MCI

mild cognitive impairment

Identifying those with cognitive impairment

March, 2012

A brief questionnaire designed to identify those with Alzheimer’s has been found to be useful in also identifying those with MCI. A large study confirms the value of such tools but also points to their limitations

New data from the ongoing validation study of the Alzheimer's Questionnaire (AQ), from 51 cognitively normal individuals (average age 78) and 47 aMCI individuals (average age 74), has found that the AQ is effective in identifying not only those with Alzheimer’s but also those older adults with mild cognitive impairment.

Of particular interest is that four questions were strong indicators of aMCI. These related to:

  • repeating questions and statements,
  • trouble knowing the date or time,
  • difficulties managing finances, and
  • decreased sense of direction.

The AQ consists of 21 yes/no questions designed to be answered by a relative or carer. The questions fall into five categories: memory, orientation, functional ability, visuospatial ability, and language. Six of these questions are known to be predictive of AD and are given extra weighting, resulting in a score out of 27. A score above 15 was indicative of AD, and between 5 and 14 of aMCI. Scores of 4 or lower indicate that the person does not have significant memory problems.

The questionnaire is not of course definitive, but is intended as an indicator for further testing. Note, too, that all participants in this study were Caucasian.

The value and limitations of brief cognitive screenings

The value of brief cognitive screenings combined with offering further evaluation is demonstrated in a recent large VA study, which found that, of 8,342 Veterans aged 70+ who were offered screening (the three-minute Mini-Cog), 8,063 (97%) accepted, 2,081 (26%) failed the screen, and 580 (28%) agreed to further evaluation. Among those accepting further evaluation, 93% were found to have cognitive impairment, including 75% with dementia.

Among those who declined further evaluation, 17% (259/1,501) were diagnosed with incident cognitive impairment through standard clinical care. In total, the use of brief cognitive screenings increased the numbers with cognitive impairment to 11% (902/8,063) versus 4% (1,242/28,349) in similar clinics without this program.

Importantly, the limits of such questionnaires were also demonstrated: 118 patients who passed the initial screen nevertheless requested further evaluation, and 87% were found to have cognitive impairment, including 70% with dementia.

This should not be taken as a reason not to employ such cognitive tests! There are two points that should, I think, be taken from this:

  • Routine screening of older adults is undoubtedly an effective strategy for identifying those with cognitive impairment.
  • Individuals who pass such tests but nevertheless believe they have cognitive problems should be taken seriously.

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Nicotine patch shows benefits in mild cognitive impairment

February, 2012

A pilot study suggests that wearing a nicotine patch may help improve memory loss in older adults with mild cognitive impairment.

The study involved 74 non-smokers with amnestic MCI (average age 76), of whom half were given a nicotine patch of 15 mg a day for six months and half received a placebo. Cognitive tests were given at the start of the study and again after three and six months.

After 6 months of treatment, the nicotine-treated group showed significant improvement in attention, memory, speed of processing and consistency of processing. For example, the nicotine-treated group regained 46% of normal performance for age on long-term memory, whereas the placebo group worsened by 26%.

Nicotine is an interesting drug, in that, while predominantly harmful, it can have positive effects if the dose is just right, and if the person’s cognitive state is at a particular level (slipping below their normal state, but not too far below). Too much nicotine will make things worse, so it’s important not to self-medicate.

Nicotine has been shown to improve cognitive performance in smokers who have stopped smoking and previous short-term studies with nicotine have shown attention and memory improvement in people with Alzheimer's disease. Nicotine receptors in the brain are reduced in Alzheimer’s brains.

Because the dose is so crucial, and the effects so dependent on brain state (including, one assumes, whether the person has been a smoker or not), more research is needed before this can be used as a treatment.

Reference: 

[2736] Newhouse, P., Kellar K., Aisen P., White H., Wesnes K., Coderre E., et al.
(2012).  Nicotine treatment of mild cognitive impairment.
Neurology. 78(2), 91 - 101.

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Higher risk of mild cognitive impairment among older men

February, 2012

Significant differences in the risk of mild cognitive impairment for men and women, and in the risk of developing the two sub-types, suggests that risk factors should be considered separately for genders and sub-type.

More data from the long-running Mayo Clinic Study of Aging has revealed that, in this one part of the U.S. at least, MCI develops at an overall rate of 6.4% a year among older adults (70+), with a higher rate for men and the less-educated.

