aging

Controlling diabetes important for slowing cognitive decline

August, 2012
  • Findings from a large, long-running study adds to growing evidence that poorly controlled diabetes is associated with faster cognitive decline.

The latest finding from the large, long-running Health, Aging, and Body Composition (Health ABC) Study adds to the evidence that preventing or controlling diabetes helps prevent age-related cognitive decline.

The study involves 3,069 older adults (70+), of whom 717 (23%) had diabetes at the beginning of the study in 1997. Over the course of the study, a further 159 developed diabetes. Those with diabetes at the beginning had lower cognitive scores, and showed faster decline. Those who developed diabetes showed a rate of decline that was between that faster rate and the slower rate of those who never developed diabetes.

Among those with diabetes, those who had higher levels of a blood marker called glycosylated hemoglobin had greater cognitive impairment. Higher levels of this blood marker reflect poorer control of blood sugar.

In other words, both duration and severity of diabetes are important factors in determining rate of cognitive decline in old age.

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Benefits of omega-3 in preventing age-related cognitive decline not proven

August, 2012

A review of research into omega-3 oils' benefits for fighting cognitive decline concludes that there is no evidence, but that longer-term research is needed.

A review of three high quality trials comparing the putative benefits of omega-3 fatty acids for preventing age-related cognitive decline, has concluded that there is no evidence that taking fish oil supplements helps fight cognitive decline. The trials involved a total of 3,536 healthy older adults (60+). In two studies, participants were randomly assigned to receive gel capsules containing omega-3 PUFA or olive or sunflower oil for six or 24 months. In the third study, participants were randomly assigned to receive tubs of margarine spread for 40 months (regular margarine versus margarine fortified with omega-3 PUFA).

The researchers found no benefit from taking the omega-3 capsules or margarine spread compared to placebo capsules or margarines (sunflower oil, olive oil or regular margarine). Participants given omega-3 did not score better on the MMSE or on other tests of cognitive function such as verbal learning, digit span and verbal fluency.

The researchers nevertheless stress that longer term studies are needed, given that there was very little deterioration in cognitive function in any of the groups.

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Alzheimer's risk gene disrupts brain function in older women, but not men

August, 2012

A new study indicates that carrying the ‘Alzheimer’s gene’ may be a significant risk factor for women only.

While the ‘Alzheimer’s gene’ is relatively common — the ApoE4 mutation is present in around 15% of the population — having two copies of the mutation is, thankfully, much rarer, at around 2%. Having two copies is of course a major risk factor for developing Alzheimer’s, and it has been thought that having a single copy is also a significant (though lesser) risk factor. Certainly there is quite a lot of evidence linking ApoE4 carriers to various markers of cognitive impairment.

And yet, the evidence has not been entirely consistent. I have been puzzled by this myself, and now a new finding suggests a reason. It appears there are gender differences in responses to this gene variant.

The study involved 131 healthy older adults (median age 70), whose brains were scanned. The scans revealed that in older women with the E4 variant, brain activity showed the loss of synchronization that is typically seen in Alzheimer’s patients, with the precuneus (a major hub in the default mode network) out of sync with other brain regions. This was not observed in male carriers.

The finding was confirmed by a separate set of data, taken from the Alzheimer's Disease Neuroimaging Initiative database. Cerebrospinal fluid from 91 older adults (average age 75) revealed that female carriers had substantially higher levels of tau protein (a key Alzheimer’s biomarker) than male carriers or non-carriers.

It’s worth emphasizing that the participants in the first study were all cognitively normal — the loss of synchronization was starting to happen before visible Alzheimer’s symptoms appeared.

The findings suggest that men have less to worry about than women, as far as the presence of this gene is concerned. The study may also explain why more women than men get the disease (3 women to 2 men); it is not (although of course this is a factor) simply a consequence of women tending to live longer.

Whether or not these gender differences extend to carriers of two copies of the gene is another story.

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Exercise reduces Alzheimer's damage in brain

August, 2012

A mouse study provides more support for the value of exercise in preventing Alzheimer’s disease, and shows one of the ways in which it does so.

A study designed to compare the relative benefits of exercise and diet control on Alzheimer’s pathology and cognitive performance has revealed that while both are beneficial, exercise is of greater benefit in reducing Alzheimer’s pathology and cognitive impairment.

