Announcements

  • January 15, 2006

    The NIA’s lead program for AD research—the Neuroscience and Neuropsychology of Aging (NNA) Program—recently welcomed three new health science administrators (HSAs). Each new staff member brings a wealth of scientific and administrative expertise to the NNA as the program continues to foster a variety of research programs exploring the normal course of aging in the neuronal system and the dementias of aging.

    “We are delighted to welcome Nina Silverberg, Ph.D., Laurie Ryan, Ph.D., and Suzana Petanceska, Ph.D. They have impressive research experience and excellent science administration skills. We have truly strengthened our abilities to serve the scientific community and continue the quest to find the causes of age-related cognitive, motor, and sensory decline and of dementias such as AD,” said Marcelle Morrison-Bogorad, Ph.D., Director, NNA.

    As the Assistant Program Director for the Alzheimer’s Disease Centers (ADCs), Dr. Silverberg will be responsible for assisting Dr. Creighton (Tony) Phelps with the Centers. Specifically, she will be involved with cognitive assessment in normal aging and dementia, education cores, and minority outreach programs in the ADCs.

    Dr. Silverberg received her Ph.D. from the University of Arizona and was most recently a clinical research scientist at the Sun Health Research Institute (Arizona ADC). At the ADC, she was involved in grant development and extracting and analyzing data from the brain donation program database. Dr. Silverberg also coordinated the ADC’s American Indian outreach program. She was the principal investigator on a New Investigator Research Grant from the Alzheimer’s Association to assess the usefulness of culturally adjusted neuropsychological tools in an American Indian population. She worked closely with a neurologist and neuropsychologist in designing, carrying out, analyzing, and interpreting various investigations of AD, mild cognitive impairment (MCI), Parkinson’s disease, and normal aging.

    Dr. Petanceska is a new HSA whose portfolio spans the Neurobiology of Aging and the Dementias of Aging branches at NNA. Her duties are to manage and develop a portfolio of grants addressing aspects of normal aging related to AD pathogenesis and to assist in developing the NNA’s translational initiatives.

    Dr. Petanceska received her Ph.D. from the Sackler Institute for Graduate Biomedical Studies at New York University. Prior to coming to NNA, Dr. Petanceska was an Assistant Professor of Psychiatry and Pharmacology at the Nathan Kline Institute/New York University. She has extensive research experience in AD pathogenesis and has had a long-standing interest in AD therapeutics. Her most recent research focused on the role of disrupted sterol metabolism in the development of AD amyloidosis and the mechanisms by which estrogens and cholesterol-lowering drugs might exert neuroprotection.

    Dr. Ryan will be involved in the AD clinical trials program, which includes managing current AD clinical trials and further developing the clinical trials program by identifying goals, research questions, and appropriate investigators. She will also be responsible for helping to stimulate research in the clinical trials portfolio, including pilot and large-scale clinical trials for AD treatment, modification of disease progression, and prevention.

    Dr. Ryan received her Ph.D. in clinical psychology with specialty training in neuropsychology at Louisiana State University in Baton Rouge. Her professional interests as a neuro-psychologist center on the neurocognitive and behavioral manifestations of disorders affecting central nervous system function such as AD and traumatic brain injury. She was most recently the Assistant Director for Research and Senior Neuropsychologist for the Defense and Veterans Brain Injury Center, Department of Neurology, at the Walter Reed Army Medical Center in Washington, DC, where she was responsible for overseeing clinical research development and implementation in particular clinical trials. Dr. Ryan has also served as an Assistant Professor of Neurology, Uniformed Services University of the Health Sciences in Bethesda, Maryland.

  • April 15, 2009

    The Alzheimer's disease (AD) research community lost a legendary figure and guiding light on September 16, 2008, when Dr. Robert Katzman, 82, died at his home in La Jolla, CA, after a long illness. He was professor emeritus of neurosciences and former chair of the Department of Neurosciences at the University of California San Diego School of Medicine. From 1964 to 1984, he was chair of neurology at the Albert Einstein College of Medicine in New York. He retired from UC San Diego in 2002.

