Announcements

  • October 1, 2014

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    Are you interested in the genetics of late-onset Alzheimer’s disease? Did you know that the NIA has a database that gives you access to a broad range of genetics and genomics data? It’s called the NIA Genetics of Alzheimer's Disease Data Storage Site, or NIAGADS, and it is an essential research resource for scientists investigating Alzheimer’s disease. In a new blog post, Dr. Marilyn Miller, Program Director for the NIA’s Division of Neuroscience, discusses the data available to investigators via NIAGADS, and the partnerships that support the database. Dr. Miller goes into detail about important aspects of NIAGADS, such as the Genomics Database and new data that will be available soon.

    Blog post – NIAGADS! We have data!

    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.

  • September 24, 2014

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    During the fiscal year 2014, NIA was affected by a number of events and challenges. As the fiscal year winds down, Dr. Robin Barr, director of the Division of Extramural Activities, looks back on the changes and surprises that occurred, including an expanded research agenda, a budget increase, and an unexpected influx of well-written applications.

    Read the full blog post: Oh, what a year it was!

    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.

  • September 18, 2014

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    Every third week in September, the NIA celebrates National Postdoc Appreciation Week. This week’s blog post thanks postdocs for their vital contributions to aging research. The post, by Dr. Jennifer Illuzzi, a postdoc with NIA’s Intramural Research Program, discusses the many ways postdoctoral fellows make significant contributions, and highlights the opportunities available for postdocs at the NIH and NIA.

    Read the full blog post: We appreciate postdocs

    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.

  • September 15, 2014

    Researchers have long wondered why some older people remain cognitively normal despite having abnormal levels of beta-amyloid in their brains, a hallmark of Alzheimer’s disease. While research has shown that older adults with Mild Cognitive Impairment (MCI), which often leads to Alzheimer’s, frequently have increased activity in the hippocampus compared to their cognitively healthy peers, scientists questioned what the hyperactivity represented. Was it helping to compensate for declining brain function or signaling onset of the disease? New NIA-supported brain imaging research has deepened our understanding of this complex puzzle by showing increased activity in several cortical regions of the brain may help compensate for amyloid build-up and help prevent onset of dementia or slow rate of progression.

    Dr. Jeremy Elman, of the Life Sciences Division of the U.S. Department of Energy's Lawrence Berkeley National Laboratory, and colleagues at the Helen Willis Neuroscience Institute, University of California, Berkeley, reported the findings online Sept. 14, 2014 in Nature Neuroscience. The work was funded by NIA and the McKnight Brain Research Foundation, through the Foundation for the National Institutes of Health (FNIH), under a joint effort since 2007 to identify age-related changes in the brain and cognition.

    The researchers used functional magnetic resonance imaging (fMRI) to assess the brain activity of volunteers tasked with memorizing pictures of scenery and then asked the group questions about the images. The volunteers included 22 young adults and 49 cognitively normal older people; among the latter, positron emission tomography (PET) brain imaging showed 16 with abnormal levels of beta-amyloid and 33 free of deposits. While both groups of older volunteers did equally well in remembering the images, those with beta-amyloid in their brains had greater brain activity while performing the memorization task. The researchers also noted that in both young adults and in older volunteers with abnormal levels of beta-amyloid, greater activity in the visual and memory areas of the brain correlated directly with success in recalling picture details. In contrast, for older adults free of amyloid, lower brain activity in areas not generally associated with vision and memory predicted how well they remembered details.

    The researchers concluded increased brain activity in older people with amyloid deposits may help compensate for the neurodegeneration wrought by Alzheimer’s disease. Interestingly, the study adds a new piece to the complex puzzle of Alzheimer’s with the finding that older brains with amyloid function more like younger brains than do older brains free of amyloid. More research is needed to explore this dynamic as well as the various and complex mechanisms involved in Alzheimer’s and healthy cognitive aging.

    Reference: Elman J.A., et al. Neural compensation in older people with brain amyloid-β deposition. Nature Neuroscience. Published online Sept. 14, 2014. doi:10.1038/nn.3806

  • September 10, 2014

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    The NIH announced a change in grant application resubmission policy in April. With the policy change, investigators now have a real choice when it comes to revising a grant application that is not funded. A new NIA blog post may assist these investigators with important decisions about their next steps. Dr. Robin Barr, director of the Division of Extramural Activities, compares initial grant applications and revisions of those applications and discusses success rates for various types of investigators. Please read this blog post for more on the policy change and NIA data on probability of funding.

