Amanda Roberts of Scripps Research; Alex Dopico of the University of Tennessee Health Science Center; and Gregg Homanics of the University of Pittsburgh.
This work was supported by funding from the National Institutes of Health (AA020913, AA006420, AA026685, AA027636, AA027372, AA020889, AA010422, AA021491, AA013498, AA011560, AA007456)
About Scripps Research
Scripps Research is an independent, nonprofit biomedical institute ranked one of the most influential in the world for its impact on innovation by Nature Index. We are advancing human health through profound discoveries that address pressing medical concerns around the globe. Our drug discovery and development division, Calibr, works hand-in-hand with scientists across disciplines to bring new medicines to patients as quickly and efficiently as possible, while teams at Scripps Research Translational Institute harness genomics, digital medicine and cutting-edge informatics to understand individual health and render more effective healthcare. Scripps Research also trains the next generation of leading scientists at our Skaggs Graduate School, consistently named among the top 10 US programs for chemistry and biological sciences. Learn more at www.scripps.edu.
JOURNAL
Molecular Psychiatry
Study highlights barriers to contraceptive access for disabled Medicare enrollees
PITTSBURGH — Contraceptive use is low among reproductive-aged people with disabilities who are enrolled in Medicare, according to a new study from the University of Pittsburgh that highlights how lack of contraceptive coverage by Medicare may prevent disabled enrollees from accessing contraception.
Published today in the January issue of Health Affairs, the study provides the first national overview of contraceptive use among enrollees in Medicare, the government health insurance for people over 65 and for people with qualifying disabilities. The researchers say that policy changes are needed to expand contraception coverage in Medicare and to ensure more equitable health care for people with disabilities, who already face barriers to reproductive health care and have higher rates of pregnancy complications and deaths than nondisabled people.
“The federal government requires that commercial insurers and Medicaid cover all contraceptive methods without cost sharing, but there is no similar requirement for Medicare, which means that disabled enrollees may not be able to access contraception or their preferred method of contraception,” said lead author Jacqueline Ellison, Ph.D., M.P.H., assistant professor in the Department of Health Policy and Management at the Pitt School of Public Health. “People with disabilities are already marginalized and experience barriers to accessing health care. It is unjust that they face additional cost-related barriers to receiving their contraceptive method of choice.”
Medicare does not require coverage for contraception to prevent pregnancies but may cover certain contraceptives for clinical indications such as endometriosis. Oral contraception may also be covered by Part D, an optional drug coverage benefit that costs extra. Patients may also be covered for other contraceptive methods by enrolling in Medicare Advantage, which is provided by private companies that contract with Medicare, but the scope of coverage depends on the company.
This complicated insurance landscape means that people with disabilities may not be able to access contraception or may be forced to pay out of pocket to access their preferred method of contraception.
In 2019, Medicare was the primary health insurance coverage for about 1.38 million reproductive-aged females with disabilities: About 941,000 had traditional Medicare and about 444,000 had Medicare Advantage. To understand more about patterns of contraceptive use among this population, Ellison and her team used two databases of insurance claims to analyze a study sample representing 17.2% of traditional Medicare and 9.5% of Medicare Advantage populations.
The researchers found that contraceptive use was low among reproductive-aged females with disabilities. Just 14.3% of traditional Medicare enrollees and 16.3% of those with Medicare Advantage had an insurance claim for contraception in 2019. In comparison, another study found that about 25% of reproductive-aged females with Medicaid — which is required to cover all forms of contraception — had such a claim in 2018.
The analysis also showed variation in contraceptive methods by type of Medicare coverage. For example, Medicare Advantage enrollees were about four times more likely to use an intrauterine device and 10 times more likely to have tubal ligation than those with traditional Medicare.
“This variation isn’t due to patient preference: There’s no reason that people with Medicare Advantage would be so much more likely than those with traditional Medicare to prefer using the intrauterine device or undergoing tubal sterilization,” explained Ellison. “This is a function of Medicare not requiring coverage for the full range of contraceptive methods.”
Medicare enrollees with noncontraceptive indications — such as acne, endometriosis, menstrual pain and irregular bleeding — were nearly twice as likely to use contraceptives as those without such an indication. This finding may highlight the importance of contraceptives for reasons beyond pregnancy prevention, or it may reflect clinicians documenting such an indication to help their patients get contraception when they otherwise would not have coverage.