    Dr. Katzman was founding director of the NIA-funded Shiley-Marcos Alzheimer's Disease Research Center at UC San Diego, one of the original members of the NIA's National Advisory Council on Aging, and a founder of the Alzheimer's Association.

    Before Dr. Katzman's work on AD began in the 1960s, little time and money were spent on AD research and therapy. Many researchers and clinicians regarded AD as an interesting but rare form of "presenile dementia," mainly occurring in people under age 65. They believed that dementia in people over 65, termed "senile dementia," is mainly a product of aging, not disease. Some of these beliefs echoed the early conclusions of Dr. Alois Alzheimer, the German scientist who originally described AD in 1906.

    Dr. Katzman and his longtime collaborator, Dr. Robert Terry, changed these mistaken notions. During 3 decades of work, they demonstrated that most cases diagnosed as senile dementia were, in fact, AD. These findings redefined AD as a "major killer" and mounting public health threat.

    In 1976, Dr. Katzman published a landmark editorial, The Prevalence and Malignancy of Alzheimer's Disease, in Archives of Neurology. In 1977, Drs. Katzman and Terry organized the first national conference on AD, sponsored in part by the NIA. These efforts led to a boom in basic research and clinical trials on AD.

    "We owe Dr. Katzman a tremendous debt of gratitude," said NIA Director Dr. Richard Hodes. "He performed groundbreaking research and provided spirited advocacy on Alzheimer's disease. His accomplishments helped to realign attitudes about Alzheimer's, clarify its pervasiveness, and substantially increase the attention paid to this disease by scientists, clinicians, funding organizations, and the public."

    Dr. Katzman received many accolades and awards during his career. Among these was the prestigious Potamkin Prize for Research in Pick's, Alzheimer's, and Related Diseases, awarded in 1994 by the American Academy of Neurology.

    Dr. Claudia Kawas, University of California, Irvine, a long-time colleague, adds: "Dr. Katzman was known for his integrity, his generosity and his leadership. As a mentor and friend, he inspired and influenced the careers of many who continue in the fight against Alzheimer's disease. The gap he leaves in the field of Alzheimer's disease, and personally for his many family, friends and colleagues, will be profound."

  • April 15, 2009

    A recent study by researchers from the Texas Tech University Health Science Center and the Mayo Clinic Department of Medicine shows that raising the Mini-Mental State Examination (MMSE, a standard screening tool for dementia) "cut score" for more highly educated people increases the early accuracy of results for this group. Earlier identification of cognitive decline could aid in their treatment.

    Scores on the MMSE decrease with advanced age and less education. The standard MMSE cut score is 24, meaning that a score of 23 or below indicates possible dementia. However, a review of data for 4,248 people, including 1,141 with 16 or more years of education, suggests that a more appropriate cut score for college-educated individuals is 27. Raising the MMSE cut score for this group to 27 increased the accuracy of the classification rate from 89 to 90 percent and provided an "optimal balance" of sensitivity and specificity, the study results reveal. A cut score of 27 identified 70 of the 104 college-educated patients with dementia who were missed when a cut score of 24 was used.

    The researchers conclude that older, more highly educated patients who complain of cognitive decline and score below 27 on the MMSE should be referred for a comprehensive dementia evaluation.

    Reference:

    O'Bryant, S.E., et al. Detecting dementia with the mini-mental state examination in highly educated individuals. Arch Neurol. 2008 July. 65(7):963-67.

  • April 15, 2009

    People with increased levels of tau protein in their CSF develop late-onset AD at earlier ages than do others with the disease, according to a study by researchers at the Washington University School of Medicine in St. Louis. The levels of this protein in CSF may provide a potential biomarker to identify people who may develop AD sooner than others do. The levels of both beta-amyloid and tau—two proteins whose abnormalities characterize AD—in CSF vary widely in individuals with the disease.

    The investigators used genotyping to pinpoint the association between MAPT, the gene that encodes tau, and AD. They found four genetic variants of MAPT that were associated with higher levels of tau, but the higher tau levels were found only in the presence of beta-amyloid deposits. The researchers also confirmed that the genetic variants of MAPT influenced the age at onset of AD clinical symptoms but had no effect on the overall risk of developing AD.

