Alzheimers

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.

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:

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.

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.