    Read the full blog post: To resubmit or not?

    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.

  • September 10, 2014

    Many people who have been affected by Alzheimer’s wonder how they can help combat this devastating disease. Volunteering to participate in research is one powerful way. Right now, at least 70,000 volunteers are needed for more than 150 active Alzheimer’s and related clinical trials and studies in the United States. All kinds of people, including healthy older adults, can join in this critical research.

    cover of publicationParticipating in Alzheimer’s Research: For Yourself and Future Generations, a new booklet from the National Institute on Aging at NIH, explores:

    • how to find Alzheimer's and related studies that might be right for you
    • benefits and potential risks to consider
    • what happens when you join a trial or study
    • how safety is protected
    • questions to ask

    Read, download, or order free copies of Participating in Alzheimer’s Research online or call the ADEAR Center at 1-800-438-4380.

    Stay connected! Subscribe to NIA's Alzheimer's Clinical Trials list to receive monthly e-alerts about new trials and studies. 

  • August 27, 2014

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    Every summer, early career researchers from diverse backgrounds come from all over the U.S. to spend a week at the National Institute on Aging’s 2014 Butler-Williams Scholars Program. They explore the best of NIA’s science, learn about grantsmanship, share challenges, and make new connections.

    What is important to these early career researchers? Dr. Marie Bernard, deputy director of the NIA, examines changing trends in a new blog post. “We have to know these things in order to get the right people in the research training pipeline, and to convince them to stay in research,” Dr. Bernard emphasizes, “The young researchers I’m interacting with have big ideas that will remake research and medicine.”

    Read the full blog post: The next generation: what will it take to keep them in research?

    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.

  • August 15, 2014

    Subject: Dr. Etienne Sibille September 4 at the GeroScience Interest Group (GSIG) summer seminar
    When: Thursday, September 4, 2014, 12:00 PM – 1:00 PM
    Where: Lipsett Amphitheater, Building 10, NIH
    Title: "Age-by-Disease interactions in the Human Brain: Evidence & Model"

    NOTE: This seminar is open to the public, but please allow time to clear security.

    Import this event into Outlook or other calendars as an ICS file (Outlook, 9K).

    The Trans-NIH GeroScience Interest Group (GSIG) cordially invites you to its summer seminar, featuring Dr. Etienne Sibille. Dr. Sibille is the Campbell Family chair in Clinical Neuroscince, in the Campbell Family Mental Health Research Institute , Centre for Addiction and Mental Health (CAMH), in the Department of Psychiatry at the University of Toronto. Dr. Sibille’s research goals have consistently focused on translational research aimed at identifying the cellular and molecular bases of depression, and specifically of the mood and affect dysregulation components of the illness. Studies in his laboratory encompass parallel investigations in postmortem brains of depressed and control subjects, and in genetic and environmental rodent models, with the aims of characterizing the primary pathology of depression and assessing causal links between identified molecular changes or candidate neurotransmitter systems and mood regulation. Current projects include translating human postmortem findings on the role of the GABA microcircuitry in mood regulation, and specifically of reduced somatostatin-positive dendritic targeting interneuron function. In addition, they have demonstrated that biological pathways affected during aging of the human brain largely overlap with neuropsychiatric and other neurological disease pathways and may in fact promote diseases, together providing a compelling rationale for investigating aging and diseases simultaneously. These latter hypotheses are now being tested in parallel in the human postmortem brain and in large epidemiological studies of subjects at the “vigor-to-frailty transition.”

    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. Jovier Evans at jevans1@mail.nih.gov or at 301/443-6328 or Dr. Ron Kohanski at kohanskir@mail.nih.gov or at 301/496-6402.

    Please send your questions related to the seminar to jevans1@mail.nih.gov or kohanskir@mail.nih.gov.

  • August 15, 2014

    Two new NIH-supported studies have shown that a person’s epigenome—the chemical modifications, or marks, on our DNA that turn gene activity on and off—may influence Alzheimer’s disease-related changes in the brain.  The two groups of researchers examined brain tissue donated by volunteers with Alzheimer’s and those free of the disease and linked a specific epigenome marker, DNA methylation, with Alzheimer’s pathology in the brain. Because the epigenome can be affected by lifestyle and the environment, these findings may offer new targets for therapies to delay, prevent or treat Alzheimer’s disease.

