Alzheimers

Alzheimer's & other dementias

Major depression more than doubles risk of dementia among adults with diabetes

March, 2010

Both diabetes and clinical depression are known to be risk factors for dementia. Now a study that tracked nearly 4000 diabetics over 5 years has found having both increased the risk 2.7-fold.

Both diabetes and clinical depression are known to be risk factors for dementia. Now a study that tracked nearly 4000 diabetics over 5 years has found having both increased the risk 2.7-fold. Nearly 8% of the diabetics with major depression (36 of 455) developed dementia over the five years, compared to 4.8% of those with diabetes alone (163 of 3382). Those who developed dementia within 2 years of being diagnosed with depression were excluded. Depression is common among people who have diabetes.

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Mother’s Alzheimer’s greater risk factor than father’s

March, 2010

A brain scanning study adds to evidence that having a mother with Alzheimer’s is a greater risk factor than having a father with Alzheimer’s.

A brain scanning study using Pittsburgh Compound B, involving 42 healthy individuals (aged 50-80), of whom 14 had mothers who developed Alzheimer's, 14 had fathers with Alzheimer's, and 14 had no family history of the disease, has found that those with a maternal history had 15% more amyloid-beta plaques than those with a paternal history, and 20% more than those with no family history. The findings add to evidence that having a mother with Alzheimer’s is a greater risk factor than having a father with Alzheimer’s. The groups did not differ in age, gender, education, or apolipoprotein E (ApoE) status.

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[335] Mosconi, L., Rinne J. O., Tsui W. H., Berti V., Li Y., Wang H Y., et al.
(2010).  Increased fibrillar amyloid-β burden in normal individuals with a family history of late-onset Alzheimer’s.
Proceedings of the National Academy of Sciences. 107(13), 5949 - 5954.

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Having greater purpose in life associated with reduced Alzheimer's risk

March, 2010
  • Data from a large long-running study has found that greater purpose in life was associated with a substantially reduced risk of developing Alzheimer's disease, as well as a reduced risk of mild cognitive impairment and a slower rate of cognitive decline.

Data from over 900 community-dwelling older adults participating in the Rush Memory and Aging Project has found that greater purpose in life was associated with a substantially reduced risk of developing Alzheimer's disease, as well as a reduced risk of mild cognitive impairment and a slower rate of cognitive decline. Specifically, those scoring in the top 10% of a purpose in life measure (4.2 out of 5) were approximately 2.4 times more likely to remain free of Alzheimer's disease than individuals in the bottom 10% (score of 3.0). The association was independent of sociodemographic status, depression, neuroticism, social network size, and number of chronic health conditions.

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Factors predicting conversion of mild cognitive impairment to Alzheimer’s identified

March, 2010

New analysis reveals the most important factors for predicting whether amnestic-MCI would develop into Alzheimer’s within 2 years were hyperglycemia, female gender and having the Alzheimer's gene.

An analysis technique using artificial neural networks has revealed that the most important factors for predicting whether amnestic mild cognitive impairment (MCI-A) would develop into Alzheimer’s within 2 years were hyperglycemia, female gender and having the APOE4 gene (in that order). These were followed by the scores on attentional and short memory tests.

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Tabaton, M. et al. 2010. Artificial Neural Networks Identify the Predictive Values of Risk Factors on the Conversion of Amnestic Mild Cognitive Impairment. Journal of Alzheimer's Disease, 19 (3), 1035-1040.

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Untreated vision problems linked to dementia in the elderly

March, 2010

Data from over 600 older adults has revealed that those with very good or excellent vision had a 63% reduced risk of dementia over the 8.5-year study period, while those with poorer vision who did not visit an ophthalmologist had a 9.5-fold increased risk of Alzheimer disease. The findings point to the need for older adults to seek treatment for their eye problems.

Data from 625 elderly Americans, followed for an average of 8.5 years, has revealed that those with very good or excellent vision at the beginning of the study had a 63% reduced risk of dementia over the study period. Those with poorer vision who did not visit an ophthalmologist had a 9.5-fold increased risk of Alzheimer disease and a 5-fold increased risk of cognitively impaired but no dementia. For the very-old (90+), 78% who maintained normal cognition had received at least one previous eye procedure compared with 51.7% of those with Alzheimer disease. The findings point to the need for older adults to seek treatment for their eye problems. The study raises the possibility that poor vision is not simply a symptom of developing dementia, but a contributing factor — possibly through its effect on curtailing activities which would help prevent it.