“People with disabilities are more vulnerable to interference by guardians and clinicians in their reproductive decision making,” said Ellison. “It’s critical that, while ensuring access to the full range of contraceptive methods, we protect people with disabilities against such interference by ensuring contraceptive care provided in the Medicare program is truly person-centered.”
Other authors on the study were Sabnum Pudasainy, M.S., Deirdre Quinn, Ph.D., M.P.H, Sonya Borrero, M.D., M.S., Iris Olson, M.P.H., Qingwen Chen, M.S., and Marian Jarlenski, Ph.D., M.P.H., all of Pitt; and Meghan Bellerose, M.P.H., and Theresa I. Shireman, Ph.D., of Brown University.
This research was supported by the National Institute for Reproductive Health (5717077).
Contraceptive Use Among Traditional Medicare And Medicare Advantage Enrollees
ARTICLE PUBLICATION DATE
8-Jan-2024
Vaccine boosts innate immunity in people with dormant immune cells
Epigenetic cell states predict whether or not an individual profits from the “wake-up call” to the innate immune system that is provided by the BCG vaccine
Humans are protected by two branches of the immune system. Innate immunity provides built-in defense against widespread characteristics of bacteria and viruses, while adaptive immunity memorizes individual pathogens that a person has already encountered. Vaccines teach the adaptive immune system about new pathogens without having to go through an actual infection. This has greatly contributed to human health, but requires a specific vaccine for each major pathogen.
Some vaccines not only teach the adaptive immune system about a specific pathogen, but also increase the overall vigilance of our body’s innate immune cells. The BCG vaccine, which teaches our adaptive immune system to fight tuberculosis bacteria, has been shown to reduce infant mortality independent of its protection against tuberculosis. This observation can be explained by the concept of “trained immunity” – the idea that innate immune cells can switch between dormant and vigilant states, and are more effective at fighting infection when in their vigilant state.
Not every immune cell needs training
Inducing trained immunity by drugs or vaccines could confer protection in times of high infection risk, for example following a major surgery or during future pandemics before tailored vaccines become available. However, trained immunity is highly variable between individuals, and it is not well understood who may profit from inducing trained immunity.
To investigate this issue, a team led by Mihai Netea (Radboud University Medical Center) and Christoph Bock (CeMM & Medical University of Vienna) vaccinated 323 healthy volunteers with BCG and analyzed the effects on the immune system. They found that the induction of trained immunity was most effective in individuals with dormant innate immunity, which was reflected in a characteristic epigenetic cell state that predicted the vaccine response (Moorlag SJCFM, Folkman L, ter Horst R, Krausgruber T, et al. Immunity. 2024).
The team identified 213 individuals as trained immunity responders and 78 as non-responders, based on whether or not their production of inflammatory mediators had increased at day 90 after BCG vaccination – at a point when the acute response has subsided, but trained immunity is expected to persist. Trained immunity responders produced fewer mediators before vaccination and started with more dormant innate immune cells than non-responders. In other words, the non-responders already had the higher immune vigilance that the BCG vaccine induced in the responders.
Epigenetic regulation of immune balance
Both genetic and environmental factors contributed to this variability, but the most interesting differences were observed in the epigenetic states of the immune cells. Epigenetic cell states, implemented through changes in chromatin accessibility that make genes easier or harder to activate, reflect the regulatory plasticity of a cell and its ability to respond rapidly to changes in its environment, making them strong candidates for regulating trained immunity.
Indeed, in response to BCG vaccination, trained immunity responders gained open chromatin at genes involved in innate immunity, while non-responders carried such open chromatin independent of BCG vaccination, with no further increase following the vaccination. This finding explains how epigenetics allows immune cells to switch between different levels of immune vigilance, which contributes to the need to balance immune activity to provide protection against pathogens while avoiding unnecessary and harmful immune responses.
The study also clarifies a previously observed association between scar development at the site of BCG vaccination on the skin and lower child mortality. Previously, scar formation at the vaccine injection site was interpreted as a sign of a strong immune response to the vaccine. However, the team’s analyses offer an alternative explanation: it seems that scar formation reflects strong immunity prior to vaccination, and these individuals may be better protected against infections independent of BCG vaccination.
