Announcements

  • June 1, 2012

    In the brain, neurons use tightly controlled chemical and electrical signals to communicate with one another in complex networks. Low levels of a protein that facilitates these signals are associated with Alzheimer’s-related memory problems in a mouse model of the disease, according to NIH-supported scientists at the University of California, San Francisco. Restoring levels of the protein, known as Nav1.1, improved learning and memory in the mice and increased lifespan.

    The investigators measured brain-wave activity in mouse models with high levels of beta-amyloid, a pathological hallmark of Alzheimer’s, in the brain. They found that specific abnormalities occurred during periods of reduced gamma-wave oscillations, a type of brain wave involved in regulating learning and memory. They further found that Nav1.1 levels in specialized nerve cells known as parvalbumin cells were decreased in these mice, suggesting an association between reduced Nav1.1 levels and abnormal brain-wave activity. The mice also had impaired memory and decreased lifespan compared with normal mice. However, when Nav1.1 levels were restored, brain-wave activity returned to normal, memory improved, and lifespan increased, despite the continued presence of high levels of beta-amyloid in the brain.

    Further research is needed to see if these findings might extend from mice to humans. But, these observations provide important clues about a potential mechanism involved in network and cognitive dysfunctions. Gamma wave alterations like those addressed in this Alzheimer’s study also occur in other neurological disorders, including epilepsy, autism, and schizophrenia, suggesting that these findings may have implications for these conditions as well.

    Reference: Verret L., et al. Inhibitory interneuron deficit links altered network activity and cognitive dysfunction in Alzheimer model. Cell 149: 708-721, April 27, 2012.

  • June 1, 2012

    In two recent studies, NIA-supported investigators identified a surprising new candidate drug treatment for Alzheimer’s disease (AD) and determined a potential mechanism of action for the compound.

    In the first study, researchers demonstrated that bexarotene, a skin cancer drug, reversed AD symptoms in a mouse model of the disease. Researchers at Case Western Reserve University School of Medicine in Cleveland found that within 72 hours of treatment, bexarotene reversed social, cognitive, and olfactory deficits and cleared beta amyloid—a pathological hallmark of AD—from the mice’s brains. Bexarotene treatment was effective in both early and later stages of Alzheimer’s in the mice. The investigators emphasize that while these findings are promising, there is further need for translational research from the animal studies to examine the efficacy of bexarotene in people with AD.

    A second article by researchers at the Indiana University School of Medicine in Indianapolis established a potential mechanism of action for bexarotene. Investigators with the Alzheimer’s Disease Neuroimaging Initiative (ADNI) genotyped 103 ADNI participants and identified a variant of the DHCR 24 gene that was associated with lower brain amyloid levels compared to people without the gene, suggesting that this variant may have a neuroprotective effect. Researchers believe that bexarotene may act through the DHCR 24 pathway, providing further support for continued investigation of bexarotene. Specifically, these findings encourage more studies to evaluate the gene’s possible role in AD pathogenesis.

    References:

    Cramer, P. E., et al. ApoE-directed therapeutics rapidly clear β-amyloid and reverse deficits in AD mouse models. Science. 2012 Mar 23;335(6075):1503-6. Epub 2012 Feb 9.

    Swaminathan S., et al. Amyloid pathway-based candidate gene analysis of [11C]PiB-PET in the Alzheimer's Disease Neuroimaging Initiative (ADNI) cohort, Brain Imaging and Behavior, (2012) 6:1-15. 8.

  • July 25, 2012

    Registration is now open for “Unveiling the NIH Toolbox,” a free scientific conference to be held September 10-11 in Bethesda, Maryland. The meeting will present the NIH Toolbox for Assessment of Neurological and Behavioral Function— a set of brief but comprehensive neurological and behavioral health measurements designed for use particularly in large-scale research studies such as epidemiological studies or clinical trials. Developed by a team of more than 250 scientists from nearly 100 academic institutions, the NIH Toolbox provides a battery of on-line and royalty-free measures of motor, cognitive, sensory and emotional function for study participants aged 3 to 85 years. Developed under the auspices of the NIH Blueprint for Neuroscience Research, a coalition that creates new tools and resources to advance neuroscience research, the highly anticipated NIH Toolbox promotes economies of scale and enhanced efficiency in measurement.

    The meeting will feature lectures, interactive demonstrations, and panel discussions about the development, testing and use of the NIH Toolbox in biomedical research. An optional “Administering the NIH Toolbox” training workshop follows the conference on September 12-15. To register for the conference and/or training workshop, or to learn more about the NIH Toolbox, go to www.nihtoolbox.org.

  • August 8, 2013

    The NIA Grants for Early Medical/Surgical Specialists’ Transition to Aging Research (GEMSSTAR) program provides research grant support to early-stage physicians seeking to bridge their clinical specialty with aging research. This program particularly targets clinician-scientists who have recently completed their residency or fellowship training and are embarking on their first faculty position. In order to receive NIA-funded support for their research project, successful candidates must also secure non-NIH funds to support an individual Professional Development Plan.

    The receipt date for RFA-AG-14-010 is October 21, 2013.

    See detailed information and FAQs »

  • July 12, 2012

    Posiphen, a drug candidate designed and developed by researchers in the NIA’s Intramural Research Program, has been shown in three small, early studies to be well-tolerated and to reduce the generation of amyloid and tau protein—the hallmarks of Alzheimer’s disease—in older people at risk for developing the disorder. The series of dosing, tolerability, and “proof of mechanism” studies was conducted by an international group of investigators testing a pill form of the drug Posiphen during trials of seven to ten days in healthy volunteers and those with mild cognitive impairment (MCI), a condition that often progresses to Alzheimer’s. The report of the research appeared online July 11, 2012 in the Journal of Neurology, Neurosurgery & Psychiatry.

