• 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:

  • 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   

  • 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 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, 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.”

  • June 5, 2012

    The Spring-Summer issue of Links: Minority Research & Training is now available! With this issue, Links has gone green, becoming an online-only publication. Enjoy the same great content, including findings from health disparities research, profiles of current and emerging leaders in the field, and highlights from NIA training programs, and also look for new features—videos!—in upcoming issues.

    The Spring-Summer issue includes:

    New to Links? The twice-yearly newsletter is part of NIA’s initiative to address health disparities and support scientists representing underserved populations. Subscribing is easy. We also invite you to visit NIA’s Minority Aging and Health Disparities web page, where you’ll find information about the Health Disparities Research Persons Network, training opportunities, and more.

  • May 30, 2012

    The National Institutes of Health is a partner in the new Next Avenue, a national public media project launched May 14, 2012, by PBS, focused on the growing 50+ population. NIH is collaborating with Next Avenue to share health information with this older audience, and the National Institute on Aging (NIA) is coordinating NIH’s participation in this effort.

     Next Avenue centers on an extensive website — Its “channels” focus on topic areas including health and wellness, money and security, caregiving, work and purpose, and living and learning. The site also includes information and perspectives with articles and blogs written by Next Avenue staff journalists and guest contributors.

     NIH is a primary content partner for health information on the site. “We are excited to be working with public television on Next Avenue,” said NIA Director Richard J. Hodes, M.D. “It is important that the free, evidence-based health and wellness information from NIA and other NIH institutes, much of it based on the research we support and conduct on behalf of the public, is offered to as broad an audience as possible.”

     Next Avenue was developed and is led by Twin Cities Public Television (tpt).


  • May 18, 2012

    'Alzheimer's Disease Research Summit 2012; Path to Treatment and Prevention. May 14-15, 2012, National Institutes of Health, Bethesda, MD.'The Alzheimer’s Disease Research Summit 2012: Path to Treatment and Prevention, held May 14-15, 2012, brought together leading experts on Alzheimer’s disease and other complex diseases to identify research priorities and strategies needed to accelerate the development of successful therapies. The Summit was attended by an international group of some 500 researchers, clinicians and members of the broader Alzheimer’s community who contributed actively to the Summit process through extensive input and discussion during the course of the meeting. The topics that were discussed included the current understanding of this complex disorder, the need for more basic research into the pathobiology of Alzheimer’s disease, existing models and approaches to drug development, and new ideas to speed development of effective interventions for treatment and prevention.

    View a 5-minute video about the Alzheimer's Disease Research Summit featuring NIH officials and grantees.

    The recommendations from the Summit, organized by a subgroup of the 57 speakers and panelists and based on the full Summit discussions, will help guide both the public and private sectors toward meeting research goals set forth in the National Plan to Address Alzheimer's Disease, a national strategy announced at the Summit by Health and Human Services Secretary Kathleen Sebelius to accelerate research and improve clinical care and services.

    Specifically, the Summit agenda and the initial recommendations presented here outline a blueprint for an integrated, multidisciplinary research agenda. The recommendations focus on a spectrum of basic discovery and translational research activities critical to the development of disease-modifying as well as symptomatic therapies across the disease continuum for the cognitive as well as neuropsychiatric symptoms of Alzheimer’s disease, and they identify the types of infrastructures, resources, and new public private partnerships needed to successfully implement this translational agenda.

    Several overarching and transformative concepts were identified by Summit participants as critical to achieving success in Alzheimer’s disease therapy development, and these emerged repeatedly among the themes brought forward by the different workgroups:

    • Recognize the heterogeneity and the multifactorial nature of the disease.
    • Employ new research paradigms such as systems biology and network pharmacology.
    • Enable rapid and extensive sharing of data, disease models, and biological specimens.
    • Build new multidisciplinary translational teams and create virtual and real spaces where these teams can operate.
    • Develop strategies to overcome intellectual property barriers to Alzheimer’s disease drug development.
    • Develop new public-private partnerships.
    • Establish a National Institutional Review Board (IRB) for Alzheimer’s disease clinical research.