Enhancing immune vigilance
These results not only provide new insights into immune biology and the role of epigenetics, but also guide the development of future therapeutics. “We can envision a new class of drugs that deliberately wake up a dormant immune system,” Netea says. “Elderly people could receive a boost of their immune system prior to a planned hospital stay, and it may be possible to reactivate the suppressed immune system in patients with cancer. Several pharmaceutical companies are already pursuing ways to induce trained immunity without having to rely on the BCG vaccine.”
The new study provides important guidance for such endeavors. First, a better understanding of the biological pathways underlying trained immunity may uncover novel therapeutic targets. Second, the study shows that such therapeutics are only likely to benefit individuals with dormant innate immunity, who can be identified through chromatin profiling or functional immune assays. Third, no overshooting immune responses were observed in individuals with high innate immunity prior to vaccination, which bodes well for the safety of future trained immunity inducing drugs.
Bock summarizes: “Our study highlights the close connection between epigenetic cell states and trained immunity, allowing the human body to switch between vigilant and dormant innate immunity. This process is variable across individuals and may be exploited with precision medicine.”
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The study “Multi-omics analysis of innate and adaptive responses to BCG vaccination reveals epigenetic cell states that predict trained immunity” was published in Immunity on January 9, 2024. DOI: 10.1016/j.immuni.2023.12.005
Authors: Moorlag SJCFM*, Folkman L*, ter Horst R*, Krausgruber T*, Barreca D, Schuster LC, Fife V, Matzaraki V, Li W, Reichl S, Mourits VP, Koeken VACM, de Bree LCJ, Dijkstra H, Lemmers H, van Cranenbroek B, van Rijssen E, Koenen HJPM, Joosten I, Xu C-J, Li Y, Joosten LAB, van Crevel R, Netea MG#, Bock C# (* Contributed equally # Senior authors)
Funding: This study was supported by a Marie Skłodowska-Curie Actions Individual Fellowship (L.F.), an EMBO Postdoctoral Fellowship (R.t.H.), the European Research Council (M.G.N. and C.B.), the European Union’s Horizon 2020 research and innovation program (M.G.N. and L.A.B.J.), the Netherlands Organization for Scientific Research (M.G.N.), and two Austrian Science Fund Special Research Area grants (C.B.).
Christoph Bock is a Principal Investigator at the CeMM Research Center for Molecular Medicine of the Austrian Academy of Sciences and Professor of [Bio]Medical Informatics at the Medical University of Vienna. He is also the scientific coordinator of the Biomedical Sequencing Facility at CeMM, member of the Human Cell Atlas Organizing Committee, fellow of the European Lab for Learning and Intelligent Systems (ELLIS), and co-founder of a Vienna-based start-up company (Myllia Biotechnology). He has received major research awards, including an ERC Starting Grant (2016-2021), an ERC Consolidator Grant (2021-2026), the Otto Hahn Medal of the Max Planck Society (2009), the Overton Prize of the International Society for Computational Biology (2017), and the Erwin Schrödinger Prize of the Austrian Academy of Sciences (2022).
Mihai Netea heads the division of Experimental Medicine, Department of Internal Medicine, Radboud University Medical Center in Nijmegen. He is scientific founder of the biotech start-up companies Trained Therapeutix Discovery and Lemba, and of the biotech incubator Biotrip. He is mainly interested in understanding the memory traits of innate immunity (trained immunity) and has received major grants such as ERC Consolidator (2012-2017) and ERC Advanced (2019-2024). He is elected fellow of the Infectious Diseases Society of America, recipient of the van Loghem Award of the Netherlands Society of Immunology, and of the Spinoza Prize (2016). Since 2016 he is a member of the Netherlands Royal Academy of Sciences (KNAW).
The CeMM Research Center for Molecular Medicine of the Austrian Academy of Sciences is an international, independent and interdisciplinary research institution for molecular medicine under the scientific direction of Giulio Superti-Furga. CeMM is oriented towards medical needs and integrates basic research and clinical expertise to develop innovative diagnostic and therapeutic approaches for precision medicine. Research focuses on cancer, inflammation, metabolic and immune disorders, and rare diseases. The Institute's research building is located on the campus of the Medical University and the Vienna General Hospital.
The Medical University of Vienna is one of the most traditional medical education and research facilities in Europe. With almost 8,000 students, it is currently the largest medical training center in the German-speaking countries. With 6,000 employees, 30 departments and two clinical institutes, 13 medical theory centers and numerous highly specialized laboratories, it is one of Europe's leading research establishments in the biomedical sector. MedUni Vienna also has a medical history museum, the Josephinum.
