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    Home > Active Ingredient News > Study of Nervous System > An inventory of the latest advances in aging research

    An inventory of the latest advances in aging research

    • Last Update: 2021-03-02
    • Source: Internet
    • Author: User
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    January 31, 2021 // --- Everyone is destined to face an old day from birth.
    development of science and technology may be able to alleviate the rate of aging.
    but carefully screened for specific methods.
    such as the recently popular "stem cell therapy" to prevent aging research projects, the actual effect may not be as effective as it is advertised.
    , can advances in science and technology ease the aging process? What can we do to slow down the pace of aging? In response to these questions, the editor has compiled some recent research progress on aging, hoping to inspire readers and friends.
    1.Science: Inhibiting the breakdown of glutamine, which inhibits renal glutaminease dependence, eliminates aging cell doi:10.1126/science.abb5916; Doi:10.1126/science.abf6368 In a new study, researchers from research institutions such as the University of Tokyo, Keeto University and Kyusju University in Japan found that glutamine decomposition, which inhibits kidney-type glutamatease (KGA) dependence in mice, can eliminate aging cells.
    the study was published in the January 15, 2021 issue of the journal Science, under the title "Senolysis by glutaminolysis resedion ameliorates agency age-associated disorders."
    paper, they describe the use of RNA interference (RNAi) to find enzymes needed for senescing cells to survive, which then induce their death.
    images from University of Tokyo.
    study involved using RNA interference to find enzymes needed for senescing cells to survive.
    this prompted them to study glutamine metabolism carefully, especially glutaminease 1 (glutaminase 1, GLS1).
    tests have shown that it is critical to the survival of senescing cells.
    , the researchers inhibited the glutamine enzyme 1 pathway in the mice.
    these changes had time to work, they found that suppressing this pathway led to the death of senescing cells.
    long term, they found that it also reduced age-related organ problems and obesity-related health problems.
    2.Nature interpretation! Scientists reveal immune drivers that induce the body's brain to age! doi:10.1038/s41586-020-03160-0 Scientists from Institutions such as Stanford University Medical Center have revealed the immune drivers that induce brain aging in a recent study published in the international journal Nature entitled "Restoring metabolism of myeloid cells reverses decline in the ageing".
    As if the Smokey Bear (the U.S. forest fire mascot) gets angry and starts to fire rather than extinguish fires, this may roughly describe the behavior of certain cells in the body's immune system, which become increasingly irritable as the body ages, not only not extinguishing the body's "fire", but causing chronic inflammation of the flame.
    Scientists have long believed that reducing inflammation slows the body's aging process, delaying age-related diseases such as heart disease, Alzheimer's disease, cancer and weakness;
    In the study, researchers from Stanford University Medical Center gave a clear answer, finding that if the results obtained in cell cultures in older mice and humans could be applied to the human body, it might suggest that pharmacological methods could be used to restore mental cognitive ability in older adult skirts.
    3. Can this "exercise protein" improve motor ability and extend life? doi:10.1038/s41467-020-20790-0 Everyone wants to grow old healthy, but the inevitable consequence of aging is a decline in metabolism and motor ability.
    new research shows that a hormone produced by the human body during exercise injected into laboratory mice of different ages can improve their motor skills and increase the life expectancy of older mice.
    this study provides a new research idea to solve the problem of decreasing the body's motor ability in the process of aging.
    so how is this hormone found and where is it produced? In fact, the peptide, made up of 16 amino acids, was discovered in the mitochondrial genome of the University of California Lee team back in 2015.
    protein is expressed in different tissues of the body, such as muscle tissue, and decreases as the body ages.
    does it play in mitochondrials? We know that mitochondrials are the source of energy for cells, and mitochondrials also play an important role in regulating metabolism through communication with other tissue cells, which is the ability to tell other cells or tissues how to use energy by releasing signals.
    mitochondrials play an important role in human metabolism and movement.
    if the mitochondrial is damaged or the mitochondrial function decreases with age, the mitochondrial's "communication ability" decreases and the body's ability to coordinate movement decreases.
    the protein (MOTS-c) discovered by Lee's team is the key to mitochondrial communication.
    researchers also call it the mitochondrial hormone or mitokine.
    4.Cell Rep: NAD plus can restore age-related muscle degeneration doi:10.1016/j.celrep.2020.108660 As we age, our muscles become weaker and people become hobbled.
    , however, the underlying causes of the biological processes and biomarkers that define muscle aging have not yet been determined.
    Now, a team of scientists from the Johan Auwerx laboratory at the EPFL School of Life Sciences looks at the similarities between muscle aging and degenerative muscle disease from another perspective.
    found protein aggregates deposited in skeletal muscles during natural aging, preventing this build-up from harmful features that prevent muscle aging.
    the study was published in the journal Cell Reports.
    photo source: www.pixabay.com.
    auwerx explains:
    During age-related muscle disease, it is difficult for our cells to maintain proper protein folding, causing these misfolded proteins to precipitate and form toxic protein aggregates in the muscles.
    most prominent component of these protein aggregates is β-amyloid, just like amyloid plaques in the brains of Alzheimer's patients.
