Dave B and Alvaro have had an interesting (albeit, brief) discussion in their comments about the subject of the hypothetical “cognitive reserve” that stands between each one of us, and the timing of the onset of Alzheimer’s Disease (AD).

First, Dave B said that while he saw ample evidence that most cognitively capable (“highly educated”) individuals that were in his studies at Medical College of Georgia seemed to be far removed from any danger of AD in their immediate future (in strong contrast to individuals in his studies who were poorly educated, and/or were less cognitively active), he saw no clear evidence in the literature that convincingly demonstrated that the onset of Alzheimer’s Disease could be delayed by cognitive training or enrichment.

Alvaro questioned this conclusion by citing studies (there are about a hundred in the literature) that first argued, about a decade ago, that individuals who were more cognitively active were protected by a greater “cognitive reserve” that gave them more protection from an end-of-life collapse into AD than was afforded to cognitively-dormant individuals.

Dave B countered by noting that such claims are generally plagued by the old chicken vs egg problem: Does your larger “cognitive reserve” merely reflect the co-inheritance of a neurology that generally assures that you’re a) with it, and b) you won’t develop AD — and that to the inexorable extent that you sustain or lose ‘a’, you can count on also sustaining or losing ‘b’? That being full of fun and playing lots of games and dancing and seeing the world and developing lots of new fun hobbies and reading like a bandit and doing your sudoku and crossword and jigsaw puzzles and still having fun in life is just exactly the kind of thing that an individual who is very unlikely to develop AD is inclined to do, whether they like it or not?!! He might also have noted that by the usual interpretation of “cognitive reserve”, having a big one does NOT protect you from the onset of Alzheimer’s pathology. To the contrary, it means that the pathology has to progress over a longer period before you meet the behavioral criteria for receiving the Alzheimer’s label. You’ve GOT the pathology. You just have more memory and cognitive ability to lose before anyone notices!

This question of whether brain fitness exercises of the best sort delays the onset of the pathology itself is difficult (and very expensive) to answer, and no “gold standard” study has yet been conducted that provides an unequivocal confirmation that this can be achieved. We have initiated a large study that will ultimately answer this question, but it shall take months to complete it. What ARE we certain of, at this point in time?

1) The cognitive performance abilities (memory, reasoning, fluency, et alia) of most of us (the average individual) peak(s) in the third decade of life, and declines systematically and continuously from that early young-adult epoch, forward to the end of life.

2) The average more-cognitively-competent 25-year-old has a longer path, in forward years, before they cross a performance threshold that would put them measurably “at risk” for AD onset. In this sense, most more-cognitive-competent individuals (irregardless of their formal education) have greater “cognitive reserve”, and a lower probability of collapsing into AD than do less-cognitively-competent individuals, through each passing decade.

3) A cognitively competent youngster can sustain their “edge” (cognitive reserve) by leading an active, rich, mentally-challenging life. If you’re quick of wit and thought and action as a young woman or man, and you stay mentally active and agile in maturity, you’re probably still sitting on a pretty good cognitive reserve!

4) With appropriately designed “brain fitness exercises” like those produced by Posit Science, it is possible to significantly improve one’s cognitive performance abilities, at any age. Such improvements presumably bucks up your “cognitive reserve”, irregardless of the level of protection that you are carrying forward from earlier life, at the time you initiate traing. You’re hypothetically safer, because after training, you have correspondingly farther to decline before your measured performance abilities label you as “at risk” for, or in the clutches of AD.

5) Our collaborators at UCSF, UC Davis and Stanford have tracked the maintenance of such improvements in MCI patients who are at risk for AD onset, and have shown that Posit Science Brain Fitness Program-trained patients are a) can substantially improve their standing, by standard assessment criteria, within this high-risk category; and b) that trained patients sustain their BFP-driven improvements in memory and cognition without further training, over a period of at least several months. Again, we hypothesize that these gains provide them with a greater, on-the-spot “cognitive reserve”, i.e., can be expected to delay symptomatic AD onset.

6) If useful training is not discontinued (as it was in the UCSF/UCD/Stanford study), it should be possible to drive the cognitive abilities of the average older individual a long distance in the direction of ‘greater safety’ (greater ‘cognitive reserve’).

7) In animals, appropriate training CAN substantially delay the onset of the Alzheimer’s pathology itself. It is highly likely that this shall also be true in human populations. We now have markers for pathology in living humans that makes it possible for us to directly determine if this is or is not the case. It shall take a little time, but before too long we’ll know the answer to this key question.

8) In the meantime, keep working on your “cognitive reserve”, because training-driven improvements can certainly delay your loss of function, and may well save your bacon!

Dave B indicates that if such exercises actually DO delay the onset of AD pathology, then we must consider how they could conceivably delay the hundred-and-and-one complex pathological sequelae that characterize the disease. I agree. That is why the growing number of studies arguing that AD pathology can be delayed by providing animal models in which AD shall develop with “rich environments” are so important. Dave seems to suggest that because there are several hundred aspects of change that affect the older brain as it collapses into AD, it may be impossible to explain how a little brain fitness training can delay them.

I don’t agree, David. It is possible that even a single fundamental change of the right sort (e.g., a slow loss of the ability of the forebrain to produce and release acetylcholine, which shall degrade the brain’s abilty to learn and remember, shall radically alter the dynamics of blood perfusion coupled to brain activity, and can trigger widespread consequences for brain metabolism, homeostasis and immune responses) would have a MYRIAD of pathological consequences. There are several scenarios that might provide that important basis for linking a an unhealthy, unfit brain to those pathological processes that we collectively describe as AD. This particular aspect of the science of aging research has been almost completely neglected. I know that DaveB has the talent and skills to make real progress in this area. As your studies progress, David, keep us all in the know about what you are discovering about this key scientific issue!