FLORIDA STATE UNIVERSITY ASSOCIATE PROFESSOR OF SOCIOLOGY MATT HAUER LED A STUDY THAT FOUND THAT INDIRECT PROCESSES COULD CREATE 5.3 TO 18 TIMES THE NUMBER OF CLIMATE MIGRANTS AS THOSE DIRECTLY DISPLACED BY RISING SEAS. THE WORK WAS PUBLISHED BY THE PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES.
As climate change fuels sea level rise, younger people will migrate inland, leaving aging coastal populations — and a host of consequences — in their wake, a study by Florida State University researchers finds.
While destination cities will work to sustainably accommodate swelling populations, aging coastal communities will confront stark new challenges, including an outflow of vital human infrastructure such as health care workers, said Associate Professor of Sociology Matt Hauer, lead author of the study published in the Proceedings of the National Academy of Sciences.
“In the destination communities where populations are increasing you’ll need more dentists, doctors, service workers, construction workers, etc.,” Hauer said. “So by people moving, you affect other people’s likelihood of moving. You get a demographic amplification.”
Previous studies estimated where people are likely to move as a changing climate affects livability. Hauer’s study also incorporates demographic data and secondary effects that revealed a host of challenges awaiting both the coastal “sender” communities and their destination counterparts.
“Imagine young families moving out of areas like Miami and moving to other locations and starting a family there,” he said. “And just by the fact that there’s more people who have moved there, these indirect population processes draw even more people.”
The study concluded that these indirect processes could create 5.3 to 18 times the number of climate migrants as those directly displaced by rising seas. It also found that by 2100, median age in coastal communities could spike as much as 10 years.
“Think about who are more unlikely to move and who will be left behind in these communities; it tends to be the oldest,” Hauer said. “Because migration is most likely to occur in more youthful populations, areas experiencing accelerated out-migration could face accelerated population aging.”
Doctoral student Sunshine Jacobs and computational scientist Scott Kulp co-authored the study with Hauer.
The researchers developed a migration model that uses sea level rise data from Climate Central and information about migration patterns from the U.S. Internal Revenue Service. That tool allowed them to predict migration on a county-by-county basis across the country. Jacobs said the model can be adapted to research different hazards that go beyond encroaching seas.
“We only looked at sea level rise,” she said. “Imagine other hazards that we know cause people to move, like heat events, wildfires and economic hazards. The future uses and implications of the model are amazing.”
This work was supported by the State of Louisiana, the American Society of Adaptation Professionals, the New York State Energy Research Development Authority, and the Great Lakes Integrated Sciences Assessment.
In recent years, research has begun to reveal that the lines of communication between the body’s organs are key regulators of aging. When these lines are open, the body’s organs and systems work well together. But with age, communication lines deteriorate, and organs don’t get the molecular and electrical messages they need to function properly.
A new study from Washington University School of Medicine in St. Louis identifies, in mice, a critical communication pathway connecting the brain and the body’s fat tissue in a feedback loop that appears central to energy production throughout the body. The research suggests that the gradual deterioration of this feedback loop contributes to the increasing health problems that are typical of natural aging.
The study — published Jan. 8 in the journal Cell Metabolism — has implications for developing future interventions that could maintain the feedback loop longer and slow the effects of advancing age.
The researchers identified a specific set of neurons in the brain’s hypothalamus that, when active, sends signals to the body’s fat tissue to release energy. Using genetic and molecular methods, the researchers studied mice that were programmed to have this communication pathway constantly open after they reached a certain age. The scientists found that these mice were more physically active, showed signs of delayed aging, and lived longer than mice in which this same communication pathway gradually slowed down as part of normal aging.
“We demonstrated a way to delay aging and extend healthy life spans in mice by manipulating an important part of the brain,” said senior author Shin-ichiro Imai, MD, PhD, the Theodore and Bertha Bryan Distinguished Professor in Environmental Medicine and a professor in the Department of Developmental Biology at Washington University. “Showing this effect in a mammal is an important contribution to the field; past work demonstrating an extension of life span in this way has been conducted in less complex organisms, such as worms and fruit flies.”
These specific neurons, in a part of the brain called the dorsomedial hypothalamus, produce an important protein — Ppp1r17. When this protein is present in the nucleus, the neurons are active and stimulate the sympathetic nervous system, which governs the body’s fight or flight response.
