Shrinking Telomeres May Foretell Dementia

Telomeres are the end caps of chromosomes, protecting the DNA complexes from deterioration during cell division. Telomere shortening is considered a marker of cellular aging, and prematurely shortened telomeres have been linked to increased risk of cancers, heart disease, dementia and death.  Lawrence Honig, from Columbia University (New York, USA), and colleagues assessed DNA samples from participants enrolled in the Washington Heights-Inwood Community Aging Project.  The team used real-time polymerase chain reaction (PCR) to determine mean telomere length in 1,983 patients who had a mean age of 78 and who were followed for mortality for a mean of 9.3 years. During the study, 190 patients (9.6%) developed incident dementia.  Confirming findings of previous studies, the researchers found that telomere length was inversely related to age and was shorter in men than in women.  Further, they found that patients who died during follow-up had shorter mean telomere length than survivors, and the association remained even after adjusting for age, sex, education, and apolipoprotein E genotype status.  The team also determined that patients who developed dementia had significantly shorter telomere length (6,131 base pairs for prevalent cases and 6,315 base pairs for incident cases, as compared with 6,431 base pairs for those remaining dementia-free.)   The study authors conclude that: “Our findings suggest that shortened leukocyte [telomere length] is associated with risks for dementia and mortality and may therefore be a marker of biological aging.”

Honig LS, Kang M, Schupf N, Lee JH, Mayeux R. “Association of Shorter Leukocyte Telomere Repeat Length With Dementia and Mortality.” Arch Neurol.,  July 23, 2012.

Alzheimer’s Disease Claimed Half Million Lives in One Year in US

While the US Centers for Disease Control & Prevention (CDC) filed vital statistics for 2008 listing official number for deaths from Alzheimer's disease at 82,000, Bryan James, from Rush University (Illinois, USA), and colleagues contend that the CDC statistics were based on death certificates, and fail to factor in chronic coexisting conditions that leave people weak and fragile and thereby lead to death.  The team analyzed data collected in the Religious Orders Study (began in 2004) and the Rush Memory and Aging Project (began in 1997), the total of both following 2,500 older men and women with cognitive tests and other exams. Autopsy data were available for more than 80% of the approximately 1,000 participants who have died so far. Deaths among participants who developed incident Alzheimer's disease during follow-up were far more common than in those remaining dementia-free:  of 516 who developed Alzheimer's disease, 68.0% died, compared with 32.3% of those without incident Alzheimer's. Median time to death for participants who developed Alzheimer's disease was 2.7 years.  The data from the two Rush cohorts were then extrapolated to the entire US population, using vital statistics data from 2007. Careful to distinguish deaths with Alzheimer's disease and deaths from the disease, the team estimates that 477,800 deaths in 2007 could be attributable to Alzheimer's disease.  Noting that reduction of the frequency of diagnostic assessments leads to underestimates of the attributable risk, the study authors submit that deaths from Alzheimer's disease may be six times more common than official statistics indicate.

"Senior Moments" Not a Normal Part of Aging

Aging is not the cause of so-called “senior moments”, mild memory lapses often experienced by older people. Robert S Wilson, PhD a neuropsychologist at Rush University Medical Center, and colleagues studied data of 354 Catholic nuns, priests, and brothers who had annual clinical evaluations for up to 13 years and who underwent brain autopsy after death. The annual clinical evaluations included detailed testing of cognitive function. The researchers found that cognitive function gradually declined with age until the last four to five years of life, when it declined rapidly. As the researchers expected, pathologic lesions, such as neurofibrillary tangles, cerebral infarction, and Lewy bodies, were related to rapid cognitive decline. However, results also showed that the presence of lesions was strongly predictive of mild changes in cognitive function, such as memory lapses. Indeed, the presence of Lewy bodies and cerebral infarction doubled the rate of gradual memory decline, whilst virtually no decline in cognitive function was noted in participants who were free of lesions. “The very early mild cognitive changes once thought to be normal aging are really the first signs of progressive dementia, in particular Alzheimer’s disease.” said  Dr Wilson. “The pathology in the brain related to Alzheimer’s and other dementias has a much greater impact on memory function in old age than we previously recognized. Our study finds that Alzheimer’s disease and related dementias are the root cause of virtually all loss of cognition and memory in old age. They aren’t the only contributing factors; other factors affect how vulnerable we are to the pathology and to its effects.  But the pathology does appear to be the main force that is driving cognitive decline in old age.”

Wilson RS, Leurgans SE, Boyle PA, Schneider JA, Bennett DA. Neurodegenerative basis of age-related cognitive decline. Neurology. 2010 Sep 15.

$200 Billion Tab for Alzheimer’s Care in US

The Alzheimer's Association (Illinois, USA) issued its “2012 Alzheimer’s Disease Facts and Figures.”  The Association reveals that 5.4 million Americans are living with Alzheimer's Disease, and the disorder affects one in eight older Americans. As the sixth leading cause of death in the United States, the bill for caring for Alzheimer's patients is staggering. This year, the tab for direct indirect costs of Alzheimer's disease and other dementias in the United States will reach an estimated $200 billion. The report warns that in the absence of advances in prevention and treatment, the cost of caring for patients with Alzheimer's disease and other dementias could reach $1.1 trillion (in 2012 dollars) by 2050, a trend driven by an aging population.  Additionally, the Association identified that Alzheimer's caregivers -- mostly family members -- provided 17.4 billion hours of unpaid care, assisting in various activities of daily living.  Those responsibilities came with large amounts of emotional stress and depression, as well as sacrifices at work.

“2012 Alzheimer’s Disease Facts and Figures.” Alzheimer’s Association, March 2012.

