Previous research has pointed to an association between not having teeth and a higher risk of cognitive decline and dementia. One reason might have to do with inflammation — inflammation is a well-established risk factor, and at least one study has linked gum disease to a higher dementia risk. Or it might have to do with the simple mechanical act of chewing, reducing blood flow to the brain. A new study has directly investigated chewing ability in older adults.

The Swedish study, involving 557 older adults (77+), found that those with multiple tooth loss, and those who had difficulty chewing hard food such as apples, had a significantly higher risk of developing cognitive impairments (cognitive status was measured using the MMSE). However, when adjusted for sex, age, and education, tooth loss was no longer significant, but chewing difficulties remained significant.

In other words, what had caused the tooth loss didn’t matter. The important thing was to maintain chewing ability, whether with your own natural teeth or dentures.

This idea that the physical act of chewing might affect your cognitive function (on a regular basis; I don’t think anyone is suggesting that you’re brighter when you chew!) is an intriguing and unexpected one. It does, however, give even more emphasis to the importance of physical exercise, which is a much better way of increasing blood flow to the brain.

The finding also reminds us that there are many things going on in the brain that may deteriorate with age and thus lead to cognitive decline and even dementia.

There's quite a bit of evidence now that socializing — having frequent contact with others — helps protect against cognitive impairment in old age. We also know that depression is a risk factor for cognitive impairment and dementia. There have been hints that loneliness might also be a risk factor. But here’s the question: is it being alone, or feeling lonely, that is the danger?

A large Dutch study, following 2173 older adults for three years, suggests that it is the feeling of loneliness that is the main problem.

At the start of the study, some 46% of the participants were living alone, and some 50% were no longer or never married (presumably the discrepancy is because many older adults have a spouse in a care facility). Some 73% said they had no social support, while 20% reported feelings of loneliness.

Those who lived alone were significantly more likely to develop dementia over the three year study period (9.3% compared with 5.6% of those who lived with others). The unmarried were also significantly more likely to develop dementia (9.2% vs 5.3%).

On the other hand, among those without social support, 5.6% developed dementia compared with 11.4% with social support! This seems to contradict everything we know, not to mention the other results of the study, but the answer presumably lies in what is meant by ‘social support’. Social support was assessed by the question: Do you get help from family, neighbours or home support? It doesn’t ask the question of whether help would be there if they needed it. So this is not a question of social networks, but more one of how much you need help. This interpretation is supported by the finding that those receiving social support had more health problems.

So, although the researchers originally counted this question as part of the measure of social isolation, it is clearly a poor reflection of it. Effectively, then, that leaves cohabitation and marriage as the only indices of social isolation, which is obviously inadequate.

However, we still have the interesting question re loneliness. The study found that 13.4% of those who said they felt lonely developed dementia compared with 5.7% of those who didn’t feel this way. This is a greater difference than that found with the ‘socially isolated’ (as measured!). Moreover, once other risk factors, such as age, education, and other health factors, were accounted for, the association between living alone and dementia disappeared, while the association with feelings of loneliness remained.

Of course, this still doesn’t tell us what the association is! It may be that feelings of loneliness simply reflect cognitive changes that precede Alzheimer’s, but it may be that the feelings themselves are decreasing cognitive and social activity. It may also be that those who are prone to such feelings have personality traits that are in themselves risk factors for cognitive impairment.

I would like to see another large study using better metrics of social isolation, but, still, the study is interesting for its distinction between being alone and feeling lonely, and its suggestion that it is the subjective feeling that is more important.

This is not to say there is no value in having people around! For a start, as discussed, the measures of social isolation are clearly inadequate. Moreover, other people play an important role in helping with health issues, which in turn greatly impact cognitive decline.

Although there was a small effect of depression, the relationship between feeling lonely and dementia remained after this was accounted for, indicating that this is a separate factor (on the other hand feelings of loneliness were a risk factor for depression).

A decrease in cognitive score (MMSE) was also significantly greater for those experiencing feelings of loneliness, suggesting that this is also a factor in age-related cognitive decline.

The point is not so much that loneliness is more detrimental than being alone, but that loneliness in itself is a risk factor for cognitive decline and dementia. This suggests that we should develop a better understanding of loneliness, how to identify the vulnerable, and how to help them.

Caffeine has been associated with a lower of developing Alzheimer's disease in some recent studies. A recent human study suggested that the reason lies in its effect on proteins involved in inflammation. A new mouse study provides more support for this idea.