The study involved 1,450 older adults (aged 70-89), who underwent memory testing every 15 months for an average of three years. By the end of the study period, 296 people had developed MCI, a rate of 6.4% per year. For men, the rate was 7.2% compared to 5.7% for women.

It should be noted that these rates apply to a relatively homogeneous group of people. Participants come from one county in Minnesota, an overwhelmingly white part of the U.S.

MCI comes in two types: amnestic (involving memory loss) and non-amnestic. Amnestic MCI was more than twice as common as non-amnestic MCI. The incidence rate of aMCI was also higher for men (4.4%) than women (3.3%), as was the risk of naMCI (2% vs 1.1%).

Those who had less education also had higher rates of MCI. For aMCI, the rate for those with 12 years or less of education was 4.3%, compared to 3.25% for those with more education. Similarly, for naMCI, the rates were 2% and 1%, respectively.

While the great majority of people diagnosed with MCI continued to have the disorder or progressed to dementia, some 12% were later re-diagnosed as not having it. This, I would presume, probably reflects temporary ‘dips’ in cognitive performance as a consequence of physical or emotional problems.

The differences between aMCI and naMCI, and between genders, suggest that risk factors for these should be considered separately.

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'Exergames' may provide greater cognitive benefit for older adults

February, 2012

An intriguing pilot study finds that regular exercise on a stationary bike enhanced with a computer game-type environment improves executive function in older adults more than ordinary exercise on a stationary bike.

We know that physical exercise greatly helps you prevent cognitive decline with aging. We know that mental stimulation also helps you prevent age-related cognitive decline. So it was only a matter of time before someone came up with a way of combining the two. A new study found that older adults improved executive function more by participating in virtual reality-enhanced exercise ("exergames") that combine physical exercise with computer-simulated environments and interactive videogame features, compared to the same exercise without the enhancements.

The Cybercycle Study involved 79 older adults (aged 58-99) from independent living facilities with indoor access to a stationary exercise bike. Of the 79, 63 participants completed the three-month study, meaning that they achieved at least 25 rides during the three months.

Unfortunately, randomization was not as good as it should have been — although the researchers planned to randomize on an individual basis, various technical problems led them to randomize on a site basis (there were eight sites), with the result that the cybercycle group and the control bike group were significantly different in age and education. Although the researchers took this into account in the analysis, that is not the same as having groups that match in these all-important variables. However, at least the variables went in opposite directions: while the cybercycle group was significantly younger (average 75.7 vs 81.6 years), it was significantly less educated (average 12.6 vs 14.8 years).

Perhaps also partly off-setting the age advantage, the cybercycle group was in poorer shape than the control group (higher BMI, glucose levels, lower physical activity level, etc), although these differences weren’t statistically significant. IQ was also lower for the cybercycle group, if not significantly so (but note the high averages for both groups: 117.6 vs 120.6). One of the three tests of executive function, Color Trails, also showed a marked group difference, but the large variability in scores meant that this difference was not statistically significant.

Although participants were screened for disorders such as Alzheimer’s and Parkinson’s, and functional disability, many of both groups were assessed as having MCI — 16 of the 38 in the cybercycle group and 14 of the 41 in the control bike group.

Participants were given cognitive tests at enrolment, one month later (before the intervention began), and after the intervention ended. The stationary bikes were identical for both groups, except the experimental bike was equipped with a virtual reality display. Cybercycle participants experienced 3D tours and raced against a "ghost rider," an avatar based on their last best ride.

The hypothesis was that cybercycling would particularly benefit executive function, and this was borne out. Executive function (measured by the Color Trails, Stroop test, and Digits Backward) improved significantly more in the cybercycle condition, and indeed was the only cognitive task to do so (other cognitive tests included verbal fluency, verbal memory, visuospatial skill, motor function). Indeed, the control group, despite getting the same amount of exercise, got worse at the Digits Backward test, and failed to show any improvement on the Stroop test.

Moreover, significantly fewer cybercyclists progressed to MCI compared to the control group (three vs nine).

There were no differences in exercise quantity or quality between the two groups — which does argue against the idea that cyber-enhanced physical activity would be more motivating. However, the cybercycling group did tend to comment on their enjoyment of the exercise. While the enjoyment may not have translated into increased activity in this situation, it may well do so in a longer, less directed intervention — i.e. real life.