Poor Sleep May Be Early Signal of Alzheimer’s Disease

In lab animal studies, disrupted sleep has been shown to cause a build-up in beta-amyloid markers characteristic of Alzheimer's Disease. Washington University School of Medicine (Missouri, USA), researchers report that signs of these beta-amyloid plaques ts can be detected in cognitively normal people who experience frequent awakenings and a habit of lying awake.  Yo-El Ju and colleagues analyzed data collected in the Adult Children Study, in which half the subjects have a family history of Alzheimer's. For this analysis, 100 participants, ages 45 to 80 years, were given standardized assessments and shown to be cognitively normal. Participants wore an actigraph for 14 days to measure sleep in an objective fashion; sleep diaries and questionnaires were used to gather subjective measures. The researchers also measured levels of amyloid beta-42 in cerebrospinal fluid and looked for increased retention of Pittsburgh compound B during amyloid imaging by positron emission tomography -- 25% of participants had preclinical signs of Alzheimer's. On average, participants spent about eight hours in bed, as measured by both actigraph results and subjective reports, but average sleep time on the actigraph was 6.5 hours because of brief awakenings during the night. Those who woke up more than five times an hour were more likely to have abnormal biomarkers indicating amyloid pathology. And more of those with low sleep efficiency – defined as sleep time divided by time in bed of less than 85% – had such signs compared with those with high sleep efficiency. Further studies to establish correlation of causality are needed, to establish the role of disrupted sleep as a factor in Alzheimer's Disease.

Huang Y, Potter R, Sigurdson W, Santacruz A, Shih S, Ju YE, et al.  “Effects of age and amyloid deposition on A[beta] dynamics in the human central nervous system. Arch Neurol. 2012 Jan;69(1):51-8.

Vitamins & Healthy Fats Promote Mental Acuity

A diet rich in key vitamins and healthy fats may help older men and women to stay cognitively sharp, as well as reduce brain shrinkage associated with Alzheimer’s Disease.  Conversely, a “junk food” diet (characterized by high trans fat intake) predicts lower cognitive scores, as well as reduced total cerebral brain volume.  G.L. Bowman, from Oregon Health and Science University (or guide, USA), and colleagues completed a study that specifically measured a wide range of blood nutrient levels and correlated them to performance on mental acuity tests.  The researchers enrolled 104 people, average age 87 years, none of whom experienced special risk factors for memory or mental acuity. The team tested 30 different nutrient biomarkers in their blood, and 42 participants also had MRI scans to measure their brain volume. The most favorable cognitive outcomes and brain size measurements were associated with two dietary patterns – high levels of marine fatty acids, and high levels of vitamins B, C, D and E. In contrast, consistently worse cognitive performance was associated with a higher intake of the type of trans-fats found in baked and fried foods, margarine, fast food and other less-healthy dietary choices. The researchers conclude that:  "Distinct nutrient biomarker patterns detected in plasma are interwpretable and account for a significant degree of variance in both cognitive function and brain volume.”

G.L. Bowman, L.C. Silbert, D. Howieson, H.H. Dodge, M.G. Traber, B. Frei, et al. ”Nutrient biomarker patterns, cognitive function, and MRI measures of brain aging.” Neurology, December 28, 2011.

More than Half of Alzheimer's Cases May Be Preventable

Over half of all Alzheimer's disease cases could potentially be prevented through lifestyle changes and treatment or prevention of chronic medical conditions, according to researchers from San Francisco VA Medical Center (California, USA).  Deborah Barnes and colleagues analyzed data from studies around the world involving hundreds of thousands of participants, and concluded that worldwide, the biggest modifiable risk factors for Alzheimer's disease are, in descending order of magnitude, low education, smoking, physical inactivity, depression, mid-life hypertension, diabetes and mid-life obesity.  In the United States, the team found that the biggest modifiable risk factors are physical inactivity, depression, smoking, mid-life hypertension, mid-life obesity, low education and diabetes.  The researchers report that: “A 10 to 25% reduction in all seven risk factors could potentially prevent as many as 1.1 to 3.0 million Alzheimer’s Disease] cases worldwide and 184,000 to 492,000 cases in the [United States].”`

Deborah E Barnes, Kristine Yaffe. “The projected effect of risk factor reduction on Alzheimer's disease prevalence.”  The Lancet Neurology, July 19, 2011.

Healthy Diet May Offset Alzheimer’s Risks

Apolipoprotein E (APOE), created by the apolipoprotein E. gene, is a molecule that is generally acknowledged as a known contributor to Alzheimer’s Disease.  APOE is a lipoprotein and known to be influenced by the good oil found in fish. Daniel Michaelson, from Tel Aviv University (Israel), and colleagues, engaged under a joint European Commission grant known as LIPIDIDIET, introduced three different kinds of diet: a normal diet, a "bad" diet high in cholesterol, and a "good" diet high in fish oil, to a mouse model of Alzheimer’s Disease.    The team found that a rich in omega-3  fatty acids, and low in cholesterol,  significantly reduced the negative effects of the APOE4 gene.   The researchers urge that:  "The main take-away message here is that good diets can alleviate the effects of bad genes. This approach can be applied to specifically counteract the negative effects of Alzheimer's disease-related genes."

Daniel Michaelson. “ApoE4 Potentiates the Pathological Effects of the Amyloid Cascade and Impairs Anti A-beta Defense Mechanisms” (Abstract #912).  Presentation at the 10th International Conference on Alzheimer’s and Parkinson’s Diseases, March 12, 2011.

New Research on Molecular Mechanisms and

Prevention of Alzheimer 's Disease

Stanislaw R. Burzynski, MD

2009 A4M Orlando Conference.

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