seniors

Common Alzheimer's medication helps skills necessary for safe driving

August, 2010

The most common type of Alzheimer's drugs (cholinesterase inhibitors) was associated with improved attention and driving skills in those with early stage Alzheimer's.

A study involving outpatients with early stage Alzheimer’s found that their performance on some computerized tests of executive function and visual attention, including a simulated driving task, improved significantly after three months of taking cholinesterase inhibitors. Specifically, the drug treatment was associated with an improved ability to accurately maintain lane position during the simulated driving task; to accurately and quickly detect a target in a visual search task; to more quickly complete computerized mazes.

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Cognitive ability, not age, predicts risky decisions

July, 2010

A new study provides evidence that it's not age per se that affects the quality of decision-making, but individual differences in processing speed and memory.

A study involving 54 older adults (66-76) and 58 younger adults (18-35) challenges the idea that age itself causes people to become more risk-averse and to make poorer decisions. Analysis revealed that it is individual differences in processing speed and memory that affect decision quality, not age. The stereotype has arisen no doubt because more older people process slowly and have poorer memory. The finding points to the need to identify ways in which to present information that reduces the demand on memory or the need to process information very quickly, to enable those in need of such help (both young and old) to make the best choices. Self-knowledge also helps — recognizing if you need to take more time to make a decision.

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Teenage physical activity reduces risk of cognitive impairment later

July, 2010

A large long-running study reveals that physical activity is always important for women wanting to prevent cognitive impairment in old age, but being active in adolescence is most important.

A large longitudinal study, comparing physical activity at teenage, age 30, age 50, and late life against cognition of 9,344 women, has revealed that women who are physically active at any point have a lower risk of cognitive impairment in late-life compared to those who are inactive, but teenage physical activity is the most important. When age, education, marital status, diabetes, hypertension, depressive symptoms, smoking, and BMI were accounted for, only teenage physical activity status remained significantly associated with cognitive performance in old age. Although becoming active later in life didn’t make up for being inactive in adolescence, it did significantly reduce the risk of cognitive impairment compared to those who remained physically inactive. The findings are a strong argument for greater effort in increasing physical activity in today's youth.

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Abdominal fat at middle age associated with greater risk of dementia

July, 2010

More evidence that excess abdominal fat, independent of your overall BMI, places otherwise healthy, middle-aged people at greater risk for dementia later in life.

A study involving 733 participants from the Framingham Heart Study Offspring Cohort (average age 60) provides more evidence that excess abdominal fat places otherwise healthy, middle-aged people at greater risk for dementia later in life. The study also confirms that a higher BMI (body mass index) is associated with lower brain volumes in both older and middle-aged adults. However the association between visceral fat and total brain volume was independent of BMI. Visceral fat differs from subcutaneous fat in that it is buried deeper, beneath the muscles, around the organs. While it can only be seen by CT imaging, a pot belly or thick waist suggests its presence. For women (who become particularly vulnerable to this after menopause), a waistline above 88 cm is regarded as signaling a dangerous amount of visceral fat. Regular vigorous exercise, and consumption of polyunsaturated fats rather than saturated fats, is recommended.

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Looking after a spouse with dementia greatly increases your own risk of dementia

July, 2010

A long-running study has revealed that caring for a spouse with dementia is as strong a risk factor for developing Alzheimer's as having the 'Alzheimer's gene'.

A 12-year study involving 1,221 married couples ages 65 or older (part of the Cache County (Utah) Memory Study) has revealed that husbands or wives who care for spouses with dementia are six times more likely to develop Alzheimer’s themselves than those whose spouses don't have it. The increased risk is of comparable size to having the ‘Alzheimer's gene’. The researchers speculate that the great stress of caregiving might be responsible for the increased dementia risk, emphasizing the need for greater caregiver support.

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[1583] Norton, M. C., Smith K. R., Østbye T., Tschanz JA. T., Corcoran C., Schwartz S., et al.
(2010).  Greater Risk of Dementia When Spouse Has Dementia? The Cache County Study.
Journal of the American Geriatrics Society. 58(5), 895 - 900.

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Alzheimer's expressed differently in carriers and noncarriers of the Alzheimer’s gene

July, 2010
  • A new study reveals that having the 'Alzheimer's gene' doesn't simply increase your risk of developing Alzheimer's, but affects how the brain is damaged.

A comprehensive study reveals how the ‘Alzheimer's gene’ (APOE ε4) affects the nature of the disease. It is not simply that those with the gene variant tend to be more impaired (in terms of both memory loss and brain damage) than those without. Different parts of the brain (and thus different functions) tend to be differentially affected, depending on whether the individual is a carrier of the gene or not. Carriers displayed significantly greater impairment on tests of memory retention, while noncarriers were more impaired on tests of working memory, executive control, and lexical access. Consistent with this, carriers showed greater atrophy in the mediotemporal lobe, and noncarriers greater atrophy in the frontoparietal area. The findings have implications both for diagnosis and treatment.

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Animal studies indicate caffeine may slow dementia and cognitive decline but human studies less conclusive

July, 2010

Several recent studies and reviews suggest that the benefits of caffeine for age-related cognitive impairment and dementia are limited. It may be that the association only exists for women.

A special supplement in the Journal of Alzheimer's Disease focuses on the effects of caffeine on dementia and age-related cognitive decline. Here are the highlights:

A mouse study has found memory restoration and lower levels of amyloid-beta in Alzheimer’s mice following only 1-2 months of caffeine treatment. The researchers talk of “ a surprising ability of moderate caffeine intake to protect against or treat AD”, and define moderate intake as around 5 cups of coffee a day(!).

