Announcements

  • 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.

  • October 15, 2009

    An article in the Spring 2009 issue of Connections (Is a Big Belly Bad for the Brain? Examining Body Fat's Ties to Dementia) described research into links between obesity, Alzheimer’s disease, and other dementias. The article mentions studies that have found “both generalized and regional brain atrophy and changes in white matter in association with obesity." A recent 5-year study, partly funded by the NIA, amplifies earlier work, by showing that overweight or obese participants tended to have lower brain volumes in specific areas. To obtain these results, scientists at the University of Pittsburgh and the University of California, Los Angeles, applied sophisticated methods of computer analysis to high-resolution brain scans.

    This is the first time anyone has created brain maps showing a possible link between being overweight and brain degeneration in particular brain regions, according to senior investigator Dr. Paul M. Thompson. “The brains of obese people looked 16 years older than the brains of those who were lean, and the brains of overweight people looked 8 years older,” he said.

    Raji, C., et al. Brain structure and obesity. Human Brain Mapping (online ahead of print). August 6, 2009.

  • October 15, 2009

    Reduction of a protein in cerebrospinal fluid called brain-derived neurotrophic factor (BDNF) is associated with age-related cognitive decline, report scientists at the University of Washington School of Medicine in Seattle. The study confirms earlier research findings of low levels of BDNF in the cerebrospinal fluid of people with Alzheimer’s disease. Now, scientists have found reduced BDNF in older adults, including cognitively normal ones across the lifespan.

    The researchers compared BDNF levels in the cerebrospinal fluid of 128 cognitively normal people, 21 with Alzheimer’s, and 9 with mild cognitive impairment, who were given standard tests of memory and cognition. The scientists found that, as the normal participants aged, not only did their test scores fall, but also BDNF levels were lower.

    The findings suggest that reduced secretion of BDNF is associated with age-related cognitive decline in the absence of dementia or MCI and independent of the presence of the APOE e4 allele and the BDNF variant. The authors conclude that further studies are needed to validate their results. If these results are validated, scientists can look for ways to increase levels of BDNF to determine whether this restores cognition or slows its decline.

    Li, G., et al. Cerebrospinal fluid concentration of brain-derived neurotrophic factor and cognitive function in non-demented subjects. PloS One. 2009. 4(5):e5424.

  • October 15, 2009

    An NIA-funded study at Columbia University Medical Center has found an association between a Mediterranean diet and a reduced risk of mild cognitive impairment (MCI). Previous studies have found an association of this diet with a reduced risk of Alzheimer’s disease. Many people with MCI ultimately develop Alzheimer’s. A Mediterranean diet includes vegetables, legumes, fruits, cereals, fish, and mono-unsaturated fats; mild to moderate alcohol use; and low intake of saturated fats, dairy products, meat, and poultry.

    The researchers recruited 1,393 cognitively normal participants and 482 participants with MCI. Subjects were divided into three groups, characterized by low, medium, and high adherence to a Mediterranean diet. After an average 4.3 years, 275 of the cognitively normal participants had developed MCI, and 106 of the participants with MCI had progressed to Alzheimer’s disease. The high-adherence groups had a 28 percent and 48 percent lower risk of developing MCI and progressing to Alzheimer’s, respectively, than those in the low-adherence group did. Those in the medium-adherence group had a 17 percent and 45 percent lower risk of MCI and Alzheimer’s, respectively, than did those in the low-adherence group.

    Researchers speculated that a Mediterranean diet may improve cholesterol and blood sugar levels and blood vessel health or reduce inflammation, all of which have been associated with MCI, but more research is needed to determine whether it has the effect suggested in this epidemiological study.

    Scarmeas, N., et al. Mediterranean diet and mild cognitive impairment. Arch Neurol. 2009. 66(2):216-25.

  • October 15, 2009

    People with Alzheimer’s disease who had an episode of delirium experienced much faster cognitive decline than people with the disease who did not have delirium, a recent study shows. Delirium is a mental disorder characterized by restlessness, excitement, delusions, and/or hallucinations.

    Scientists from Harvard Medical School and Massachusetts General Hospital used data from the Massachusetts Alzheimer’s Disease Research Center’s patient registry to examine changes in cognitive performance over 15 years, in 408 older adults with Alzheimer’s, including 72 who developed delirium.

