seniors

Following on from studies showing that a Mediterranean-like diet may be associated with a lower risk of Alzheimer's disease and may lengthen survival in people with Alzheimer's, a six-year study of 712 New Yorkers has revealed that those who were most closely following a Mediterranean-like diet were 36% less likely to have brain infarcts (small areas of dead tissue linked to thinking problems), compared to those who were least following the diet. Those moderately following the diet were 21% less likely to have brain damage.

A new test has been developed that measures amyloid-beta oligomers in the cerebrospinal fluid, promising a reliable means of early diagnosis. In a comparison of patients with Alzheimer’s, patients with MCI that later developed into Alzheimer’s, and controls, levels of these protein fragments directly correlated with Alzheimer’s, and was more accurate than levels of the more usual amyloid plaques.

A computerized self test (CST) has been developed that is 96% accurate in diagnosing Alzheimer’s and MCI-A (compared to 71% for the MMSE and 69% for the Mini-Cognitive — tests currently in use). Moreover, the test accurately classified 91% of the six experimental groups (control, MCI, early Alzheimer's, mild to moderate, moderate to severe, and severe) as compared to 54% for the MMSE and 48% for the Mini-Cog. The brief, interactive online test is designed to be used in the primary care setting, where physicians may not have detailed training in recognizing cognitive impairments.

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.

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.

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).

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.

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.

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.

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.