It should also be remembered that the intervention was relatively short, and that other cognitive tasks might take longer to show improvement than the more sensitive executive function. This is supported by the fact that levels of the brain growth factor BDNF, assessed in 30 participants, showed a significantly greater increase of BDNF in cybercyclists.

I should also emphasize that the level of physical exercise really wasn't that great, but nevertheless the size of the cybercycle's effect on executive function was greater than usually produced by aerobic exercise (a medium effect rather than a small one).

The idea that activities that combine physical and mental exercise are of greater cognitive benefit than the sum of benefits from each type of exercise on its own is not inconsistent with previous research, and in keeping with evidence from animal studies that physical exercise and mental stimulation help the brain via different mechanisms. Moreover, I have an idea that enjoyment (in itself, not as a proxy for motivation) may be a factor in the cognitive benefits derived from activities, whether physical or mental. Mere speculation, derived from two quite separate areas of research: the idea of “flow” / “being in the zone”, and the idea that humor has physiological benefits.

Of course, as discussed, this study has a number of methodological issues that limit its findings, but hopefully it will be the beginning of an interesting line of research.  

Reference: 

[2724] Anderson-Hanley, C., Arciero P. J., Brickman A. M., Nimon J. P., Okuma N., Westen S. C., et al.
(2012).  Exergaming and Older Adult Cognition.
American Journal of Preventive Medicine. 42(2), 109 - 119.

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Diet linked to brain atrophy in old age

January, 2012
  • A more rigorous measurement of diet finds that dietary factors account for nearly as much brain shrinkage as age, education, APOE genotype, depression and high blood pressure combined.

The study involved 104 healthy older adults (average age 87) participating in the Oregon Brain Aging Study. Analysis of the nutrient biomarkers in their blood revealed that those with diets high in omega 3 fatty acids and in vitamins C, D, E and the B vitamins had higher scores on cognitive tests than people with diets low in those nutrients, while those with diets high in trans fats were more likely to score more poorly on cognitive tests.

These were dose-dependent, with each standard deviation increase in the vitamin BCDE score ssociated with a 0.28 SD increase in global cognitive score, and each SD increase in the trans fat score associated with a 0.30 SD decrease in global cognitive score.

Trans fats are primarily found in packaged, fast, fried and frozen food, baked goods and margarine spreads.

Brain scans of 42 of the participants found that those with diets high in vitamins BCDE and omega 3 fatty acids were also less likely to have the brain shrinkage associated with Alzheimer's, while those with high trans fats were more likely to show such brain atrophy.

Those with higher omega-3 scores also had fewer white matter hyperintensities. However, this association became weaker once depression and hypertension were taken into account.

Overall, the participants had good nutritional status, but 7% were deficient in vitamin B12 (I’m surprised it’s so low, but bear in mind that these are already a select group, being healthy at such an advanced age) and 25% were deficient in vitamin D.

The nutrient biomarkers accounted for 17% of the variation in cognitive performance, while age, education, APOE genotype (presence or absence of the ‘Alzheimer’s gene’), depression and high blood pressure together accounted for 46%. Diet was more important for brain atrophy: here, the nutrient biomarkers accounted for 37% of the variation, while the other factors accounted for 40% (meaning that diet was nearly as important as all these other factors combined!).

The findings add to the growing evidence that diet has a significant role in determining whether or not, and when, you develop Alzheimer’s disease.

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Common health complaints increase Alzheimer's risk

October, 2011

Two large studies respectively find that common health complaints and irregular heartbeat are associated with an increased risk of developing Alzheimer’s, while a rat study adds to evidence that stress is also a risk factor.

A ten-year study involving 7,239 older adults (65+) has found that each common health complaint increased dementia risk by an average of about 3%, and that these individual risks compounded. Thus, while a healthy older adult had about an 18% chance of developing dementia after 10 years, those with a dozen of these health complaints had, on average, closer to a 40% chance.

It’s important to note that these complaints were not for serious disorders that have been implicated in Alzheimer’s. The researchers constructed a ‘frailty’ index, involving 19 different health and wellbeing factors: overall health, eyesight, hearing, denture fit, arthritis/rheumatism, eye trouble, ear trouble, stomach trouble, kidney trouble, bladder control, bowel control, feet/ankle trouble, stuffy nose/sneezing, bone fractures, chest problems, cough, skin problems, dental problems, other problems.