    Among patients with delirium, the annual decline in cognitive skills accelerated to twice the rate before delirium. Across the entire study group, the rate of decline was three times faster in those who had delirium compared with those who did not. The researchers conclude that information from this study will provide a foundation for future studies to determine whether prevention of delirium might delay cognitive decline in patients with Alzheimer’s disease.

    Fong, T.G., et al. Delirium accelerates cognitive decline in Alzheimer’s disease. Neurology. 2009. 72:1571-75.

  • June 15, 2010

    Dr. William Markesbery

    William R. Markesbery, M.D., who for more than 30 years was director of the University of Kentucky (UK) Sanders-Brown Center on Aging, died January 30, 2010, at age 77, in Lexington, KY. Dr. Markesbery led the UK Sanders-Brown Center on Aging from its founding in 1979 and was director of its Alzheimer's Disease Center. He also held the Commonwealth Chair in Aging and was professor of neurology, pathology, neurosurgery, and anatomy and neurobiology at the UK College of Medicine.

    Dr. Markesbery's studies of Alzheimer's disease received continuous NIH support for almost 30 years. He is credited with more than 410 peer-reviewed scientific publications and received numerous awards recognizing his work to find a cure for and prevention of Alzheimer's disease. The Journal of Alzheimer's Disease rated him among the top researchers in the world for the productivity and impact of his scientific study of Alzheimer's disease.

    From 1969 to 1972, Dr. Markesbery served as a faculty member at the University of Rochester School of Medicine and Dentistry and Strong Memorial Hospital in Rochester, NY. In 1972, he returned to UK and began his longtime career as a clinician and researcher. In addition to his College of Medicine appointments, Markesbery was a consultant in neurology and neuropathology at the Veterans Affairs Medical Center in Lexington.

    In 1974, he was the first to describe a rare form of heredity muscular dystrophy, now called Finnish-Markesbery Disease. In 1981, Markesbery and colleagues published one of several studies disproving the once-popular theory that an accumulation of toxic metals, such as aluminum, plays a role in the development of Alzheimer's disease. In 1991, they published the first study to demonstrate that oxidative stress is an important part of the pathogenesis of late-onset Alzheimer's disease and is present early in the disease.

    Dr. Markesbery received the Alzheimer's Association Khachaturian Award in 2009 for Outstanding Achievements in Advancing Alzheimer's Science.

    "Throughout his education and career, Bill Markesbery demonstrated his love for the University of Kentucky and his passion for Alzheimer's disease research," said Dr. Marcelle Morrison-Bogorad, director of NIA's Division of Neuroscience. "Without the work of leaders like him, our understanding of aging and Alzheimer's disease would not be where it is. We deeply appreciate Bill's contributions. He was a truly remarkable, dedicated professional whose work improved the quality of life for older Americans of this and future generations."

  • June 15, 2010

    More rigorous and long-term studies are needed before specific life style measures to prevent Alzheimer's disease and cognitive decline can be recommended, according to an independent panel convened by the National Institutes of Health (NIH). After reviewing medical literature and hearing speakers during an April 26-28 NIH State-of-the-Science Conference on Preventing Alzheimer's Disease and Cognitive Decline, the 15-member panel of clinical and scientific experts concluded that the existing evidence for drug, dietary, exercise, and other interventions is not yet sufficient to serve as the basis for clinical recommendations.

    Other conclusions by the panel included the following: There remain important and formidable challenges in conducting research on Alzheimer's disease and cognitive decline, particularly in the area of prevention. There are numerous ongoing or planned investigations which may offer promising new insights regarding the causes and prevention of these diseases. Cognitive decline and Alzheimer's disease pose a significant burden not only on affected individuals, but also on their caregivers and society. Firm conclusions cannot be drawn about the association of modifiable risk factors with cognitive decline or Alzheimer's disease. There is an absence of highly reliable consensus-based diagnostic criteria for cognitive decline, mild cognitive impairment, and Alzheimer's disease, and the available criteria have not been uniformly applied. There is insufficient evidence to support the use of pharmaceutical agents or dietary supplements to prevent or delay cognitive decline or Alzheimer's disease. Ongoing studies may provide new insight. Large-scale, population-based studies and randomized controlled clinical trials are critically needed to investigate strategies to maintain cognitive function and to identify factors that may delay onset of Alzheimer's disease in those at risk and that may slow the progression of Alzheimer's among individuals already diagnosed with the disease.