    Specific recommendations are presented here:

    Session 1: Interdisciplinary Approach to Discovering and Validating the Next Generation of Therapeutic Targets for Alzheimer’s Disease

    1. Intensify scientific efforts to deepen the understanding of the complex pathobiology of Alzheimer’s disease, and diversify target identification to better address the multifactorial nature of the disease. These efforts should include the use of systems biology approaches and tools, as well as cutting-edge stem cell technology.
    2. Develop a better systems-level understanding of how the many discoveries that have already been made (e.g., genetic, pathological, biochemical, radiological, neuropsychological) and the contributory factors that have already been identified (e.g., Ab, tau, apoE4, a-synuclein, TDP-43, aging, proteostasis failure, mediators of inflammation, comorbidities) are related mechanistically.
    3. Facilitate the conversion of existing genetic information into mechanistic insights and therapeutic advances and continue to generate new genetic data using exome and genomic sequencing approaches to identify rare genetic variants of large functional effect.
    4. Generate new experimental models (e.g., different animal species, human induced pluripotent stem [iPS] cells, in silico models) that better simulate the multifactorial etiology of Alzheimer’s disease and use these models to identify modulators of disease pathways and to assess combination treatments which may be required to defeat this disease. Ensure that these new tools and models are freely shared.
    5. Develop in vivo imaging agents (tracers for PET scans) to assess target engagement and the burden of brain pathology to enable successful drug development for existing and new therapeutic targets.
    6. Develop robust biomarkers that can feasibly be obtained in large cohorts of volunteers, including metabolic signatures to develop and validate diagnostic, prognostic, and surrogate biomarkers for Alzheimer’s disease and biomarkers for disease subtypes.
    7. Establish links among peripheral biochemical changes (e.g. blood-based markers) and imaging and cerebrospinal fluid changes to identify and validate peripheral biomarkers of disease.
    8. Enable rapid sharing of new data via web-based resources with the capacity to store large and diverse datasets (such as data about clinical phenotypes, genetics, epigenetics, proteomics, and metabolomics) that can be used for testing different models or hypotheses at the computational level.
    9. Enable analysis of new data before publication, using approaches such as collaborative challenges open to all citizens and scientists.
    10. Maximize the use of existing infrastructure and resources (e.g., research centers, biobanks, and repositories) by publicizing their availability to researchers.
    11. Facilitate the creation of new translational teams to expedite the discovery and validation of new therapeutic targets. These teams should include epidemiologists, basic research scientists, geneticists, computational biologists, medicinal chemists, pharmacologists, toxicologists, pharmacogenomics experts, clinicians, and project managers, collaborating within and across institutions.

    Session 2: Challenges in Preclinical Therapy Development

    1. Develop infrastructure and resources to increase the likelihood that preclinical therapeutic development efforts for Alzheimer’s disease will translate to success in the clinic by:
      • Creating expert advisory committees for all aspects of preclinical and early clinical drug development to assist academic drug discovery efforts
      • Establishing a network of Alzheimer’s disease preclinical therapy centers integrated with existing and proposed translational infrastructure and resources (e.g., Alzheimer’s Disease Neuroimaging Initiative, Alzheimer’s Disease Centers)
      • Establishing an open-access resource for reviewing and publishing negative and discrepant data.
    2. Develop broad capabilities in quantitative and systems pharmacology to understand the impact of drugs on organisms, to predict dosing, to reduce toxicity, and to facilitate drug repurposing and the identification of combination therapies. This will require a wide collaboration among NIH Institutes, government, academia, industry, voluntary health organizations, and foundations including the establishment of new training programs.
    3. Increase the predictive power of preclinical testing in animal models by:
      • Establishing a standardized and rigorous process for the development and characterization of animal models, and ensuring their maximal and rapid availability to all researchers for preclinical drug development
      • Aligning the pathophysiological features of Alzheimer’s disease animal models with the corresponding stages of clinical disease using translatable biomarkers
      • Establishing guidelines for rigorous preclinical testing in animal models and reporting of both positive and negative findings.
    4. Provide an expedited review track for applications focused on drug discovery, preclinical, and clinical drug development for Alzheimer’s disease to mitigate difficulties with intellectual property and commercialization issues that are imposed by the current lengthy review/grant cycle at the NIH. Establish multi-disciplinary review panels with adequate expertise to evaluate all aspects of translational research.

