• December 8, 2015

    The death rate among middle-aged, white Americans rose significantly between 1999 and 2013, reversing a decades-long trend of improvement, new research shows. This group also reported worse physical and mental health than other age groups, according to the NIA-funded study, published online Nov. 2, 2015, in the Proceedings of the National Academy of Sciences.

    From 1978 to 1998, the death rate for U.S. non-Hispanic whites ages 45 to 54 fell 2 percent per year on average, matching the rate for some wealthy European countries, reported economists Drs. Anne Case and Angus Deaton of Princeton University. But in the following 15 years, the U.S. group’s death rate rose half a percent per year on average, while the death rate for their European peers continued to fall. The experts analyzed federal survey data.

    In the U.S., this higher death rate was unique to middle-aged whites. During the same period, the average yearly death rate decreased 1.8 percent for Hispanics and 2.8 percent for non-Hispanic blacks in the same age group. Even older Americans age 65–74 had a lower death rate than 45- to 54-year-old whites.

    Drug and alcohol poisoning, suicide, and chronic liver disease and cirrhosis drove up the death rate for white people in this age group, the analysis showed. For those aged 45–54, if the white mortality rate had held at its 1998 value, 96,000 deaths would have been avoided from 1999–2013, the researchers noted. Death rates were highest for people with the least education (a high school degree or less).

    There was also a significant rise in the proportion of middle-aged adults reporting fair or poor health in 2011–13, compared with 1997–99. Individuals reported higher rates of chronic pain, psychological distress, and difficulty with daily activities. Risk for heavy drinking also rose significantly.

    The authors noted that the increase in midlife mortality is only partly understood. Increased availability of opioid prescription drugs, chronic pain (for which opioids are often prescribed), and the economic crisis which began in 2008 may all have contributed to an increase in overdoses, suicide, and increased liver disease associated with alcohol abuse.

    Reference: Case, A., and Deaton, A. Rising morbidity and mortality in midlife among white non-Hispanic Americans in the 21st century. Proceedings of the National Academy of Sciences. doi: 10.1073/pnas.1518393112. Published online Nov. 2, 2015.

  • December 11, 2015

    A new online report provides an easy-to-read overview of recent National Institutes of Health-funded research advances and initiatives in Alzheimer’s disease and related dementias. Issued by the National Institute on Aging (NIA) at NIH, the annual report—2014-2015 Alzheimer’s Disease Progress Report: Advancing Research Toward a Cure—discusses research momentum under the National Plan to Address Alzheimer’s Disease, describes research opportunities, and summarizes scientific advances in several areas:

    • Understanding the biology of Alzheimer’s, related dementias, and the aging brain
    • Identifying genetic influences on risk for late-onset Alzheimer’s, the most common form
    • Detecting the earliest Alzheimer’s-related brain changes, including further development of biomarkers to track the onset and progression of Alzheimer’s
    • Understanding gender and racial differences in the impact of Alzheimer’s
    • Stepping up translational research enabling the design and testing of new drugs
    • Testing in clinical trials potential new therapies to prevent, delay or treat Alzheimer’s
    • Finding better ways to support caregivers

    The report includes searchable tables of NIA-funded clinical trials that are testing promising interventions for Alzheimer’s disease, mild cognitive impairment, age-related cognitive decline, delirium and dementia-related psychiatric conditions and symptoms—agitation, apathy and depression.

    Read the report online: 2014-2015 Alzheimer’s Disease Progress Report: Advancing Research Toward a Cure

  • December 2, 2015

    As animals, including humans, age or develop brain diseases such as Alzheimer’s, their brain cells may not produce enough energy to remain fully functional. A new study shows that an enzyme, SIRT3, may protect brain cells against stresses believed to contribute to energy loss. Researchers also found that physical exercise increases the expression of SIRT3, helping to protect the brain against degeneration. The results were published online Nov. 19, 2015, in Cell Metabolism.