Not all complaints are created equal. The most common complaint — arthritis/rheumatism —was only slightly higher among those with dementia. Two of the largest differences were poor eyesight (3% of the non-demented group vs 9% of those with dementia) and poor hearing (3% and 6%).

At the end of the study, 4,324 (60%) were still alive, and of these, 416 (9.6%) had Alzheimer's disease, 191 (4.4%) had another sort of dementia and 677 (15.7%) had other cognitive problems (but note that 1,023 were of uncertain cognitive ability).

While these results need to be confirmed in other research — the study used data from broader health surveys that weren’t specifically designed for this purpose, and many of those who died during the study will have probably had dementia — they do suggest the importance of maintaining good general health.

Common irregular heartbeat raises risk of dementia

In another study, which ran from 1994 to 2008 and followed 3,045 older adults (mean age 74 at study start), those with atrial fibrillation were found to have a significantly greater risk of developing Alzheimer’s.

At the beginning of the study, 4.3% of the participants had atrial fibrillation (the most common kind of chronically irregular heartbeat); a further 12.2% developed it during the study. Participants were followed for an average of seven years. Over this time, those with atrial fibrillation had a 40-50% higher risk of developing dementia of any type, including probable Alzheimer's disease. Overall, 18.8% of the participants developed some type of dementia during the course of the study.

While atrial fibrillation is associated with other cardiovascular risk factors and disease, this study shows that atrial fibrillation increases dementia risk more than just through this association. Possible mechanisms for this increased risk include:

  • weakening the heart's pumping ability, leading to less oxygen going to the brain;
  • increasing the chance of tiny blood clots going to the brain, causing small, clinically undetected strokes;
  • a combination of these plus other factors that contribute to dementia such as inflammation.

The next step is to see whether any treatments for atrial fibrillation reduce the risk of developing dementia.

Stress may increase risk for Alzheimer's disease

And a rat study has shown that increased release of stress hormones leads to cognitive impairment and that characteristic of Alzheimer’s disease, tau tangles. The rats were subjected to stress for an hour every day for a month, by such means as overcrowding or being placed on a vibrating platform. These rats developed increased hyperphosphorylation of tau protein in the hippocampus and prefrontal cortex, and these changes were associated with memory deficits and impaired behavioral flexibility.

Previous research has shown that stress leads to that other characteristic of Alzheimer’s disease: the formation of beta-amyloid.

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Which 'Senior moments' may signal mental decline

October, 2011

A very large survey of older women indicates which type of memory difficulties may signal age-related cognitive impairment possibly leading to dementia.

A telephone survey of around 17,000 older women (average age 74), which included questions about memory lapses plus standard cognitive tests, found that getting lost in familiar neighborhoods was highly associated with cognitive impairment that might indicate Alzheimer’s. Having trouble keeping up with a group conversation and difficulty following instructions were also significantly associated with cognitive impairment. But, as most of us will be relieved to know, forgetting things from one moment to the next was not associated with impairment!

Unsurprisingly, the more memory complaints a woman had, the more likely she was to score poorly on the cognitive test.

The 7 memory lapse questions covered:

  • whether they had recently experienced a change in their ability to remember things,
  • whether they had trouble remembering a short list of items (such as a shopping list),
  • whether they had trouble remembering recent events,
  • whether they had trouble remembering things from one second to the next,
  • whether they had difficulty following spoken or written instructions,
  • whether they had more trouble than usual following a group conversation or TV program due to memory problems,
  • whether they had trouble finding their way around familiar streets.

Because this survey was limited to telephone tests, we can’t draw any firm conclusions. But the findings may be helpful for doctors and others, to know which sort of memory complaints should be taken as a flag for further investigation.

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One cause of damage in older brains, and how exercise can help

September, 2011

Two mice studies indicate that an increase in a protein involved in immune response may be behind the reduced ability of older brains to create new neurons, and that exercise produces a protein that helps protect against damage caused by illness, injury, surgery and pollutants.

In the first mouse study, when young and old mice were conjoined, allowing blood to flow between the two, the young mice showed a decrease in neurogenesis while the old mice showed an increase. When blood plasma was then taken from old mice and injected into young mice, there was a similar decrease in neurogenesis, and impairments in memory and learning.

Analysis of the concentrations of blood proteins in the conjoined animals revealed the chemokine (a type of cytokine) whose level in the blood showed the biggest change — CCL11, or eotaxin. When this was injected into young mice, they indeed showed a decrease in neurogenesis, and this was reversed once an antibody for the chemokine was injected. Blood levels of CCL11 were found to increase with age in both mice and humans.