    The results indicate that beta-amyloid deposition leads to MAPT gene expression, which in turn raises tau levels and increases early neurodegeneration in late-onset AD.

    Reference:

    Kauwe, J.S., et al. Variation of MAPT is associated with cerebrospinal fluid tau levels in the presence of amyloid-beta deposition. Proc Natl Acad Sci USA. 2008 Jun 10. 105(23):8050-54.

  • April 15, 2009

    Previous studies have suggested that frailty, a common but poorly understood condition in older people, may predict the development of dementia. In this study, Rush University researchers examined 165 physically frail older adults before and after their deaths to investigate this connection. First, participants' frailty was evaluated by measuring their grip strength, timed walk, body composition, and fatigue. After death (at a mean age of 88.1 years), their brains were autopsied for evidence of AD, cerebral infarcts, and Lewy body disease.

    Regression analyses controlling for age, chronic diseases, medications, and other factors showed an association between levels of frailty and of AD pathology but no association between frailty and cerebral infarcts or Lewy body disease. A higher level of AD pathology was associated with a higher level of frailty. The link was similar in people with and without dementia.

    The researchers speculate that AD pathology may contribute to frailty by affecting parts of the brain that control movement. Or, AD and frailty may share a common cause. "These different mechanisms are not mutually exclusive and underscore the need for further studies of the relationship between AD and frailty," they conclude.

    Reference:

    Buchman, A.S., et al. Physical frailty in older persons is associated with Alzheimer disease pathology. Neurology. 2008. 71:499-504.

  • April 15, 2009

    Examination of people at risk for the rare familial form of AD may provide clues to how the disease develops in others—years before clinical symptoms appear, according to a recent study. The clues are levels of certain proteins found in plasma and cerebrospinal fluid (CSF), biomarkers that might be used to diagnose AD in its earliest preclinical stage.

    The research team, led by scientists at the University of California, Los Angeles, examined blood and CSF samples from 21 adults under age 50, most of whom had no symptoms of AD but were related to people with familial AD, a genetically inherited form of the disease. One of their biomarkers, elevated levels of plasma Aß42 (a type of beta-amyloid protein), also has been found in people with late-onset AD.

    The results confirmed and amplified what previous studies have shown: Pre-symptomatic people with the familial-AD mutation had higher levels of plasma Aß42, which declined as the disease progressed, as well as higher plasma Aß42/Aß40 ratios, than those in people without the mutation. People with the mutation had lower CSF Aß42/Aß40 ratios and higher levels of CSF tau and p-tau181 than people who did not carry the mutation. There was no significant difference between the two groups in plasma F2-isoprostane levels.

    Reference:

    Ringman, J.M., et al. Biochemical markers in persons with preclinical familial Alzheimer disease. Neurology. 2008 July. 71:85-92.

  • April 15, 2009

    Receiving a diagnosis of dementia does not prompt a strong negative reaction in most people and may even provide relief because it explains symptoms and makes patients feel less helpless, concludes a recent study.

    To gauge psychological reactions to a dementia diagnosis, researchers from Washington University in St. Louis conducted telephone interviews with patients a few days after they received a dementia diagnosis. Two tests were used: the Geriatric Depression Scale and the "State" version of the State-Trait Anxiety Inventory. Both patients and their companions took the tests. Baseline scores were obtained through comprehensive physical and neurological examinations. Of 90 study participants, 41 were diagnosed with very mild dementia, 21 with mild dementia, and 28 with no dementia.

    The researchers found no significant increase in depression in individuals or their companions, regardless of diagnostic outcome or dementia severity. The level of anxiety also did not increase—and decreased significantly in some cases.

    Reference:

    Carpenter, B.D., et al. Reaction to a dementia diagnosis in individuals with Alzheimer's disease and mild cognitive impairment. J Am Geriatr Soc. 2008. 56:405-12.

    More information for health care professionals about communicating with older patients is provided in the NIA publication Talking With Your Older Patient: A Clinician's Handbook.

  • April 15, 2009

    A combination of magnetic resonance imaging (MRI) and positron emission tomography (PET) can more accurately detect mild cognitive impairment (MCI) brain abnormalities in the early stages of their development than can either method used alone, a recent study finds. Early diagnosis of amnestic MCI is important because the condition is often a precursor to Alzheimer's disease (AD).

