Announcements

  • April 8, 2015

    Subject: Dr. Luigi Ferrucci, May 7 at the GeroScience Interest Group (GSIG) spring seminar (Open to the Public)

    When: Thursday, May 7, 2015, 12:00 PM – 1:00 PM

    Where: Masur Auditorium, Building 10, NIH

    Title: "Is Inflammation a Hallmark of Aging?"

    Open to the Public (please allow time for the NIH security check)

    The Trans-NIH GeroScience Interest Group (GSIG) cordially invites you to its spring seminar, featuring Dr. Luigi Ferrucci. Dr. Ferrucci is a geriatrician and epidemiologist who conducts research on the causal pathways leading to progressive physical and cognitive decline in older persons. Dr. Ferrucci has made major contributions in the design of many epidemiological studies conducted in the U.S. and in Europe, including the European Longitudinal Study on Aging, the "ICare Dicomano Study," the AKEA study of Centenarians in Sardinia and the Women's Health and Aging Study. He was also the Principal Investigator of the InCHIANTI study, a longitudinal study conducted in the Chianti Geographical area (Tuscany, Italy). After serving for several years as Director of the Baltimore Longitudinal Study on Aging (BLSA). Dr. Ferrucci became the Scientific Director of the NIA’s Intramural Research Program in 2011.

    The GeroScience Interest Group (GSIG) was formed to enhance opportunities for discussion of the intersection between the biology of aging and the biology of disease and conditions that are of interest across ICs. It is focused on basic biology, but with a longer view towards translation. If you are interested in learning more, please visit the GSIG web site (http://sigs.nih.gov/geroscience/Pages/default.aspx).

    The seminar will be videocast at http://videocast.nih.gov/ and archived in the GSIG web site.

    Sign Language Interpreters will be provided. Individuals with disabilities who need reasonable accommodation to participate in this event should contact Dr. Ronald Kohanski at kohanskir@mail.nih.gov or at 301/496-6402.

    Please send your questions related to the seminar to kohanskir@mail.nih.gov.

  • March 31, 2015

    Do you work with patients or clients with cognitive impairment? Visit our new online portal for free clinical practice tools, training materials, and other resources for physicians, nurses, social workers, and other professionals.

    You’ll find:

    • Tools for assessment, diagnosis, treatment, and management
    • Disease-specific information
    • Professional training and curricula
    • Information about clinical trials and studies
    • Patient communication and care tips
    • Patient and caregiver education materials

    Help us spread the word about these tools and resources. Share via social media:
    Get professional #Alzheimers/dementia care tools & materials for your practice from this @Alzheimers_NIH resource http://1.usa.gov/1aQILet

  • March 23, 2015

    Researchers are making great advances in identifying potential new ways to help diagnose, treat, and even prevent Alzheimer’s disease. But it will take many people, including older adults, volunteering for research studies and trials to help find the answers. Find out what you can do. Visit our new webpage—Volunteer for Alzheimer’s Research—to:

    • Learn more about participating in research
    • Find a clinical trial or study
    • Get an infographic and more information
    • Watch videos from researchers and study participants
    • Locate an Alzheimer’s Disease Research Center

    Help us spread the word about the importance of volunteering for Alzheimer’s research. Find social media messages on our website and share the infographic with the following message:

    YOU can make a difference in the fight against #Alz by volunteering for #clinicaltrials http://1.usa.gov/1LiwWxO pic.twitter.com/FvYn1yMhhk

  • March 16, 2015

    Age-related brain lesions known as white matter hyperintensities (WMH) have been linked to movement problems and disabilities in late life. A recent study suggests that physically active older people may have fewer movement problems caused by WMH. The study, supported in part by NIA, was published online March 11, 2015, in Neurology.

    Brain imaging shows that WMH are common in older adults, and increased WMH levels have been linked with difficulty walking and other movement problems, according to researchers led by Dr. Debra A. Fleischman of the Rush University Alzheimer’s Disease Center, Chicago.

    Previous studies suggest that physical activity may enhance brain health by increasing blood flow and other vascular functions in the brain, thus reducing WMH burden. The new study found that physically active older adults with high levels of WMH had fewer motor problems than sedentary people with a high WMH burden.

    The research team measured total daily activity for 11 days in 167 older adults (average age 80) in the Rush Memory and Aging Project. All of the participants wore movement monitors on their wrists, took movement and strength tests, and underwent brain magnetic resonance imaging to determine the extent of WMH.

    These findings suggest that higher levels of physical activity in older adults may protect against loss of motor function despite the burden of WMH. However, further studies are needed to investigate other brain mechanisms and motor pathways that may influence movement.

    Reference: Fleischman DA, et al. Physical activity, motor function, and white matter hyperintensity burden in healthy older adults. Neurology. 2015;8:1-7.

  • March 9, 2015

    Researchers led by a team from the Mayo Clinic in Rochester, Minnesota, have identified a new class of drugs called “senolytics” that target and kill aged—senescent—cells in mice. The team also found that a single dose of senolytic drugs led to improvements in the animals’ health and function.

    Previous research has shown that genetically modifying mice to remove their senescent cells extended their health span. This study, published online on March 9, 2015, in Aging Cell, and funded in part by the National Institute on Aging at NIH, is the first to pharmacologically imitate the approach in a mouse model of extremely accelerated aging.

    Senescent cells have long been implicated in aging. Some rapidly dividing cells reach a point when they can no longer safely replicate; their telomeres become too short to protect the cell’s DNA. At this point, a cell will either destroy itself through a process called apoptosis, become dysfunctional (and potentially cancer-prone), or turn replication off but continues to survive. The cells that turn off are known as senescent. They can perform some functions, but they also release molecules that may increase risk for a variety of diseases, including cancer. 