    Posiphen was determined to readily enter the brain and in cerebrospinal fluid tests, scientists found that the drug lowered levels of amyloid, tau, and inflammation—all key targets in the effort to find therapies for Alzheimer’s. Researchers believe the drug may work by inhibiting the production of neurotoxic products that derive from amyloid precursor protein, or APP, and result in the accumulation of abnormal clumps of amyloid. While the finding is preliminary, it does provide key data to move the drug forward for further human testing.

    Reference: Maccecchini, M., et al. Posiphen as a candidate drug to lower CSF amyloid precursor protein, amyloid-b peptide and s levels: target engagement, tolerability and pharmacokinetics in humans. Journal of Neurology, Neurosurgery & Psychiatry. Doi: 10.1136/jnnp-2012-302589.

  • June 29, 2012

    The creation of the first iteration of the Common Alzheimer Disease Research Ontology (CADRO) is a collaborative effort between the National Institute on Aging (NIA) and the Alzheimer’s Association (AA). The project began in May 2010 for the purpose of conducting a comparative analysis of the NIA and AA Alzheimer’s disease (AD) research portfolios. See International Alzheimer's Disease Research Portfolio.

    The purpose of this effort is to inform the development of a comparative analysis of research portfolios among multiple funders of AD research, inform strategic planning and priority-setting, and support coordination by federal and non-federal agencies supporting AD research in the United States and internationally.

    The ultimate goal of this project is to support communication and facilitate in the sharing of priorities among federal and non-federal agencies that support AD research.

    For more information see CADRO.

  • June 25, 2012

    Investigators have identified interventions that extend lifespan in model systems. For example, caloric restriction (CR) – a reduction in caloric intake while maintaining adequate nutrition – has been shown to increase insulin sensitivity, improve health, and extend lifespan in several organisms.  Although scientists do not fully understand the mechanisms through which CR may work, it is generally believed that it functions at least in part through inhibition of the protein complex mTORC1. Another intervention, the immunosuppressive drug rapamycin, extends the lifespans of yeast, flies, and mice, also by inhibiting mTORC1. However, unlike CR, long-term use of rapamycin causes insulin resistance in rodents; in humans, that could lead to diabetes and decreased lifespan.

    NIH-supported investigators recently found that rapamycin disrupts a second protein complex, mTORC2, in mice, and that mTORC2 is required for efficient equilibrium between glucose production and consumption. When scientists decoupled protein complexes mTORC1 and mTORC2 in mice, they found that decreasing mTORC1 signaling alone extended lifespan without changes in glucose tolerance or insulin sensitivity. However, reduction in mTORC2 activity was associated with impaired insulin sensitivity in the liver and no increase in life span.  

    These findings suggest  that rapamycin confers longevity through inhibition of mTORC1 and negatively effects glucose control through inhibition of mTORC2.The investigators note that a compound that would inhibit just mTORC1 might provide many of the same benefits of rapamycin on health and longevity, without the side effects that currently limit rapamycin’s utility.

    Reference: Lamming DW, Le Y, Katajisto P, et al. Rapamycin-induced insulin resistance is mediated by mTORC2 loss and uncoupled from longevity. Science 335: 1638-1643, 2012. PubMed: http://www.ncbi.nlm.nih.gov/pubmed/22461615

  • July 10, 2012

    Taking the Next Step:   Grants Technical Assistance Workshop is an interactive forum for pre- and post-doctoral students and recent recipients of Ph.D., M.D., or related doctoral degrees with the National Institute on Aging, the world's largest funding source for research on aging and geriatrics. During this intensive 1.5 day workshop attendees will gain an understanding of the NIH grants process from application to award, and NIA staff will discuss research priorities and opportunities in the basic biology of aging, neuroscience, behavioral and social research and clinical geriatrics and gerontology. Attendees will have the opportunity to meet in small groups with NIA staff representative of their field of interest. A session focused on research and funding opportunities in health disparities and aging will highlight this GSA pre-conference workshop.

    Applications are due July 20, 2012.

    The deadline for applications has been extended until August 10th.

    See more information and application.

  • June 11, 2012

    The Round 1 beta release public use files for the National Health and Aging Trends Study (NHATS) are now available at www.nhats.org.   

  • June 6, 2012

    The National Institute on Aging and NIH are working with a team of federal agencies to encourage older adults to register as organ donors. Led by the Health Resources and Services Administration and launched during Older Americans Month in May 2012, the new campaign seeks to increase knowledge and interest about organ donation to people 50 and older, who comprise the majority of people receiving organ transplants.

    Last year, 60 percent of the people receiving organ transplants were 50 and older. Today, more than 114,000 people of all ages are on the waiting list for an organ.

    At the same time, more than 99 million people in the U.S. today are age 50 or older. But, more than 20 percent believe that they are too old to register as an organ donor.

    The website www.organdonor.gov now features information on organ donation geared toward people 50+. The site attempts to dispel myths about organ donation with advancing age and provides answers to several frequently asked questions. At www.organdonor.gov, you can find specific instructions on how to register to be an organ donor in your state. You can also register for organ donation when you renew your driver’s license.

    “Age doesn’t make you ineligible to sign up, nor do you have to be in perfect health,” says NIA Deputy Director Marie A. Bernard, M.D. “Your ability to donate is determined by a doctor at the time of death.

    “More people today are living healthier lives and know about the importance of living and eating well and exercising,” Dr. Bernard continues. “That means we’re in better shape than ever. We’re also able to be donors and recipients at later ages than anyone might have imagined. The NIA joins the effort to encourage people 50 and older to think about organ donation and the power such a gift has to save lives and health of family, friends, and neighbors.”

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