In the study, two groups of mice, one of which had been given caffeine, were exposed to hypoxia, simulating what happens in the brain during an interruption of breathing or blood flow. When re-oxygenated, caffeine-treated mice recovered their ability to form a new memory 33% faster than the other mice, and the caffeine was observed to have the same anti-inflammatory effect as blocking interleukin-1 (IL-1) signaling.

Inflammation is a key player in cognitive impairment, and IL-1 has been shown to play a critical role in the inflammation associated with many neurodegenerative diseases.

It was found that the hypoxic episode triggered the release of adenosine, the main component of ATP (your neurons’ fuel). Adenosine is released when a cell is damaged, and this leakage into the environment outside the cell begins a cascade that leads to inflammation (the adenosine activates an enzyme, caspase-1, which triggers production of the cytokine IL-1β).

But caffeine blocks adenosine receptors, stopping the cascade before it starts.

The finding gives support to the idea that caffeine may help prevent cognitive decline and impairment.

Memory problems in those with mild cognitive impairment may begin with problems in visual discrimination and vulnerability to interference — a hopeful discovery in that interventions to improve discriminability and reduce interference may have a flow-on effect to cognition.

The study compared the performance on a complex object discrimination task of 7 patients diagnosed with amnestic MCI, 10 older adults considered to be at risk for MCI (because of their scores on a cognitive test), and 19 age-matched controls. The task involved the side-by-side comparison of images of objects, with participants required to say, within 15 seconds, whether the two objects were the same or different.

In the high-interference condition, the objects were blob-like and presented as black and white line-drawings, with some comparison pairs identical, while others only varied slightly in either shape or fill pattern. Objects were rotated to discourage a simple feature-matching strategy. In the low-interference condition, these line-drawings were interspersed with color photos of everyday objects, for which discriminability was dramatically easier. The two conditions were interspersed by a short break, with the low interference condition run in two blocks, before and after the high interference condition.

A control task, in which the participants compared two squares that could vary in size, was run at the end.

The study found that those with MCI, as well as those at risk of MCI, performed significantly worse than the control group in the high-interference condition. There was no difference in performance between those with MCI and those at risk of MCI. Neither group was impaired in the first low-interference condition, although the at-risk group did show significant impairment in the second low-interference condition. It may be that they had trouble recovering from the high-interference experience. However, the degree of impairment was much less than it was in the high-interference condition. It’s also worth noting that the performance on this second low-interference task was, for all groups, notably higher than it was on the first low-interference task.

There was no difference between any of the groups on the control task, indicating that fatigue wasn’t a factor.

The interference task was specifically chosen as one that involved the perirhinal cortex, but not the hippocampus. The task requires the conjunction of features — that is, you need to be able to see the object as a whole (‘feature binding’), not simply match individual features. The control task, which required only the discrimination of a single feature, shows that MCI doesn’t interfere with this ability.

I do note that the amount of individual variability on the interference tasks was noticeably greater in the MCI group than the others. The MCI group was of course smaller than the other groups, but variability wasn’t any greater for this group in the control task. Presumably this variability reflects progression of the impairment, but it would be interesting to test this with a larger sample, and map performance on this task against other cognitive tasks.

Recent research has suggested that the perirhinal cortex may provide protection from visual interference by inhibiting lower-level features. The perirhinal cortex is strongly connected to the hippocampus and entorhinal cortex, two brain regions known to be affected very early in MCI and Alzheimer’s.

The findings are also consistent with other evidence that damage to the medial temporal lobe may impair memory by increasing vulnerability to interference. For example, one study has found that story recall was greatly improved in patients with MCI if they rested quietly in a dark room after hearing the story, rather than being occupied in other tasks.

There may be a working memory component to all this as well. Comparison of two objects does require shifting attention back and forth. This, however, is separate to what the researchers see as primary: a perceptual deficit.

All of this suggests that reducing “visual clutter” could help MCI patients with everyday tasks. For example, buttons on a telephone tend to be the same size and color, with the only difference lying in the numbers themselves. Perhaps those with MCI or early Alzheimer’s would be assisted by a phone with varying sized buttons and different colors.

The finding also raises the question: to what extent is the difficulty Alzheimer’s patients often have in recognizing a loved one’s face a discrimination problem rather than a memory problem?

Finally, the performance of the at-risk group — people who had no subjective concerns about their memory, but who scored below 26 on the MoCA (Montreal Cognitive Assessment — a brief screening tool for MCI) — suggests that vulnerability to visual interference is an early marker of cognitive impairment that may be useful in diagnosis. It’s worth noting that, across all groups, MoCA scores predicted performance on the high-interference task, but not on any of the other tasks.

So how much cognitive impairment rests on problems with interference?