    The researchers, from the National Institute on Aging (NIA) and the University of Pennsylvania, examined MRI and PET images from 30 elderly participants in NIA's Baltimore Longitudinal Study of Aging to distinguish people with aMCI from people who were aging normally. They looked at spatial patterns of brain atrophy and reduced blood flow in dozens of regions of the brain.

    MRI data alone produced an 87 percent accuracy rate for aMCI diagnosis, and PET data alone produced a 50 percent accuracy rate. However, when the two were combined, researchers obtained a 90 to 100 percent accuracy rate—"an excellent diagnostic value" for this method.

    Reference:

    Fan Y., et al. Structural and functional biomarkers of prodromal Alzheimer's disease: a high-dimensional pattern classification study. Neuroimage. 2008. 41:277-85.

  • April 15, 2009

    The Rosalyn Carter Leadership in Caregiving Award is among the most prestigious awards in the caregiving field. This award, presented annually by the Rosalyn Carter Institute of Caregiving, recognizes programs that develop and implement innovative approaches to promote collaborations between community agencies and caregiving researchers that bridge the gap between science and practice.

    One of two 2008 awards recognizes the REACH VA program, implemented by the Veterans Health Administration (VHA) Geriatrics and Extended Care Unit in partnership with the Memphis VA Medical Center. REACH VA focuses on "education, safety for the patient, support for the caregiver, and skills building to help caregivers manage difficult patient behaviors and decrease their own stress." The goal of REACH VA is "to implement an effective intervention to decrease caregiver stress and improve the management of patient behaviors throughout the VHA system."

    REACH VA is the first national clinical translation of a proven dementia behavioral intervention, REACH II (Resources for Advancing Alzheimer's Caregiver Health). REACH II is a social and behavioral research effort funded by NIA and the National Institute of Nursing Research. The goal of REACH II is to translate the results of research in caregiver support into evidence-based community practices. REACH VA has made it possible to broadly implement the findings from the REACH II research project. Clinical staffs from VA Home-Based Primary Care programs in 36 cities and 19 states have volunteered to learn and deliver the intervention to caregivers of dementia patients.

    The second winner of the 2008 award is Minnesota's NYU Caregiver Intervention Project, designed and implemented by the Minnesota Board on Aging and the Alzheimer's Association Minnesota/North Dakota Chapter, in partnership with New York University's Dr. Mary Mittelman and Cynthia Epstein. The goals of the project are to develop and improve appropriate supportive services for people with Alzheimer's disease and to integrate these services into long-term care-, home-, and community-based systems. The project uses the care model developed by Dr. Mittelman and funded in part by NIA. In the journal Neurology, Dr. Mittelman and colleagues report that nursing home placement for patients with AD who received their care intervention was delayed a median of 557 days, due in large part to improvements in caregiver social support, learned responses to patient behavior problems, and symptoms of depression.

  • October 15, 2009

    A new “dementia risk index” can accurately predict which older adults will develop dementia within 6 years, according to a study in Neurology. Some of the factors that may predict dementia—age, poor performance on cognitive tests, and the apolipoprotein E ε4 gene—are well known. Others, such as ventricular enlargement, not drinking alcohol, and being underweight, are less well known. The tool could be developed for use in clinical and research settings to target prevention and treatment strategies for high-risk individuals.

    Researchers at the University of California, San Francisco, devised the index by studying 3,375 participants from the Cardiovascular Health Cognition Study, part of the larger Cardiovascular Health Study of people 65 and older. Of the participants, 14 percent developed dementia during the 6-year study. Fifty-six percent of participants with high scores on the 15-point index developed dementia, compared with 23 percent with mid-range scores and 4 percent with low scores.

    The study lays the groundwork for development of a shorter, simpler index that would be easier to use in a doctor’s office, yet have the same predictive accuracy, the researchers write.

    Reference:

    Barnes, D.E., et al. Predicting risk of dementia in older adults: the late-life dementia risk index. Neurology. 2009. Epub. May 13, 2009.

Pages