The fight or flight response is well known for having broad effects throughout the body, including causing increased heart rate and slowed digestion. As part of this response, the researchers found that the neurons in the hypothalamus set off a chain of events that triggers neurons that govern white adipose tissue — a type of fat tissue — stored under the skin and in the abdominal area. The activated fat tissue releases fatty acids into the bloodstream that can be used to fuel physical activity. The activated fat tissue also releases another important protein — an enzyme called eNAMPT — which returns to the hypothalamus and allows the brain to produce fuel for its functions.
This feedback loop is critical for fueling the body and the brain, but it slows down over time. With age, the researchers found that the protein Ppp1r17 tends to leave the nucleus of the neurons, and when that happens, the neurons in the hypothalamus send weaker signals. With less use, the nervous system wiring throughout the white adipose tissue gradually retracts, and what was once a dense network of interconnecting nerves becomes sparse. The fat tissues no longer receive as many signals to release fatty acids and eNAMPT, which leads to fat accumulation, weight gain and less energy to fuel the brain and other tissues.
The researchers, including first author Kyohei Tokizane, PhD, a staff scientist and a former postdoctoral researcher in Imai’s lab, found that when they used genetic methods in old mice to keep Ppp1r17 in the nucleus of the neurons in the hypothalamus, the mice were more physically active — with increased wheel-running — and lived longer than control mice. They also used a technique to directly activate these specific neurons in the hypothalamus of old mice, and they observed similar anti-aging effects.
On average, the high end of the life span of a typical laboratory mouse is about 900 to 1,000 days, or about 2.5 years. In this study, all of the control mice that had aged normally died by 1,000 days of age. Those that underwent interventions to maintain the brain-fat tissue feedback loop lived 60 to 70 days longer than control mice. That translates into an increase in life span of about 7%. In people, a 7% increase in a 75-year life span translates to about five more years. The mice receiving the interventions also were more active and looked younger — with thicker and shinier coats — at later ages, suggesting more time with better health as well.
Imai and his team are continuing to investigate ways to maintain the feedback loop between the hypothalamus and the fat tissue. One route they are studying involves supplementing mice with eNAMPT, the enzyme produced by the fat tissue that returns to the brain and fuels the hypothalamus, among other tissues. When released by the fat tissue into the bloodstream, the enzyme is packaged inside compartments called extracellular vesicles, which can be collected and isolated from blood.
“We can envision a possible anti-aging therapy that involves delivering eNAMPT in various ways,” Imai said. “We already have shown that administering eNAMPT in extracellular vesicles increases cellular energy levels in the hypothalamus and extends life span in mice. We look forward to continuing our work investigating ways to maintain this central feedback loop between the brain and the body’s fat tissues in ways that we hope will extend health and life span.”
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Tokizane K, Brace CS, Imai S. DMHPpp1r17 neurons regulate aging and lifespan in mice through hypothalamic-adipose inter-tissue communication. Cell Metabolism. Jan. 8, 2024. https://doi.org/10.1016/j.cmet.2023.12.011
This work was supported by the National Institute on Aging of the National Institutes of Health (NIH), grant numbers AG037457 and AG047902; the American Federation for Aging Research; the Tanaka Fund at Washington University School of Medicine; a Glenn Foundation for Medical Research Postdoctoral Fellowship; and a Tanaka Scholarship. The content is solely the responsibility of the authors and does not necessarily represent the official views of the NIH.
About Washington University School of Medicine
WashU Medicine is a global leader in academic medicine, including biomedical research, patient care and educational programs with 2,800 faculty. Its National Institutes of Health (NIH) research funding portfolio is the third largest among U.S. medical schools, has grown 52% in the last six years, and, together with institutional investment, WashU Medicine commits well over $1 billion annually to basic and clinical research innovation and training. Its faculty practice is consistently within the top five in the country, with more than 1,800 faculty physicians practicing at 65 locations and who are also the medical staffs of Barnes-Jewish and St. Louis Children’s hospitals of BJC HealthCare. WashU Medicine has a storied history in MD/PhD training, recently dedicated $100 million to scholarships and curriculum renewal for its medical students, and is home to top-notch training programs in every medical subspecialty as well as physical therapy, occupational therapy, and audiology and communications sciences.