    Senescent cells are not dead. In fact, they cannot die (on their own). This characteristic was key for determining a drug target.

    The two senolytic drugs tested, dasatinib and quercetin, were effective individually, but more powerful when used together. Days after a single dose, aged mice showed a notable improvement in heart function. Also, a single dose reversed the damaging effects of radiation on a limb, leading to a lasting improvement in exercise capacity. Longer term, periodic use of the drugs delayed a variety of age-related symptoms, including osteoporosis and frailty.

    While dasatinib is an FDA-approved cancer drug, and quercetin has been used by humans as an antioxidant supplement, the researchers cautioned that it is far too early to suggest that they be considered as a clinical intervention for aging. More research is needed to determine whether these and other senolytics have similar effects and are safe in animal models before studies regarding any application in humans can be designed and tested.

    Reference: Zhu Y, et al. The Achilles’ Heel of Senescent Cells: From Transcriptome to Senolytic DrugsAging Cell. 2015 Mar 9. doi: 10.1111/acel.12344 [Epub ahead of print]

  • March 4, 2015

    Dr. Nancy Nadon, lead scientist for NIA’s Intervention Testing Program, discusses the importance of using female, along with male, mice when determining the effects of compounds on health and longevity.

  • February 27, 2015

    Animal models are an essential resource in the research enterprise. Studies in flies, worms, mice, and even yeast, have led to breakthroughs in treating major health problems in humans, such as cancer, diabetes, and heart disease. These animals are also important in studying the basic biology of aging. They might not look anything like us on the outside, but deep in the cells, they share similar biological mechanisms and genes that contribute to physical changes and diseases associated with age. In addition, because most of these animals have a relatively short lifespan, researchers can test disease—and aging—interventions in a timely way.

    Now, researchers at the Stanford University School of Medicine have identified a new animal model for research on aging: the African turquoise killifish. It is the shortest lived vertebrate bred in the lab, with a lifespan of approximately 4 to 6 months. That is six times shorter than the lifespan of mice. Also, unlike mice, killifish have a similar telomere length to that of humans. This makes them particularly suited for studying genetics and telomere-related diseases.

    To help with future investigations, the Stanford scientists have developed a biological toolkit of the killifish and made it publically available to the research community. The toolkit includes the sequenced genome of the killifish, with a mapped location of specific genes involved in aging and age-related diseases; genomic data sets and gene models from experiments on 13 genes thought be associated with aging; and stable lines of fish with mutations in select genes.

    Reference: Harel I, et al. A platform for rapid exploration of aging and diseases in a naturally short-lived vertebrate, Cell, 2015, www.ncbi.nlm.nih.gov/pubmed/25684364.

  • February 25, 2015

    Cartoon of four people in conversation.

    The NIA announces an updated funding policy with important new information for Alzheimer’s disease researchers seeking grants. This year, fiscal year 2015, the NIA received an additional $25 million for research on Alzheimer’s disease. Dr. Robin Barr, Director of the Division of Extramural Activities, explains, “This year, we are moving to establish a separate, enhanced payline for Alzheimer’s funding while still reserving some support for initiatives and strategic priorities. In making that choice, we now expect that Alzheimer’s research will continue to have an enhanced payline relative to other fields in future years.”

    See the full blog post: Alzheimer's Disease Funding: Interim Update on Payline

    The NIA blog publishes weekly with information on grants and funding policy, research priorities, scientific meetings, and topics of interest to researchers and others in the scientific community. Subscribe to get it weekly in your email inbox, or grab the RSS feed.

  • February 23, 2015

    Researchers at UCLA’s David Geffen School of Medicine recently published the first study that provides definitive evidence that people with Down syndrome age at a faster rate. In the Feb. 9, 2015, online issue of Aging Cell, researchers led by Dr. Steve Horvath reported that they have applied an “epigenetic clock” developed for normal aging to tissues from people with Down syndrome.

    Down syndrome is not only associated with intellectual disability, but also with a group of clinical symptoms of accelerated aging. These include premature wrinkling and grey hair, early menopause, reduced immune function, and Alzheimer’s disease. Until now, it has not been clear whether these symptoms are actually due to accelerated aging processes in Down syndrome.

    The research team analyzed brain, blood, and buccal (cheek) tissue samples from up to 87 people with Down syndrome and calculated their epigenetic clock measure from patterns of DNA methylation. They found that Down syndrome did accelerate this measure of aging in all individuals, but that different types of tissue aged at different rates. For example, brain tissue shows a greater age acceleration effect (11 years) than blood (about 4 years). No sign of accelerated aging was seen in the buccal tissue.

    Reference: Horvath S, et al. Accelerated epigenetic aging in Down syndrome. Aging Cell. 2015 Feb 9. doi: 10.1111/acel.12325. [Epub ahead of print]

  • February 18, 2015

    Cartoon of four people in conversation.

    This is an extremely difficult time in aging research. Dr. Richard J. Hodes, NIA director, describes some of the challenges that lie ahead, as well as what the next fiscal year will bring. “While the scientific and fiscal challenges are very real, it is still an exciting time to be in aging and Alzheimer’s research,” writes Dr. Hodes.

    See the full blog post: Supporting Aging Research in Challenging Times

    The NIA blog publishes weekly with information on grants and funding policy, research priorities, scientific meetings, and topics of interest to researchers and others in the scientific community. Subscribe to get it weekly in your email inbox, or grab the RSS feed.

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