The study involved mice genetically engineered with a mutation in the APP gene (a familial risk factor for Alzheimer’s), who were given either a standard diet or a high-fat diet (60% fat, 20% carbohydrate, 20% protein vs 10% fat, 70% carbohydrate, 20% protein) for 20 weeks (from 2-3 to 7-8 months of age). Some of the mice on the high-fat diet spent the second half of that 20 weeks in an environmentally enriched cage (more than twice as large as the standard cage, and supplied with a running wheel and other objects). Others on the high-fat diet were put back on a standard diet in the second 10 weeks. Yet another group were put on a standard diet and given an enriched cage in the second 10 weeks.

Unsurprisingly, those on the high-fat diet gained significantly more weight than those on the standard diet, and exercise reduced that gain — but not as much as diet control (i.e., returning to a standard diet) did. Interestingly, this was not the result of changes in food intake, which either stayed the same or slightly increased.

More importantly, exercise and diet control were roughly equal in reversing glucose intolerance, but exercise was more effective than diet control in ameliorating cognitive impairment. Similarly, while amyloid-beta pathology was significantly reduced in both exercise and diet-control conditions, exercise produced the greater reduction in amyloid-beta deposits and level of amyloid-beta oligomers.

It seems that diet control improves metabolic disorders induced by a high-fat diet — conditions such as obesity, hyperinsulinemia and hypercholesterolemia — which affects the production of amyloid-beta. However exercise is more effective in tackling brain pathology directly implicated in dementia and cognitive decline, because it strengthens the activity of an enzyme that decreases the level of amyloid-beta.

Interestingly, and somewhat surprisingly, the combination of exercise and diet control did not have a significantly better effect than exercise alone.

The finding adds to the growing pile of evidence for the value of exercise in maintaining a healthy brain in later life, and helps explain why. Of course, as I’ve discussed on several occasions, we already know other mechanisms by which exercise improves cognition, such as boosting neurogenesis.

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Review of working memory training programs finds no broader benefit

July, 2012

A meta-analysis of 23 studies has found no evidence that working memory training has wider cognitive benefits for normally developing children and healthy adults.

I have said before that there is little evidence that working memory training has any wider benefits than to the skills being practiced. Occasionally a study arises that gets everyone all excited, but by and large training only benefits the skill being practiced — despite the fact that working memory underlies so many cognitive tasks, and limited working memory capacity is thought to negatively affect performance on so many tasks. However, one area that does seem to have had some success is working memory training for those with ADHD, and researchers have certainly not given hope of finding evidence for wider transfer among other groups (such as older adults).

A recent review of the research to date has, sadly, concluded that the benefits of working memory training programs are limited. But this is not to say there are no benefits.

For a start, the meta-analysis (analyzing data across studies) found that working memory training produced large immediate benefits for verbal working memory. These benefits were greatest for children below the age of 10.

These benefits, however, were not maintained long-term (at an average of 9 months after training, there were no significant benefits) — although benefits were found in one study in which the verbal working memory task was very similar to the training task (indicating that the specific skill practiced did maintain some improvement long-term).

Visuospatial working memory also showed immediate benefits, and these did not vary across age groups. One factor that did make a difference was type of training: the CogMed training program produced greater improvement than the researcher-developed programs (the studies included 7 that used CogMed, 2 that used Jungle Memory, 2 Cognifit, 4 n-back, 1 Memory Booster, and 7 researcher-developed programs).

Interestingly, visuospatial working memory did show some long-term benefits, although it should be noted that the average follow-up was distinctly shorter than that for verbal working memory tasks (an average of 5 months post-training).

The burning question, of course, is how well this training transferred to dissimilar tasks. Here the evidence seems sadly clear — those using untreated control groups tended to find such transfer; those using treated control groups never did. Similarly, nonrandomized studies tended to find far transfer, but randomized studies did not.

In other words, when studies were properly designed (randomized trials with a control group that is given alternative treatment rather than no treatment), there was no evidence of transfer effects from working memory training to nonverbal ability. Moreover, even when found, these effects were only present immediately and not on follow-up.