    Scientists at NIH’s National Institute on Aging Intramural Research Program, Baltimore, used a new mouse model to investigate whether they could aid brain cells called neurons in resisting the energy-depleting stress caused by neurotoxins and other factors. They found a biochemical hero in SIRT3, located in mitochondria, the cell’s powerhouses. SIRT3 is part of the sirtuin family of proteins, which are thought to play an important role in aging, stress resistance, and metabolic regulation.

    The researchers, led by Mark Mattson, Ph.D., of NIA’s Laboratory of Neurosciences, found that mice that did not produce SIRT3 became highly sensitive to cellular stress when exposed to neurotoxins that cause neurodegeneration and cell death. In mouse models of Huntington’s disease and epilepsy, mice with SIRT3 deficiency had greater brain neuron degeneration and associated behavioral symptoms than those with sufficient SIRT3 after exposure to certain toxins.

    In addition, normal mice that exercised on running wheels for 30 days had significantly higher SIRT3 levels in neurons of the hippocampus, a brain region important for learning and memory, than mice that did not exercise. Researchers concluded that running helped protect neurons against cell death in mice by increasing SIRT3 levels.

    The researchers also found that they could protect neurons against stress using a gene-therapy technology to increase levels of SIRT3 in neurons. Neurons without SIRT3 were significantly more vulnerable to toxic stress than those with SIRT3.

    The findings suggest that bolstering mitochondrial function and stress resistance by increasing SIRT3 levels may offer a promising therapeutic target for protecting against age-related cognitive decline and brain diseases.

    Reference: Cheng A., et al. Mitochondrial SIRT3 mediates adaptive responses of neurons to exercise, and metabolic and excitatory challenges. Cell Metabolism. Published online Nov. 19, 2015.

  • December 1, 2015

    This Notice serves to communicate NIH’s priority areas of health economics research.

    Applicants and potential applicants for NIH research grants are advised to consult with NIH program officers in Institutes and Centers (IC) appropriate to their proposed topic if they have questions about the alignment of their research with IC program priorities.

    You may read the full Notice on the NIH Grants website.

  • November 16, 2015

    If you live in a residentially segregated area with comparatively high rates of crime and violence, limited access to healthy foods, and inadequate health care, it's going to affect your health. Public health professionals who ignore this reality do so at our peril, Carl V. Hill says.

    Hill, PhD '05, believes that to address health disparities in the U.S., new steps - and an interdisciplinary team approach - are needed, "because these disparities are created and sustained at environmental, sociocultural, behavioral, and biological levels."

    To read more, go to University of Michigan School of Public Health newsletter “Findings”, Fall 2015 issue.

  • November 16, 2015

    Heidi Williams, Class of 1957 Career Development Assistant Professor in the Economics Department at MIT, was awarded a 2015 MacArthur Fellowship. The citation recognizes her as

    “….an economist unraveling the causes and consequences of innovation in health care markets. Williams combines finely grained empirical observations and custom-designed data collection methods to build entirely new datasets about technological changes in health care. In addition, her creative methods for determining causal inference, and keen understanding of regulatory law, biological science, and medical research, have allowed her to trace the interplay among institutions, market behavior, and public policy–relevant outcomes.“

    During her studies for her PhD, Dr. Williams was a trainee supported by an NIA T32 institutional training grant, led by David Wise. She is now Principal Investigator for a project “Empirical Studies of the Development and Diffusion of Medical Technologies,” managed by NIA with funds from the NIH Common Fund program in Health Economics.

    All of us at NIA/BSR are delighted to congratulate Heidi Williams on this well deserved recognition of her work!

  • November 12, 2015

    The National Institute on Aging has been working to stimulate health disparities research related to aging. An opportunity is currently available for researchers interested in aging, stress, resilience, and health disparities. There are also exciting, new funding opportunities for Alzheimer’s Disease research that focuses on health disparities.