    The panel's final consensus statement can be found at http://consensus.nih.gov/2010/alzstatement.htm. NIA's ongoing Alzheimer's research program is actively investigating a variety of strategies to prevent or delay Alzheimer's and cognitive decline, including lifestyle strategies. You can find out more about the evidence thus far and what is being tested, including approaches like exercise and high blood pressure control, in the NIA booklet Can Alzheimer's Disease Be Prevented?

  • June 15, 2010

    People with early-onset Alzheimer's disease and "mixed dementias" are now eligible to receive social security benefits more quickly, thanks to an expansion of the Social Security Administration's (SSA's) Compassionate Allowance Program. According to the SSA, the purpose of the program is to waive the standard waiting period for benefits in order to "provide benefits quickly to applicants whose medical conditions are so serious that their conditions obviously meet disability standards."

    In a meeting on July 29, 2009, Alzheimer's experts and representatives from Alzheimer's Disease Centers (ADCs), as well as people struggling with these diseases, testified before SSA officials about the nature and effects of early-onset Alzheimer's and other dementias.

    NIA Deputy Director Dr. Marie Bernard explained the functions of the NIA, Alzheimer's Research Centers, and NIA's major Alzheimer's research initiatives, as well as the information and resources provided by the ADEAR Center. Among those testifying, Dr. David Bennett, Director of the ADC at the Rush University Medical Center, Chicago, provided an overview of the diseases. Sandra Weintraub, of the Northwestern ADC, explained how cognitive decline in early-onset disease is measured and differentiated from normal aging. Dr. Daniel Marson, Director of the University of Alabama at Birmingham ADC, testified on the impact of Alzheimer's disease on the capacity to work. Susan Frick, of the Rush ADC, testified regarding the emotional effects of Alzheimer's on people's ability to work. Darby Morhardt, also from Rush, discussed how families struggling with neurodegenerative diseases such as early-onset Alzheimer's have a host of psychological, social, family, and financial issues that are different from those of most people over 65.

  • June 15, 2010

    Allopregnanolone, a metabolite of the hormone progesterone that is made in the central nervous system, reversed neurological decline and improved performance on memory tests in 3-month-old mice with characteristics of Alzheimer's disease, a recent study showed. Allopregnanolone can increase the number of neural progenitor cells of mice and humans in vitro. In this study, led by researchers at the University of California, Los Angeles, the same molecule was given in vivo to triple transgenic Alzheimer's disease mice and to normal mice to test its effect on learning and memory. Allopregnanolone was found to regenerate nerve cells significantly in a part of the hippocampus—a region of the brain important to memory—in the transgenic mice but not in the normal mice. The Alzheimer's mice not only improved their performance on a trace eye-blink conditioning test of learning and memory, but performed as well as did the normal mice.

    Allopregnanolone can reverse cognitive deficits in an Alzheimer's mouse model, perhaps by helping certain nerve cells proliferate and thrive, the authors concluded. The findings, they say, suggest further investigation of allopregnanolone for its therapeutic potential in Alzheimer's disease.

    Wang, J.M., et al. Allopregnanolone reverses neurogenic and cognitive deficits in mouse model of Alzheimer's disease. Proceedings of the National Academy of Sciences USA. 2010. 107(14):6498-503. (PDF, 690K)

  • June 15, 2010

    Older adults with strong muscles are at lower risk of developing Alzheimer's disease and mild cognitive impairment than their weaker peers, researchers report in Archives of Neurology. The study builds on previous research showing a link between grip strength and Alzheimer's risk.

    In this study, researchers at the Rush University Alzheimer's Disease Center in Chicago measured a wide range of cognitive skills and muscle strength throughout the body in 970 participants with an average age of 80 years. During nearly 4 years of follow-up, 138 people developed Alzheimer's disease. After adjusting for age and other variables, the researchers found that the strongest 10 percent of participants had a 61 percent lower risk of developing Alzheimer's, compared with the weakest 10 percent of study participants. Muscle strength and mild cognitive impairment, a condition that often precedes Alzheimer's, were similarly but less closely linked. Stronger muscles were also associated with a slower rate of cognitive decline.

    The authors surmise that a common underlying disease process could account for the association between muscle weakness and declining cognition. Replication of the results in a population-based study is important, they add.

    Boyle, P.A., et al. Association of muscle strength with the risk of Alzheimer's disease and the rate of cognitive decline in community-dwelling older persons. Archives of Neurology. 2009. 66(11):1339-44.

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