    "5.Nat Neurosci: Revealing the effects of the immune response on the aging brain Doi:10.1038/s41593-020-00745-w As humans age, the function of the body's organs gradually declines.
    Although many studies in the past have analyzed the effects of aging on the body, brain and cognitive abilities, the neurological mechanisms and environmental factors that accelerate or mitigate these effects are little known to researchers.
    is well known that the immune system and nervous system play an important role in controlling the function of many organs of the body, and previous studies have shown that both systems change significantly during the body's aging process.
    neuroscience has found that as the nervous system ages, so does the way the body controls its immune response, but researchers still don't know how aging of the nervous system affects the body's immune response and the resulting effects on brain function.
    a recent study published in the international journal Nature Neuroscience, scientists from capital medical university and Tianjin Medical University analyzed the effects of immune responses on the likelihood of an aging brain; The degeneration of s, such as embryonic cells derived from nerve fibers, increases the toxicity of natural killer cells (NK cells), which can impair nerve development and cognitive function in the brain, a type of blood cell that belongs to the human body's immune system.
    6.Science Sub-Journal: Based on genome-wide screening, Chinese scientists have identified the gene KAT7doi:10.1126/scitranslmed.abd2655 to understand the genetic and exogenetic basis of cellular aging as essential for developing interventions to slow aging.
    although cell aging is known to promote aging, many of the mechanisms that control this process are still unknown.
    In a new study, researchers from the Chinese Academy of Sciences, the University of Chinese Academy of Sciences, Peking University and Xuanwu Hospital of capital medical universities used two types of human-to-human pregenesome cells (hMPCs) that exhibit accelerated aging to conduct a full genome-wide screening based on CRISPR-Cas9.
    two hMPCs are derived from human embryonic stem cells carrying disease-causing mutations in Werner syndrome, a disease that causes accelerated aging, and Hutchinson-Gilford progeria syndrome, respectively.
    results were published in the January 6, 2021 issue of the Journal of Science Translational Medicine under the title "A genome-wide CRISPR-base screenes out of KAT7 as a driver of cellular senescence".
    the authors identified missing genes that reduce cell aging, including KAT7.
    kat7 encodes a histogenetic acetyl transferase, ranking highest in both premature hMPC models.
    ineration of KAT7 reduced the acetylation of histamine H3 lysine, inhibited the transcription of p15INK4b, and alleviated hMPC aging.
    In addition, intravenous giving lysovirus vectors encoded Cas9/sg-Kat7 can reduce liver cell aging and liver aging in physiologically aging mice as well as early-aging Zmpste24-/- mice that exhibit premature aging esophysiology, extending life.
    7.Nature: Gene editing techniques used to treat premature aging doi:10.1038/s41586-020-03086-7 In a recent study, researchers successfully used DNA editing techniques to extend the lifespan of mice with genetic variants associated with premature aging, a rare genetic disease that causes extreme premature aging in children and may significantly shorten their life expectancy.
    the study was published in the journal Nature.
    , also known as Hutchinson-Gilford premature aging syndrome, is caused by a mutation in the nucleocleic protein A (LMNA) gene, one of which changes the DNA base C to T.
    this change increases the production of toxic protein progerin, which leads to a rapid aging process.
    for the study, researchers used a ground-breaking DNA editing technique that replaced a single DNA letter with another DNA letter without damaging the DNA, and further study how changing the mutation could affect early aging symptoms in mice.
    to test the effectiveness of its base editing method, the team initially worked with the Progeria Research Foundation to obtain connective tissue cells from patients with premature aging.
    team used the basic editor of the LMNA gene in the patient's cells in a laboratory setting.
    the treatment repairs mutations in 90 percent of cells.
    8.eLife: Small molecule ISR inhibitors are expected to bring the brain back to old age: 10.7554/eLife.62048 aging is an inevitable process for all living things.
    age-related cognitive decline is a emerging global problem as life expectancy increases.
    the accumulation of misfolded proteins during aging, which leads to chronic activation of integrated stress response (integrated stress, response ISR), an evolutionaryly conservative protein stabilization program activated by endosurance stress.
    drug-like small molecule ISR inhibitor (drug-like small molecules ISR inhibitor, ISRIB) has been shown to save behavioral and cognitive impairments caused by traumatic brain injury, and it is not clear whether similar methods can reduce age-related cognitive impairment.
    images from eLife, 2020, doi:10.7554/eLife.62048.
    a new study, Karen Krukowski et al. expanded the use of ISRIB: using it to rapidly reverse spatial memory impairment and improvement in preclinical models of aging in mice
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