    In July of 2015, the Office of Special Populations successfully posted a Funding Opportunity Announcement for administrative supplements entitled Aging Research to Address Health Disparities. The announcement was intended to expand existing research in specific areas of interest to include development of new measures to facilitate research on the behavioral and social mechanisms leading to disparities in health; addition of sub-group analyses to existing studies; studies focused on racial, ethnic or gender disparities in stress-responses; and studies focused on racial or ethnic disparities in functional, physiologic, or metabolic outcomes across the life span and in old age.

    The administrative supplement supports the NIA’s health disparity goals of (1) understanding environmental and sociocultural factors and related behavioral and biological mechanisms that diminish health and reduce life expectancy for populations that experience health disparities, (2) developing strategies to increase life expectancy among aging adults and improve the health status of elders from underserved and disadvantaged populations, and (3) using research insights and advances to inform policy that reduces health disparities. The parent projects that were supported cover a broad range of research areas (see below).

    We look forward to learning of valuable findings that inform health disparities research related to aging!

    PI Name (Contact) Institution Parent Project Title
    Sun, Liou
    Board of Trustees of Southern Illinois University
    The Effects Of Early Life Nutritional And Hormonal Signals On Mammalian Aging (Health Disparities Admin Supplement)
    Fillingim, Roger B.
    Bradley, Laurence
    Goodin, Burel R.
    University of Florida Board of Trustees
    Ethnic Differences In Responses To Painful Stimuli
    Kasper, Judith
    Thorpe, Roland
    Johns Hopkins University
    Racial Disparities In Mobility Disability Among Older Men
    Mangione, Carol
    Paz, Sylvia
    University of California Los Angeles
    Center For Health Improvement Of Minority Elderly
    Kapteyn, Arie
    Barcellos, Silvia
    Carvalho, Leandro
    University of California Los Angeles
    Roybal Center For Health Decision Making And Financial Independence In Old Age
    Johnson, Sterling C.
    University of Wisconsin-Madison
    Wisconsin Registry For Alzheimer’s Prevention: Biomarkers For Preclinical Ad
    Wharton, Whitney
    Emory University
    Preclinical Alzheimer's Disease Biomarkers: Effects Of Midlife Vascular Factors
    Small, Scott A.
    The Trustees of Columbia University in the City of New York
    Determinants Of Racial Disparities In Alzheimer’s Disease
    Erlandson, Kristine Mace
    University of Colorado Denver
    Barriers And Facilitators To Exercise Maintenance
    Polivka, Barbara J.
    University of Louisville
    Asthma In Older Adults: Identifying Phenotypes And Factors Impacting Outcomes


    --Toccara Chamberlain, NIA Office of Special Populations

  • October 23, 2015

    The National Institute on Aging (NIA), a major research component of the National Institutes of Health (NIH) and the Department of Health and Human Services (DHHS), is seeking exceptional candidates for the position of Health Scientist Administrator. This position is located in the Biological Resources Branch (BRB) and the Aging Physiology Branch (APB), in the Division of Aging Biology (DAB), National Institute on Aging. DAB is responsible for the planning, organization and direction of multidisciplinary programs of extramural research on the biology of aging and managing contract-supported resources for the research community. The incumbent in this position serves as the Program Director for grant portfolios in aging physiology (basic biology of aging of the kidney, liver, lung, and other internal organs) and in the development of novel animal models to study aging biology (from hydra to whales). The incumbent will also be required to take training to become a Contracting Officer’s Representative (COR) in order to assist with contracts that provide biological resources to the research community (e.g., aging rodent colonies, cell bank, tissue banks).

    Major Duties

    As a Health Scientist Administrator, the incumbent will:

    • Formulate, develop, and implement the scientific goals and activities of the Program
    • Formulate and recommend program goals and objectives for developing the resources needed to support the nation's potential to support research on aging;
    • Serve as a Health Scientist Administrator with scientific and administrative responsibility for the program to award and monitor grants and other funding mechanisms to support research goals of the aging research community;
    • Attend study section review meetings for research applications assigned to the portfolio under purview; and
    • Serve as alternate COR or COR on resource contracts, managing technical aspects of contracts and providing assistance to the research community using the resources.

