In theory, we know that the choices we make every day affect the fate of our bodies and brains. But the research keeps revealing unexpected, sometimes disconcerting, evidence to explain just how true this is. Recent studies are making major strides to uncover all the variables that put our brains at risk for Alzheimer’s disease. And it might have as much to do with our thoughts and behavior patterns as with our genes.
Alzheimer's risk seems to have something to do with activity in the brain’s default mode network, a collection of brain regions that seems to be “on” when we’re not thinking of anything terribly profound (hence the term "default"). It seems to be be responsible for mind-wandering or “undirected mentation,” according to a new study, and to self-referential thoughts. These “me” thoughts aren’t necessarily positive, since they’re usually about personal stressors and worries. In fact, when queried randomly, people whose minds are wandering say they’re less happy while it wanders. (For a discussion of how the default mode network, or DMN, relates to chronic unhappiness, see last month's post.)
But when we’re using our brains for serious business (solving problems, crunching numbers), the cells of the default mode quiet down, and the active, goal-directed areas of the brain take over. In this way, the default network is said to be “anti-correlated” with the problem-solving networks.
So how does this relate to dementia?
Alzheimer’s disease is characterized by plaque build-up in the brain, and it’s known that these amyloid plaques tend to accumulate in the DMN. But why and how they build up in this region has not been well understood.
But a recent study at Washington University has made some exciting discoveries about why plaques may build up in the default networks of Alzheimer’s patients. Using mice as subjects, the team found that the more lactate was present in certain areas (lactate is a product of neuronal activity), the more amyloid-beta peptide was also present. Amyloid-beta is a precursor of full-blown plaques and, ultimately, dementia.
In fact, the researchers also directly showed that when the mice’s whiskers were stimulated and certain neurons were more active as a result, more amyloid-beta was also present (the reverse was true too). These findings strongly link increasing neural activity to the buildup of amyloid-beta. The idea that more brain cell activity could lead to more amyloid-beta build up is an exciting, if sobering, finding.
David Holtzman, senior author of the study, says that the findings could mean that “people whose default mode networks have an average increase in activity relative to others may be at increased risk to get Alzheimer’s disease later in life and the converse may also be true (less activity in this network, less risk).” In other words, it’s possible that people vary naturally in the activity of their default networks. Now, of course, it’s just a matter of figuring out why some of us have more or less activity in these areas.
What specific variables could be responsible? Holtzman says that “some of the things that may be able to modify the amount of time the default mode is on are sleep and depression. So people with poor sleep or long periods of depression may be at increased risk for Alzheimer’s. This is not proved but is being actively studied.”
In fact, recent work has found that depressed people have significant changes in the ways their DMNs respond to certain stimuli. Certain parts of the DMN in depressed people fail to quiet down as normal people’s would when they are concentrating on specific images. The same study found that other areas in the DMN are turned on more than in controls. Intuitively, the idea that depression could change activity in the DMN makes sense, since depression is linked to problems with concentration and attention, as well as with the tendency for rumination.
Another possibility, as Holtzman suggests, is that sleep – or lack of sleep – affects DMN activity. In the current study, his team found that there was more amyloid-beta accumulation during the night hours, when mice are typically awake, compared to daytime hours. Alzheimer’s is well known to be linked to sleep problems. This connection, theoretically, could work both ways, such that the disease disturbs one’s sleep pattern, and lack of sleep in turn leads to more amyloid-beta buildup.
The authors also suggest that education could play a role, although this relationship is less clear-cut. In fact, earlier research has shown that more educated people appear to be at less risk for Alzheimer’s. Holtzman and his colleagues write that since “default network activity is suppressed during cognitively demanding tasks, one possibility is that education reduces Alzheimer’s disease risk by reducing neuronal activity and [amyloid-beta] generation within the default network.”
On the other hand, it’s hard to tease apart whether more education is actually reducing one’s risk or whether it’s just harder to see symptoms in more intellectual people. Holtzman points out that “it is possible that people who are more cognitively active might be able to delay the onset of dementia but this is still controversial. It may be that it is simply harder to detect dementia in the early stages the greater the intellectually ability.”
Still, Holtzman says that “it is certainly possible there are environmental ways to decrease DMN activity such as meditation or by training, but this needs to be further studied to be proved.” In fact, meditation has recently been shown to decrease activity in the DMN, and it’s conceivable that other methods of changing thought patterns so that the mind is wandering less and focusing more could also help reduce risk over the long term. It seems like almost any activitythat forces the problem-solving areas of the brain to engage and DMN to quiet down (diving into work you love, or maybe even attempting a Sudoku) might be able to help keep the brain healthy for longer.
While much is still theoretical, the new evidence is certainly beginning to change the way we think about brain diseases. And while researchers continue to explore how we can reduce amyloid-beta levels in the brain (whether by changing behaviors, thought processes, or by pharmacological methods), the best advice is probably to stay as cognitively active as you can, get some rest, and perhaps most importantly, be as happy as you can be.