    The independently-run, epigenome-wide association studies (EWAS) reported online in Nature Neuroscience on August 17, 2014, were led by: Philip L. De Jager, M.D., Ph.D., Brigham and Women's Hospital, Boston, in collaboration with co-author David Bennett, Ph.D., Rush University Medical Center, Chicago; and by Jonathan Mill, Ph.D., of the University of Exeter Medical School and King’s College London, in collaboration with colleagues in the United Kingdom and United States.  

    Because the epigenome determines gene expression—that is, which genes are active and what proteins they produce—it can impact health and longevity. These new studies show for the first time that DNA methylation may impact specific gene regions, several of which are thought to play a role in Alzheimer’s disease risk, onset and progression.

    • Dr. De Jager’s team analyzed samples from 708 donated brains from the Religious Orders Study and Rush Memory and Aging Project led by Dr. Bennett. They found that greater methylation levels correlated with Alzheimer's disease in 71 of the 415,848 markers analyzed. The 71 markers were found in the ANK1 and RHBDF2 genes, as well as in ABCA7 and BIN1 genes (two known Alzheimer’s risk variants.) They also identified nearby genes with altered expression that may be related to Alzheimer’s: ANK1, CDH23, DIP2A, RHBDF2, RPL13, RNF34, SERPINF1 and SERPINF2. This work was funded in part by the National Institute on Aging (NIA) at NIH. 
    • Dr. Mill’s team analyzed brain tissue from nearly 300 donated brains in the U.S. and U.K. They linked higher levels of DNA methylation in the ANK1 gene to greater levels of Alzheimer’s pathology, especially in brain regions known to be susceptible to the disease. This research was primarily funded by the NIH Epigenomics Roadmap Initiative, which seeks to accelerate research into the relatively new and fast-developing area of epigenetics. NIA also provided support.

    References:

    De Jager PL., et al. Alzheimer's disease: early alterations in brain DNA methylation at ANK1, BIN1, RHBDF2 and other loci. Nature Neuroscience, published online Aug. 17, 2014; DOI:10.1038/nn.3786

    Lunnon K., et al. Methylomic profiling implicates cortical deregulation of ANK1 in Alzheimer's disease. Nature Neuroscience, published online Aug. 17, 2014; DOI:10.1038/nn.3782  

  • August 15, 2014

    Preliminary findings from a study by National Institute on Aging (NIA) scientists and colleagues showed that a blood test for Alzheimer’s-related proteins may accurately predict who might be at risk for the disease years before symptoms develop. The test measured the levels of several tau and amyloid proteins—the hallmarks of Alzheimer’s disease—in exosomes, microscopic organelles shed by brain cells.

    The study by Dimitrios Kapogiannis, Ph.D., and Edward Goetzl, M.D., both of the NIA Intramural Research Program, Baltimore, and researchers at the Mayo Clinic, Rochester, Minn.; University of Kentucky, Lexington; Georgetown University, Washington, D.C.; University of California, San Francisco; and the University of Rochester, N.Y., appeared online in the August 15, 2014 issue of Alzheimer’s & Dementia. The work was funded by NIA, the University of Kentucky, Lexington, and Nanosomix, Inc.

    Compared to those free of the disorder, the blood test showed people with Alzheimer’s had higher elevations of three proteins (p-5396-tau, p-181 tau, and Ab42) in exosomes. The test was 96 percent accurate in distinguishing between these two groups. Significantly, the investigators also found elevated levels of these proteins in blood samples collected from cognitively healthy older people who later developed dementia within one to ten years.

    While this case-controlled study needs to be replicated, it offers intriguing insights into novel ways to detect Alzheimer’s disease at its earliest stages. The work was funded by NIA, the University of Kentucky, Lexington, and Nanosomix, Inc.

    Reference: Fiandaca MS, et al. Identification of pre-clinical Alzheimer’s disease by a profile of pathogenic proteins in neurally-derived blood exosomes: a case-control study. Alzheimer’s & Dementia. http://dx.doi.org/10.1016/j.jalz.2014.06.008.

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