    Session 3: Whom to Treat, When to Treat, and What Outcomes to Measure

    1. Initiate treatment trials in asymptomatic, at-risk individuals (e.g., individuals at risk genetically, older adults positive for biomarkers for Alzheimer’s disease) using uniform biomarkers and cognitive outcomes, informed by data from Alzheimer’s disease trials using patients with more advanced disease.
    2. Collect DNA and other biosamples from these studies to enable subsequent interrogation based on treatment response and predictors of decline in the groups receiving placebo.
    3. Expand large-scale registries and natural history cohorts of healthy individuals from early midlife to late-life, as well as individuals with subjective and/or objective cognitive impairment and use the data generated to inform clinical trial design. These cohorts should be population-based and should oversample underrepresented ethnic minorities and groups with lower education.
    4. Develop, validate, and standardize sensitive neuropsychological and other clinical and behavioral measures to detect and track the earliest clinical manifestations of Alzheimer’s disease and to predict long-term clinical and functional outcomes. These measures should be sensitive to change and capture the variability in cognitive function that may be an important predictor of treatment response.
    5. Optimize biomarkers for detecting and monitoring the progression of Alzheimer’s disease, and focus particularly on standardization. These biomarkers will be used to elucidate the temporal trajectories over the course of preclinical and prodromal Alzheimer’s disease, to assess the proximity to onset of clinical symptoms, and to predict long-term clinical response to treatment.
    6. Develop treatments for patients with symptomatic Alzheimer’s disease and support proof of concept studies to validate novel targets for cognitive and neuropsychiatric symptoms across all disease stages.
    7. Develop approaches to stratify and individualize treatments based on the heterogeneity of symptomatic patient populations.
    8. Support broad infrastructure changes that will accelerate and improve the efficiency of prevention initiatives, including the formation of a national centralized Institutional Review Board for multi-center Alzheimer’s disease trials and the development of agreements for data sharing of de-identified data from both placebo and treatment arms via public databases.

    Session 4: Drug Repurposing and Combination Therapy

    1. Expand publicly available libraries of drugs, drug signatures, and Alzheimer’s disease tissues and publicize their availability to the Alzheimer research community. Consider including cell-type and region-specific expression differences in the brain and periphery at varying stages of Alzheimer’s disease, as different stages may require different drugs. Expression libraries from cognitively normal adults positive for amyloid imaging and CSF Alzheimer’s biomarkers and from centenarians without dementia could be used to identify Alzheimer’s disease-resistant expression signatures that correlate with specific drug signatures for prevention studies.
    2. Maintain rigor in the development of repurposed drugs with respect to scientific rationale, as well as design of clinical trials. Provide adequate prior clinical trial evidence for safety in populations with or at risk for Alzheimer’s disease.
    3. The optimal therapy for Alzheimer’s disease may involve the use of drug combination cocktails and require different composition of these cocktails at different stages of the illness. To facilitate the development of effective combination therapies, develop translational workgroups that include experts in network biology and network pharmacology.
    4. Encourage the evaluation of drugs that simultaneously target multiple disease pathways (e.g., insulin, selective estrogen receptor modulators).
    5. Develop translational groups across institutions that focus on specific therapy development efforts (e.g., apoE therapeutics, combinatorial therapeutic strategies, drug repurposing, neuropsychiatric symptoms).

    Session 5: Nonpharmacological Interventions

    1. Integrate epidemiological studies with mechanistic research to explore underlying pathways by which risk and protective factors contribute to the disease process.
    2. Continue to identify the molecular mechanisms by which non-pharmacological interventions operate and employ systems biology approaches to examine brain health in relation to, and in concert with, other organ systems.
    3. Initiate rigorously designed clinical trials in asymptomatic and cognitively impaired older adults to establish the effectiveness of physical exercise, cognitive training, and the combination of these interventions for Alzheimer’s disease treatment and prevention.
    4. Combine nonpharmacological (e.g., behavioral, lifestyle, environmental) interventions with pharmacological treatments to maximize possible therapeutic benefit. Use epidemiologic information, mechanistic research in animal models, and network analysis to inform trial design and drug selection.
    5. Develop standard outcome measures to enable data comparisons across studies. These include but are not limited to ecologically valid measures of real world function, quality of life, and physical and cognitive function.
    6. Pursue the science of behavioral change for successful implementation of effective nonpharmacological interventions.
    7. Invest in research to develop technologies that promote prevention and treatment trials, clinical care, caregiver support, and in-home monitoring.

    Session 6: New Models of Public Private Partnerships

    1. Promote and enable partnerships across all sectors involved in basic, translational, and clinical research to successfully implement an integrated translational research agenda.
    2. Increase awareness of the importance and value of public private partnerships among federal agencies, other stakeholder organizations, and the public and engage the full spectrum of the Alzheimer’s disease community in various partnership activities for the advancement of AD therapy development.
    3. Enable partnerships for:'
      • Data sharing (with standardized ontologies and metadata)
      • Creating, validating and sharing tools for translational research (e.g., instruments and biomarkers, animal models, high-throughput screening assays, iPS cells).
      • Expanding the precompetitive space using new models of public private partnerships such as the Arch2POCM partnership for target validation and also for product development partnerships.
    4. Develop a National Institutional Review Board for Alzheimer’s disease studies accessible to both public and private funding research organizations.

