Our rule when reading about “Ten Misconceptions About Aging” is that you read about prior “misconceptions” before your are entitled to read about this current one, MC #6. If you haven’t done your homework, see blogs on this subject on November 7th, December 5th, April 29th, May 1st and May 5th. Then come back and read about……

Misconception 6. Alzheimers Disease pathology (amyloid plaques; neurofibrillary tangles) directly causes memory and cognitive losses in aging.

Most scientists now understand that while AD pathology and cognitive performance abilities are correlated for large populations (the more “diseased” your brain, on the statistical average, the greater your cognitive difficulties), the individual variability in the relationship between your behavior and the physical expressions of this “disease” is great. One of the first demonstrations of this fact came from the “Nun Study” led by the University of Kentucky professor David Snowdon, who showed that brain pathology documented at autopsy did not always jibe with behaviorally assessments and quality of life, documented in a large order of Roman Catholic nuns. Those studies described examples of Sisters with relatively advanced “pathology” who were doing remarkably well behaviorally; as well as other sisters with milder pathology who were (behaviorally, and in their quality of life) doing poorly.

At about the same time, a second autopsy study conducted from the brains of Swedes near retirement age (approximately 65) revealed that a substantial proportion of those normal individuals had frank AD pathology. A Swedish scientist told me that on the basis of this evidence, the government in Stockholm debated whether or not they should reconsider the automatic renewal of driver’s licenses for retired citizens, given the fact that, on the basis of brain pathology, such a large proportion of them “had Alzheimers”. It took them awhile to come to an alternative conclusion: If the disease is defined in terms of functional (behavioral) criteria, maybe the onset of pathology does not equate with the onset of the “Disease”.

The conclusion that a large proportion of “normal” folk (circa 40% over 65) have a significant degree of ongoing AD pathology has been elaborated in a number of more recent studies by scientists who have developed labels for marking amyloid bodies (and with less precision, microtubular “tangles”) in living subjects, recorded using positron emission tomography (PET imaging). These latter studies show that if you’re over 70 and normal, there’s an even-money chance that your brain appears to be in AD’s clutches, and that as with the nuns, you (your cognitive abilities; your quality of life) can be in pretty bad shape or pretty good shape, with essentially equivalent evident AD pathology.

Over-riding these issues of disease progression is a simple question: How DO the functional losses used to define AD relate to/arise from this pathology?! After all, cognitive decline begins in the 3rd or 4th decade of life, and losses are relatively steady decade by decade, over time. The losses recorded in AD appear to be a predictable, accelerated extension of losses that have been progressing in most individuals for decades. How are AD losses DIFFERENT? In what sense are AD-generated losses SPECIAL? How, EXACTLY, does the disease pathology account for the losses?

In my view, AD pathology represents one of the most severe of a long list of factors that simply degrade the ability of the brain to translate what it sees, hears, feels, smells and tastes in actions crucial for controlling thought and action and self-reference. While AD pathology leads to memory and cognitive losses (of course), the consequences of the advancing brain damage incurred in the “illness” are non-specific, and are not directly related to specific neurological processes. Amyloid bodies are known to poison (disable) the cortical circuitry within its neighborhood; each “tangle”-filled neuron is taken off-line, no longer capable of contributing to the representation of perceptions or to make its contribution to cognition or action control. As AD progresses, amyloid “bombs” rain down on the brain, and tangle-filled neurons progressively remove more and more neurons from cortical circuits.

We and other scientists have hypothesized that if an individual is making the most out of their brain machinery by engaging it in ways that continuously sharpen and strengthen its resolving power, they can continue to do pretty well, even in the face of significant amyloid-body poisoning and tangled-neuron losses. On the other hand, if the brain has not been taken very good care of, and is already a poor resolver from the time of onset of the pathology, it shall not take too much additional AD-contributed pathology to ultimately-profoundly disable it.

So if you’re a normal 70-year-old who happens to have a brain that is polka-dotted with growing numbers of amyloid plaques, take heart, because frank pathology does NOT mean certain disaster. But on other hand, for prudence’s sake, get thee to the brain gym, because it may just save your bacon.