A review of studies into the relation between caffeine intake, diabetes, cognition and dementia, concludes that indications that coffee/caffeine consumption is associated with a decreased risk of Type 2 diabetes and possibly also with a decreased dementia risk, cannot yet be confirmed with any certainty.

A study involving 351 older adults without dementia found the association between caffeine intake and cognitive performance disappeared once socioeconomic status was taken into account.

A study involving 641 older adults found caffeine consumption was significantly associated with less cognitive decline for women only. Supporting this, white matter lesions were significantly fewer in women consuming more than 3 units of caffeine per day (after adjustment for age) than in women consuming less.

A Portuguese study involving 648 older adults found that caffeine intake was associated with a lower risk of cognitive decline in women, but not significantly in men.

A review of published studies examining the relation between caffeine intake and cognitive decline or dementia shows a trend towards a protective effect of caffeine, but because of the limited number of epidemiological studies, and the methodological differences between them, is unable to come up with a definitive conclusion.

A review of published epidemiological studies looking at the association between caffeine intake and Parkinson’s Disease confirms that higher caffeine intake is associated with a lower risk of developing Parkinson’s Disease (though this association may be stronger for men than women). Other studies provide evidence of caffeine’s potential in treatment, improving both the motor deficits and non-motor symptoms of Parkinson’s.

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Arendash, G.W. & Cao, C. Caffeine and Coffee as Therapeutics Against Alzheimer’s Disease. Journal of Alzheimer's Disease, 20 (Supp 1), 117-126.
Biessels, G.J. Caffeine, Diabetes, Cognition, and Dementia. Journal of Alzheimer's Disease, 20 (Supp 1), 143-150.
Kyle, J., Fox, H.C. & Whalley, L.J. Caffeine, Cognition, and Socioeconomic Status. Journal of Alzheimer's Disease, 20 (Supp 1), 151-159.
Ritchie, K. et al. Caffeine, Cognitive Functioning, and White Matter Lesions in the Elderly: Establishing Causality from Epidemiological Evidence. Journal of Alzheimer's Disease, 20 (Supp 1), 161-161
Santos, C. et al. Caffeine Intake is Associated with a Lower Risk of Cognitive Decline: A Cohort Study from Portugal. Journal of Alzheimer's Disease, 20 (Supp 1), 175-185.
Santos, C. et al. Caffeine Intake and Dementia: Systematic Review and Meta-Analysis. Journal of Alzheimer's Disease, 20 (Supp 1), 187-204.
Costa, J. et al. Caffeine Exposure and the Risk of Parkinson’s Disease: A Systematic Review and Meta-Analysis of Observational Studies. Journal of Alzheimer's Disease, 20 (Supp 1), 221-238.
Prediger, R.D.S. Effects of Caffeine in Parkinson’s Disease: From Neuroprotection to the Management of Motor and Non-Motor Symptoms. Journal of Alzheimer's Disease, 20 (Supp 1), 205-220.

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Extending lifespan has mixed effects on learning and memory

July, 2010

Although roundworm research suggesting different effects at different ages is concerned with genetic manipulation, we may speculate that restricting your food intake is a bad idea for young adults but good for the old, while reducing sugar may be better for the young than it is for the old.

Studies on the roundworm C. elegans have revealed that the molecules required for learning and memory are the same from C. elegans to mammals, suggesting that the basic mechanisms underlying learning and memory are ancient, and that this animal can serve as a testing ground for treatments for age-related memory loss. Intriguingly, a comparison of two known regulators of longevity — reducing calorie intake and reducing activity in the insulin-signaling pathway (achieved through genetic manipulation) — has found that these two treatments produce very different effects on memory. While dietary restriction impaired memory in early adulthood, it maintained memory with age. On the other hand, reduced insulin signaling improved early adult memory performance but failed to preserve it with age. These different effects appear to be linked to expression of CREB, a protein known to be important for long-term memory. Young roundworms with defective insulin receptors had higher levels of CREB protein, while those worms genetically altered to eat less had low levels, but the level did not diminish with age. These findings add to our understanding of why memory declines with age.

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Promise of drug therapy for age-related memory loss

July, 2010

Mouse studies suggest a way to reverse both normal age-related memory loss, and dementia.

Although research has so far been confined to mouse studies, researchers are optimistic about the promise of histone deacetylase inhibitors in reversing age-related memory loss — both normal decline, and the far more dramatic loss produced by Alzheimer’s. The latest study reveals that memory impairment in the aging mouse is associated with altered hippocampal chromatin plasticity, specifically with the failure of histone H4 lysine 12 acetylation, leading to a failure to initiate the gene expression program associated with memory consolidation. Restoring this acetylation leads to the recovery of cognitive abilities.

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Test of implantable cardioverter defibrillator linked to cognitive problems

March, 2010

A study involving patients given on implantable cardioverter defibrillator (ICD) reveals that more than a third of participants had significant cognitive problems six weeks and six and 12 months after ICD surgery. Although most regained their normal abilities within 12 months, a few (10%) first developed difficulties at that point.

An implantable cardioverter defibrillator (ICD) is a small electronic device that monitors and regulates heartbeat, and many have been implanted in patients — an estimated 114,000 in the U.S. in 2006. Part of the implantation process involves ventricular defibrillation testing, which temporarily disrupts brain activity by causing a drop in blood pressure and blood flow to the brain. In a study involving 52 patients having cognitive tests several days before ICD surgery and again six weeks and six and 12 months afterwards, more than a third of participants had significant cognitive problems six weeks and six and 12 months after ICD surgery. Attention, short-term memory of visual words and objects, and auditory (spoken) words were most commonly affected. Although most patients regained their normal abilities by 12 months after surgery, a few (10%) first developed difficulties at that point. The results were unrelated to measurements of anxiety, depression and quality of life.

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