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[325] Rogers, M. A. M., & Langa K. M.
(2010).  Untreated Poor Vision: A Contributing Factor to Late-Life Dementia.
Am. J. Epidemiol.. 171(6), 728 - 735.

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Alzheimer's memory problems originate with oligomers not plaques

April, 2010

While everyone agrees that amyloid-beta protein is part of the problem, not everyone agrees that amyloid plaques are the cause (or one of them) of Alzheimer’s. A new study provides convincing evidence that floating clumps called oligomers or ADDLs are the real problem.

While everyone agrees that amyloid-beta protein is part of the problem, not everyone agrees that amyloid plaques are the cause (or one of them) of Alzheimer’s. Other forms of amyloid-beta have been pointed to, including floating clumps called oligomers or ADDLs. A new study, using mice engineered to form only these oligomers, and never any plaques, throughout their lives, provides more support for this theory. Mice that never developed plaques were just as impaired by the disease as mice with both plaques and oligomers, and when a gene that converted oligomers into plaques was added to the mice, the mice were no more impaired than they had been before. This may explain why treatments aimed at removing plaques have not been successful, and offers a new approach to the treatment of Alzheimer’s.

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More evidence for benefits of Rapamycin

April, 2010

Another study using a different strain of genetically engineered mice has confirmed the finding that the transplant drug rapamycin prevented cognitive impairment.

A few months ago, I reported on an exciting finding that rapamycin, a drug currently used in transplant patients, improved memory in Alzheimer's mice. Now a different strain of mice (ones engineered to have defects in the genes that make amyloid precursor protein) has also shown improvements in learning and memory, correlated with less damage in brain tissue, after rapamycin treatment lowered levels of amyloid-beta-42. The mice given the drug performed at levels comparable with normal mice.

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New guideline on when people with Alzheimer's disease should stop driving

April, 2010

The American Academy of Neurology has updated its guidelines on when people with dementia should stop driving. The guidelines support caregivers’ instincts, but not use of the patient’s own self-rating.

The American Academy of Neurology has updated its guidelines on when people with dementia should stop driving. While the guidelines point out that this decision is a complex one that should be made by a doctor using the Clinical Dementia Rating scale, they also supported caregivers’ instincts, which have been found to often be correct. For caregivers and family members, the following warning signs are identified:

  • Decreased miles being driven
  • Collisions
  • Moving violations
  • Avoiding certain driving situations, such as driving at night or in the rain
  • Aggressive or impulsive personality traits

However, the patient’s own self-rating, and a lack of situational avoidance, are not regarded as useful evidence.

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New gene associated with increased risk of Alzheimer's

April, 2010

Another gene has been identified that appears to increase risk of Alzheimer’s. The gene is involved in influencing the body's levels of homocysteine (high levels are known to be a strong risk factor), and have also been implicated in coronary artery disease.

Another gene has been identified that appears to increase risk of Alzheimer’s. The gene, MTHFD1L, is located on chromosome six. Comparison of the genomes of 2,269 people with late-onset Alzheimer's disease and 3,107 people without the disease found those with a particular variation in this gene were almost twice as likely to develop Alzheimer's disease as those people without the variation. The gene is involved in influencing the body's levels of homocysteine (high levels are known to be a strong risk factor), and have also been implicated in coronary artery disease.

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The results were presented at the American Academy of Neurology's 62nd Annual Meeting in Toronto, April 10–17, 2010.

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Clinical trial shows intervention reduces brain atrophy in Alzheimer’s patients

April, 2010

The Phase II clinical trial of a treatment using naturally occurring antibodies has been successful in slowing (and in some cases preventing) the progression of the disease in patients with mild-to-moderate Alzheimer's. A much larger trial is now being carried out.

The Phase II clinical trial of a treatment using naturally occurring antibodies (IGIV) has achieved significantly lower rates of ventricular enlargement (6.7% vs 12.7% per year) and less whole-brain atrophy (1.6% vs 2.2% per year) than control subjects who initially received placebo. The trial ran for 18 months and involved 24 patients with mild to moderate Alzheimer's disease, of whom 16 received IGIV once or twice a month for the whole period, and 8 received a placebo for the first 6 months. Those who responded best to IGIV did not measurably decline over 18 months, and had an average rate of brain shrinkage and average rate of ventricular enlargement comparable to the rate previously reported in normal elderly individuals. Most tellingly, differences in rates were associated with dosage rates (there were four different regimens). A much larger trial is now being carried out.

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The results were presented April 13 at the American Academy of 62nd Annual Meeting in Toronto.

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