    View Summit Videocast

    To view the presentations and discussions of the Summit, which was hosted by the National Institutes of Health and the Department of Health and Human Services, with support from the private sector through the Foundation for the National Institutes of Health, go to the links below: 



  • May 9, 2012

    "The Weight of the Nation" documentary series and public awareness campaign by the cable network HBO, launching this week, features National Institutes of Health research showing how obesity affects the country's health and how interventions can turn the tide against obesity and its complications.

    The network, in consultation with NIH and other major health organizations, developed four documentaries focused on obesity. The project also includes a three-part HBO Family series for kids, 12 short features, a social media campaign, and a nationwide community-based campaign to mobilize action to move the country to a healthier weight.

    The films feature several NIH-funded clinical studies that have formed the basis of scientific evidence on the causes and consequences of being overweight or obese, including the Diabetes Prevention Program (DPP), Coronary Artery Risk Development in Young Adults (CARDIA) study, and Bogalusa Heart Study. The DPP found that even moderate weight loss can help prevent type 2 diabetes. The CARDIA study measures changes in coronary heart disease risk factors. The Bogalusa Heart Study examines how cardiovascular disease develops over time.

    “If we don't take the obesity epidemic seriously as individuals and as a nation, we will pay a serious price,” said NIH Director Francis S. Collins, M.D., Ph.D., who appears in all of the main documentaries in the series. “It's going to take diverse and rigorous research to understand the causes of obesity and to identify interventions that work in the real world. The results from federally funded research, as seen in these documentaries, can help to prevent and treat obesity and its complications.” More »

    For more information, go to NIH and the Weight of the Nation.

  • April 16, 2012

    The hippocampus, a brain region important to learning and memory, gradually loses volume as part of the normal aging process. This loss is significantly accelerated in older people with Alzheimer’s disease, especially if they have vascular problems or diabetes.   Now, an international team of researchers has identified four genes that may play a role in the age-related decline of hippocampal volume, a finding that may provide insight to risk for cognitive decline and Alzheimer’s disease. Conducted in part by NIA-funded investigators, the study appeared online April 15, 2012, in Nature Genetics.

    The findings result from the combined analyses of several genome-wide association studies (GWAS) conducted in the U.S., Canada, Europe and Australia involving thousands of participants with and without Alzheimer’s disease. GWAS analyze DNA to identify specific genetic variations associated with particular diseases. The researchers located four gene risk factors on chromosome 12 that may play a role in age-related hippocampal decline.  

    The genes implicated in the findings are involved in cell death, brain development and plasticity, oxidative stress and enzymes targeted by diabetes medications—all of which may contribute to the brain’s vulnerability to Alzheimer’s. While we need to learn more about the complex interplay between genetic risk for Alzheimer’s disease and other factors that influence its onset and progression, these genes findings on age-related declines in brain volume could lead to new approaches for the devastating hippocampal declines wrought by the disorder.

    Reference: Bis JC, et al. Common variants at 12q14 and12q24 are associated with hippocampal volume. Nature Genetics. doi:10.1038/ng.2237

  • April 13, 2012

    Plaques made up of abnormal deposits of beta-amyloid protein are a hallmark of Alzheimer’s disease. The toxic buildup begins when the beta-secretase enzyme (BACE), working in concert with a partner enzyme, snips a small fragment of amyloid precursor protein (APP) and releases beta-amyloid from the cell membrane of neurons.  The beta-amyloid can then gradually clump together to form the well-known plaques that may cause damage to brain cells. Now a new study primarily funded by NIA appearing in the April 10, 2012, issue of Nature Communications has revealed a previously unknown interaction between BACE and a large APP fragment called sAPPalpha that blocked the buildup of plaques in mice. The novel findings may lead to new therapeutic targets for Alzheimer’s researchers.

    Scientists at the University of South Florida, Tampa, discovered that the sAPPalpha fragment, which is released from neurons at synapses (the tiny gap between neurons across which neurotransmitters travel during communication), interfered with BACE activities in mouse models with Alzheimer’s pathology. Increased levels of sAPPalpha blocked the ability of BACE to snip the APP protein and reduced levels of amyloid plaque buildup in the brains of the mice. Because lower than normal sAPPalpha levels are often found in people with Alzheimer’s, restoring or enhancing these levels may be one avenue to investigate for slowing onset or progression of the disorder.    

    Reference: Obregon D, et al. Soluble amyloid precursor protein-α modulates β-secretase activity and amyloid-β generation. Nature Communications. 2012 Apr 10;3:777. doi: 10.1038/ncomms1781.