Neither was there any evidence of transfer effects, either immediate or delayed, on verbal ability, word reading, or arithmetic. There was a small to moderate effect on training on attention (as measured by the Stroop test), but this only occurred immediately, and not on follow-up.

It seems clear from this review that there are few good, methodologically sound studies on this subject. But three very important caveats should be noted in connection with the researchers’ dispiriting conclusion.

First of all, because this is an analysis across all data, important differences between groups or individuals may be concealed. This is a common criticism of meta-analysis, and the researchers do try and answer it. Nevertheless, I think it is still a very real issue, especially in light of evidence that the benefit of training may depend on whether the challenge of the training is at the right level for the individual.

On the other hand, another recent study, that compared young adults who received 20 sessions of training on a dual n-back task or a visual search program, or received no training at all, did look for an individual-differences effect, and failed to find it. Participants were tested repeatedly on their fluid intelligence, multitasking ability, working memory capacity, crystallized intelligence, and perceptual speed. Although those taking part in the training programs improved their performance on the tasks they practiced, there was no transfer to any of the cognitive measures. When participants were analyzed separately on the basis of their improvement during training, there was still no evidence of transfer to broader cognitive abilities.

The second important challenge comes from the lack of skill consolidation — having a short training program followed by months of not practicing the skill is not something any of us would expect to produce long-term benefits.

The third point concerns a recent finding that multi-domain cognitive training produces longer-lasting benefits than single-domain training (the same study also showed the benefit of booster training). It seems quite likely that working memory training is a valuable part of a training program that also includes practice in real-world tasks that incorporate working memory.

I should emphasize that these results only apply to ‘normal’ children and adults. The question of training benefits for those with attention difficulties or early Alzheimer’s is a completely different issue. But for these healthy individuals, it has to be said that the weight of the evidence is against working memory training producing more general cognitive improvement. Nevertheless, I think it’s probably an important part of a cognitive training program — as long as the emphasis is on part.

Reference: 

Melby-Lervåg, M., & Hulme, C. (2012). Is Working Memory Training Effective? A Meta-Analytic Review. Developmental psychology. doi:10.1037/a0028228
Full text available at http://www.apa.org/pubs/journals/releases/dev-ofp-melby-lervag.pdf

[3012] Redick, T. S., Shipstead Z., Harrison T. L., Hicks K. L., Fried D. E., Hambrick D. Z., et al.
(2012).  No Evidence of Intelligence Improvement After Working Memory Training: A Randomized, Placebo-Controlled Study..
Journal of Experimental Psychology: General.
Full text available at http://psychology.gatech.edu/renglelab/publications/2012/RedicketalJEPG.pdf
 

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Rapamycin makes young mice learn better and prevents decline in old mice

July, 2012

Further evidence from mice studies that the Easter Island drug improves cognition, in young mice as well as old.

I have reported previously on research suggesting that rapamycin, a bacterial product first isolated from soil on Easter Island and used to help transplant patients prevent organ rejection, might improve learning and memory. Following on from this research, a new mouse study has extended these findings by adding rapamycin to the diet of healthy mice throughout their life span. Excitingly, it found that cognition was improved in young mice, and abolished normal cognitive decline in older mice.

Anxiety and depressive-like behavior was also reduced, and the mice’s behavior demonstrated that rapamycin was acting like an antidepressant. This effect was found across all ages.

Three "feel-good" neurotransmitters — serotonin, dopamine and norepinephrine — all showed significantly higher levels in the midbrain (but not in the hippocampus). As these neurotransmitters are involved in learning and memory as well as mood, it is suggested that this might be a factor in the improved cognition.

Other recent studies have suggested that rapamycin inhibits a pathway in the brain that interferes with memory formation and facilitates aging.

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Immune system may protect against Alzheimer's

July, 2012

New studies involving genetically-engineered mice and older adult humans support a connection between the immune system and cognitive impairment in old age.

A number of studies have come out in recent years linking age-related cognitive decline and dementia risk to inflammation and infection (put inflammation into the “Search this site” box at the top of the page and you’ll see what I mean). New research suggests one important mechanism.

In a mouse study, mice engineered to be deficient in receptors for the CCR2 gene — a crucial element in removing beta-amyloid and also important for neurogenesis — developed Alzheimer’s-like pathology more quickly. When these mice had CCR2 expression boosted, accumulation of beta-amyloid decreased and the mice’s memory improved.