The chemokine was a surprise, because to date the only known role of CCL11 is that of attracting immune cells involved in allergy and asthma. It is thought that most likely it doesn’t have a direct effect on neurogenesis, but has its effect through, perhaps, triggering immune cells to produce inflammation.

Exercise is known to at least partially reverse loss of neurogenesis. Exercise has also been shown to produce chemicals that prevent inflammation. Following research showing that exercise after brain injury can help the brain repair itself, another mouse study has found that mice who exercised regularly produced interleukin-6 (a cytokine involved in immune response) in the hippocampus. When the mice were then exposed to a chemical that destroys the hippocampus, the interleukin-6 dampened the harmful inflammatory response, and prevented the loss of function that is usually observed.

One of the actions of interleukin-6 that brings about a reduction in inflammation is to inhibit tumor necrosis factor. Interestingly, I previously reported on a finding that inhibiting tumor necrosis factor in mice decreased cognitive decline that often follows surgery.

This suggests not only that exercise helps protect the brain from the damage caused by inflammation, but also that it might help protect against other damage, such as that caused by environmental toxins, injury, or post-surgical cognitive decline. The curry spice cucurmin, and green tea, are also thought to inhibit tumor necrosis factor.

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More evidence of the benefits of B vitamins in fighting cognitive decline

September, 2011
  • High daily doses of B-vitamins significantly slowed cognitive decline and brain atrophy in those with MCI, especially if they had high levels of homocysteine.

In a small study, 266 older adults with mild cognitive impairment (aged 70+) received a daily dose of 0.8 mg folic acid, 0.5 mg vitamin B12 and 20 mg vitamin B6 or a placebo for two years. Those treated with B vitamins had significantly lower levels of homocysteine at the end of the trial (high homocysteine is a known risk factor for age-related cognitive decline and dementia). Moreover, this was associated with a significantly slower rate of brain shrinkage.

However, while there were significant effects on homocysteine level, brain atrophy, and executive function, it wasn’t until results were separated on the basis of baseline homocysteine levels that we get really dramatic results.

It was the group with high homocysteine levels at the start of the study who really benefited from the high doses of B vitamins. For them, brain atrophy was cut by half, and there were clear benefits in episodic memory, semantic memory, and global cognitive function, not just executive function. Among those with high baseline homocysteine who received the placebo, significant cognitive decline occurred.

The level of B vitamins in the supplements was considerably greater than the recommended standard. However, caution must be taken in dosing yourself with supplements, because folic acid can have negative effects. Better to try and get your diet right first.

A longer and larger follow-up study is now planned, and hopefully that will tell us if such treatment can keep MCI developing into Alzheimer’s.

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Memory loss in old age the price we pay for a large brain & a long life?

September, 2011
  • Chimpanzee brains don’t shrink with age as humans’ do. It may be that cognitive impairment and even dementia are our lot because we work our brains too hard for too long.

Comparison of 99 chimpanzee brains ranging from 10-51 years of age with 87 human brains ranging from 22-88 years of age has revealed that, unlike the humans, chimpanzee brains showed no sign of shrinkage with age. But the answer may be simple: we live much longer. In the wild, chimps rarely live past 45, and although human brains start shrinking as early as 25 (as soon as they reach maturity, basically!), it doesn’t become significant until around 50.

The answer suggests one reason why humans are uniquely vulnerable to Alzheimer’s disease — it’s all down to our combination of large brain and long life. There are other animals that experience some cognitive impairment and brain atrophy as they age, but nothing as extreme as that found in humans (a 10-15% decline in volume over the life-span). (Elephants and whales have the same two attributes as humans — large brains and long lives — but we lack information on how their brains change with age.)

The problem may lie in the fact that our brains use so much more energy than chimps’ (being more than three times larger than theirs) and thus produce a great deal more damaging oxidation. Over a longer life-span, this accumulates until it significantly damages the brain.

If that’s true, it reinforces the value of a diet high in antioxidants.

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[2500] Sherwood, C. C., Gordon A. D., Allen J. S., Phillips K. A., Erwin J. M., Hof P. R., et al.
(2011).  Aging of the cerebral cortex differs between humans and chimpanzees.
Proceedings of the National Academy of Sciences. 108(32), 13029 - 13034.

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