    Candidate Qualifications

    Applicants must possess an M.D. and/or Ph.D., or equivalent degree in the biomedical sciences, with experience using mammalian laboratory animal models in cell biology, molecular biology, or animal physiology. Experience in gerontology (aging research) is desirable but not necessary. In addition, the incumbent must have demonstrated skill in interpersonal relationships and administration.

  • October 15, 2015

    Dr. Angus Deaton

    The 2015 Nobel Prize in Economic Sciences has been awarded to National Institute on Aging grantee Angus Deaton, Ph.D., of Princeton University, N.J.

    “The National Institute on Aging is proud to have supported Dr. Deaton’s work for more than 20 years,” said NIA Director Richard J. Hodes, M.D. “His work has examined how circumstances including income inequality and early childhood nutrition influence health and subjective well-being across the life course in the United States and around the world.”

    Deaton’s NIA funded research has focused on measuring poverty among the elderly in the US, the influence of income and inequality on health and mortality in high, middle, and low income countries, as well as the role of work in the decline of health at older ages. His more recent funded work focused on the measurement of subjective well-being, a self-reported quality of life measure. Dr. Deaton has examined the impact of the financial crisis on well-being in the United States as well as how subjective measures of wellbeing vary across people in different societal groups and in different countries. His funded research has been published in high-profile medical and economics journals such as PNAS, Lancet and the American Economic Review.

    Deaton has also received support from the Fogarty International Center at NIH.

    NIA congratulates Dr. Deaton on his outstanding contributions to health science.

  • September 24, 2015

    The ability to suppress inappropriate behavioral responses—known as cognitive inhibitory control—is essential for everyday living. The time required for the brain to inhibit a response is called the stop-signal reaction time. Certain conditions such as Parkinson’s disease, attention deficit hyperactivity disorder, schizophrenia, and even normal aging, can affect cognitive inhibitory control, resulting in a slower stop-signal reaction time.

    Basic studies are underway to help better understand the mechanisms behind this process, which may ultimately lead to new therapeutic targets for people with cognitive problems affecting stop signal reaction times. One new finding, reported online Sept. 14, 2015 in Nature Neuroscience, provides important new insights. Most research to date on cognitive inhibitory control and stop-signal reaction time has focused on the fronto-basal-ganglia circuit, a part of the brain that helps control movement. Now, researchers from the Laboratory of Behavioral Neuroscience at the National Institute on Aging at NIH and Johns Hopkins University provide new evidence that this cognitive function might also be controlled by the inhibition of neurons in another part of the brain, the basal forebrain, the bottom-front part of the brain typically associated with the wake and sleep states as well as with learning and memory. Changes in the basal forebrain have also been associated with age-related cognitive decline, as well as Alzheimer’s disease.

    In the study, investigators trained rats to respond to a sound, but to inhibit their response if the sound was immediately followed by a light signal. Researchers measured the rats’ stop-signal reaction times and recorded neuronal activity in the basal forebrain.

    Researchers found that the neurons in the basal forebrain of rats were silenced—not firing signals—immediately before cognitive inhibitory control. The faster the neurons were silenced, the shorter the stop-signal reaction time. This link was further established when scientists artificially silenced basal forebrain neurons and saw that the rats would no longer respond to sound even when there was no light signal. This suggests that basal forebrain neurons alone are powerful enough to exert cognitive inhibitory control over behavior in the rats.

    Reference: Mayse, J.D., et al., Basal Forebrain Neuronal Inhibition Enables Rapid Behavioral Stopping. Nature Neuroscience. E-pub Sept 14, 2015. doi: 10.1038/22.4110.