In the human study, the expression levels of thousands of genes from 691 older adults (average age 73) in Italy (part of the long-running InCHIANTI study) were analyzed. Both cognitive performance and cognitive decline over 9 years (according to MMSE scores) were significantly associated with the expression of this same gene. That is, greater CCR2 activity was associated with lower cognitive scores and greater decline.

Expression of the CCR2 gene was also positively associated with the Alzheimer’s gene — meaning that those who carry the APOE4 variant are more likely to have higher CCR2 activity.

The finding adds yet more weight to the importance of preventing / treating inflammation and infection.

Reference: 

[2960] Harries, L. W., Bradley-Smith R. M., Llewellyn D. J., Pilling L. C., Fellows A., Henley W., et al.
(2012).  Leukocyte CCR2 Expression Is Associated with Mini-Mental State Examination Score in Older Adults.
Rejuvenation Research. 120518094735004 - 120518094735004.

Naert, G. & Rivest S. 2012. Hematopoietic CC-chemokine receptor 2-(CCR2) competent cells are protective for the cognitive impairments and amyloid pathology in a transgenic mouse model of Alzheimer's disease. Molecular Medicine, 18(1), 297-313.

El Khoury J, et al. 2007. Ccr2 deficiency impairs microglial accumulation and accelerates progression of Alzheimer-like disease. Nature Medicine, 13, 432–8.

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Effect of blood pressure on the aging brain depends on genetics

July, 2012
  • For those with the Alzheimer’s gene, higher blood pressure, even though within the normal range, is linked to greater brain shrinkage and reduced cognitive ability.

I’ve reported before on the evidence suggesting that carriers of the ‘Alzheimer’s gene’, APOE4, tend to have smaller brain volumes and perform worse on cognitive tests, despite being cognitively ‘normal’. However, the research hasn’t been consistent, and now a new study suggests the reason.

The e4 variant of the apolipoprotein (APOE) gene not only increases the risk of dementia, but also of cardiovascular disease. These effects are not unrelated. Apoliproprotein is involved in the transportation of cholesterol. In older adults, it has been shown that other vascular risk factors (such as elevated cholesterol, hypertension or diabetes) worsen the cognitive effects of having this gene variant.

This new study extends the finding, by looking at 72 healthy adults from a wide age range (19-77).

Participants were tested on various cognitive abilities known to be sensitive to aging and the effects of the e4 allele. Those abilities include speed of information processing, working memory and episodic memory. Blood pressure, brain scans, and of course genetic tests, were also performed.

There are a number of interesting findings:

  • The relationship between age and hippocampal volume was stronger for those carrying the e4 allele (shrinkage of this brain region occurs with age, and is significantly greater in those with MCI or dementia).
  • Higher systolic blood pressure was significantly associated with greater atrophy (i.e., smaller volumes), slower processing speed, and reduced working memory capacity — but only for those with the e4 variant.
  • Among those with the better and more common e3 variant, working memory was associated with lateral prefrontal cortex volume and with processing speed. Greater age was associated with higher systolic blood pressure, smaller volumes of the prefrontal cortex and prefrontal white matter, and slower processing. However, blood pressure was not itself associated with either brain atrophy or slower cognition.
  • For those with the Alzheimer’s variant (e4), older adults with higher blood pressure had smaller volumes of prefrontal white matter, and this in turn was associated with slower speed, which in turn linked to reduced working memory.

In other words, for those with the Alzheimer’s gene, age differences in working memory (which underpin so much of age-related cognitive impairment) were produced by higher blood pressure, reduced prefrontal white matter, and slower processing. For those without the gene, age differences in working memory were produced by reduced prefrontal cortex and prefrontal white matter.

Most importantly, these increases in blood pressure that we are talking about are well within the normal range (although at the higher end).

The researchers make an interesting point: that these findings are in line with “growing evidence that ‘normal’ should be viewed in the context of individual’s genetic predisposition”.

What it comes down to is this: those with the Alzheimer’s gene variant (and no doubt other genetic variants) have a greater vulnerability to some of the risk factors that commonly increase as we age. Those with a family history of dementia or serious cognitive impairment should therefore pay particular attention to controlling vascular risk factors, such as hypertension and diabetes.

