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.

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.

A rat study has shown how a diet high in fructose (from corn syrup, not the natural levels that occur in fruit) impairs brain connections and hurts memory and learning — and how omega-3 fatty acids can reduce the damage.

We know that these unnaturally high levels of fructose can hurt the brain indirectly through their role in diabetes and obesity, but this new study demonstrates that it also damages the brain directly.

In the study, two groups of rats consumed a fructose solution as drinking water for six weeks. One of these groups also received omega-3 fatty acids in the form of flaxseed oil and DHA. Both groups trained on a maze twice daily for five days before starting the experimental diet. After the six weeks of the diet, the rats were put in the maze again.

Those who didn’t receive the omega-3 oils navigated the maze much more slowly than the second group, and their brains showed a decline in synaptic activity. They also showed signs of resistance to insulin. Indications were that insulin had lost much of its power to regulate synaptic function.

It’s suggested that too much fructose could block insulin's ability to regulate how cells use and store sugar for the energy required for processing information.

It’s estimated that the average American consumes more than 40 pounds of high-fructose corn syrup per year.

The findings are consistent with research showing an association between metabolic syndrome and poorer cognitive function, and help explain the mechanism. They also support the consumption of omega-3 fatty acids as a preventative or ameliorative strategy.

Now that we’ve pretty much established that sleep is crucial for consolidating memory, the next question is how much sleep we need.

A new study compared motor sequence learning in 16 people with mild obstructive sleep apnea to a matched control group (also attending the sleep clinic). There were no significant differences between the groups in total sleep time, sleep efficiency and sleep architecture (time spent in the various sleep stages), subjective measures of sleepiness, or performance on a psychomotor vigilance task (a task highly sensitive to sleep deprivation).

Nor were there any differences in learning performance during the training phase on the motor task.

But the interesting thing about consolidation is that skills usually improve overnight — your performance the next day will usually be better than it was at the end of your training. And here there was a significant difference between the groups, with the controls showing much greater overnight improvement on the motor sequence task. For sequences learned in the morning and tested 12 hours later on the same day, however, there were no differences between the groups.

So given all the factors relating to sleep that were the same between the two groups, what was the factor behind the group consolidation difference? It turns out it was (principally) the arousal index (arousals were scored on the basis of abrupt shifts in EEG frequency that last at least 3 seconds with 10 seconds of stable sleep preceding), and to a lesser extent the apnea-hypopnea index.

It seems likely, then, that arousals from sleep may (depending, presumably, on timing) interrupt the transfer of labile memories from the hippocampus to the neocortex for long-term storage. Thus, the more arousals you have, the more likely it is that this process will be interrupted.

A number of studies, principally involving rodents, have established that physical exercise stimulates the creation of new brain cells in the hippocampus. A recent study attempted to uncover more about the mechanism.

Using two drugs that work directly on muscles, producing the physical effects of exercise, the researchers compared the effects on the brain. One drug (Aicar) improves the fitness of even sedentary animals. The other drug increases the effects of exercise on animals that exercise, but has little effect on sedentary animals.

After a week of receiving one of the drugs, sedentary mice performed better on tests of memory and learning, and showed more new brain cells. These effects were significantly greater for those taking Aicar.

Because the drugs have very little ability to cross into the brain, this demonstrates that the neurogenesis results from exercise-type reactions in the muscles, not to brain responses to the drugs. Indeed, previous research has found that direct infusion of Aicar into the brain impaired learning and memory.

Aicar increases the muscles’ output of AMPK, an enzyme that affects cellular energy and metabolism. It’s speculated that some of this enzyme may enter the bloodstream and travel to the brain. Interestingly, as with neurogenesis, AMPK activity in muscles appears to decline with age. It may be that AMPK production could serve as a biomarker for neurogenesis, as well as being a target for improving neurogenesis.

These findings add weight to evidence for the value of aerobic exercise over other types of exercise (given that the mice exercise by running). However, I see that human research has found that resistance training (which is difficult to study in mice!) also increases AMPK activity.

Do note — if you are hopeful that drugs will relieve you of the need to exercise — that the benefits were not only smaller than those achieved from exercise, but also didn’t last. In those mice taking Aicar for a second week, their brains not only stopped deriving any benefit, but actually deteriorated.