This doesn’t mean that those without such a family history can safely ignore such conditions! When they get to the point of being clinically diagnosed as problems, then they are assuredly problems for your brain regardless of your genetics. What this study tells us is that these vascular issues appear to be problematic for Alzheimer’s gene carriers before they get to that point of clinical diagnosis.

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Omega-3 oil linked to lower level of Alzheimer's protein

June, 2012

A new study adds to growing evidence that higher levels of omega-3 fatty acids help protect against Alzheimer’s disease.

A new study, involving 1,219 dementia-free older adults (65+), has found that the more omega-3 fatty acids the person consumed, the lower the level of beta-amyloid in the blood (a proxy for brain levels). Consuming a gram of omega-3 more than the average per day was associated with 20-30% lower beta-amyloid levels. A gram of omega-3 equates to around half a fillet of salmon per week.

Participants provided information about their diet for an average of 1.2 years before their blood was tested for beta-amyloid. Other nutrients investigated —saturated fatty acids, omega-6 polyunsaturated fatty acids, mono-unsaturated fatty acid, vitamin E, vitamin C, beta-carotene, vitamin B12, folate and vitamin D — were not associated with beta-amyloid levels.

The results remained after adjusting for age, education, gender, ethnicity, amount of calories consumed and APOE gene status.

The findings are consistent with previous research associating higher levels of omega-3 and/or fish intake with lower risk of Alzheimer’s. Additionally, another recent study provides evidence that the brains of those with Alzheimer’s disease, MCI, and the cognitively normal, all have significantly different levels of omega-3 and omega-6 fatty acids. That study concluded that the differences were due to both consumption and metabolic differences.

Reference: 

[2959] Gu, Y., Schupf N., Cosentino S. A., Luchsinger J. a, & Scarmeas N.
(2012).  Nutrient Intake and Plasma Β-Amyloid.
Neurology. 78(23), 1832 - 1840.

Cunnane, S.C. et al. 2012. Plasma and Brain Fatty Acid Profiles in Mild Cognitive Impairment and Alzheimer’s Disease. Journal of Alzheimer’s Disease, 29 (3), 691-697.

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Computer use and exercise combo reduce odds of MCI

June, 2012

Engaging in both moderate exercise and cognitively stimulating activities has an additive effect in reducing your risk of becoming cognitively impaired.

More findings from the long-running Mayo Clinic Study of Aging reveal that using a computer plus taking moderate exercise reduces your risk of mild cognitive impairment significantly more than you would expect from simply adding together these two beneficial activities.

The study involved 926 older adults (70-93), of whom 109 (12%) were diagnosed with MCI. Participants completed questionnaires on physical exercise and mental stimulation within the previous year. Computer use was targeted in this analysis because of its popularity as a cognitive activity, and because it was particularly associated with reduced odds of having MCI.

Among the cognitively healthy, only 20.1% neither exercised moderately nor used a computer, compared to 37.6% of those with MCI. On the other hand, 36% of the cognitively healthy both exercised and used a computer, compared to only 18.3% of those with MCI. There was little difference between the two groups as regards exercise but no computer use, or computer use but no exercise.

The analysis took into account calorie intake, as well as education, depression, and other health factors. Daily calorie intake was significantly higher in those with MCI compared to those without (respective group medians of 2100 calories vs 1802) — note that the median BMI was the same for the two groups.

Moderate physical exercise was defined as brisk walking, hiking, aerobics, strength training, golfing without a golf cart, swimming, doubles tennis, yoga, martial arts, using exercise machines and weightlifting. Light exercise included activities such as bowling, leisurely walking, stretching, slow dancing, and golfing with a cart. Mentally stimulating activities included reading, crafts, computer use, playing games, playing music, group and social and artistic activities and watching less television.

It should be noted that the assessment of computer activities was very basic. The researchers suggest that in future studies, both duration and frequency should be assessed. I would add type of activity, although that would be a little more difficult to assess.

Overall, the findings add yet more weight to the evidence for the value of physical exercise and mental stimulation in staving off cognitive impairment in old age, and add the twist that doing both is much better than doing either one alone.

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