Does Nicotine Help Memory?

Contributed by: Dennis Fortier, President, Medical Care Corporation

According to a recent study published in Neurology, there may well be a relationship between memory and nicotine.  But before you run out and take up smoking, let's examine the facts.

First, the study was conducted on a small number of participants (74), all of whom had a mild, prior memory deficit, and the nicotine was delivered through a transdermal patch, not through smoking cigarettes.  After six months, those who had received a nicotine patch outperformed a placebo group on cognitive tests of attention and memory.  In fact, the group receiving nicotine improved their baseline scores while the placebo group showed a decline in thinking abilities over the six month trial.

For sure, the well-documented risks associated with smoking (which include cognitive decline) would preclude any reasonable argument about smoking to preserve brian health.  But nicotine, if delivered without the burden of smoking, has been shown to interact with receptors in the brain and improve some chemical signals along neural circuits. It is more than plausible that this is a benefit we could one day harness for improved cognition.

The major caveats on this particular study are that it was very small, the noted cognitive gains were considered minimal, and many of the authors work for companies that sell nicotine patches.  Nonetheless, this early stage work is noteworthy and bodes well for future benefits.

Memory Loss More Common in Men?

Contributed by: Dennis Fortier, President, Medical Care Corporation

There is much press this week about a study published in Neurology that measured the incidence of mild cognitive impairment (MCI) in an aging population.

MCI is a subtle loss of thinking ability, such as impaired memory or judgment, that is not severe enough to interfere with the person's normal activities of living.  The study showed about a 20% incidence rate which is squarely in line with previous estimates.

The press has been largely focused on the fact that, in this study, men between the ages of 70 and 89 years had a higher incidence of MCI than women of the same age.  This is probably true.  It is also probably easy to explain.

MCI is not a disease, it is merely a descriptor term for a certain level of cognitive impairment.  It refers to the degree of impairment that falls between normal cognition and the severe loss of function that we call dementia.  Asking "why" a person has MCI is a whole different question with a host of common answers including depression, thyroid disease, stroke, sleep disorder, Alzheimer's disease, and anxiety, to name just a few.  

The question of "why" a person has MCI was not adressed in this study, but may shed some important light on the observed gender differences.  For example, sleep disorders and certain cardiovascular conditions, like hypertension and stroke, are common causes of MCI and are somewhat more prevalent among men than women.  Clearly, conditions that impair memory and are also more common in men, could fully explain the observed gender differences in this study.  In that respect, these results are hardly surprising and, in fact, make perfect sense.

It would be truly worthy of a media frenzy if researchers controlled for each cause of MCI and still found that one gender was more susceptible than the other.  But despite many misleading headlines, that was not the case in this study.

Can Genetic Risk for Alzheimer's be Reduced?

Contributed by: Dennis Fortier, President, Medical Care Corporation

As genetic testing has become more commonplace in medicine, we have all seen frequent examples of overstatement, where writers and speakers confuse "higher risk" with "absolute certainty".  This has been an especially maddening component of arguments against testing for the APOe4 gene associated with increased risk for Alzheimer's disease.

A great many of these faulty arguments state that learning about a genetic risk for an incurable disease is pointless.  (I have refuted that argument many times but that is not the point of this post).  This week, research published in Archives of Neurology strengthens the case for genetic testing.

In a study from the University of Washington in St. Louis, more than 200 participants aged 45 to 88 reported on their physical exercise habits and submitted to spinal fluid measures or PET scans to determine the amount of accumulated amyloid protein in their brains. They also had their APOe4 status checked and researchers found that, among those who carried the APOe4 gene, regular exercisers had less amyloid load than sedentary members of the group.  Interestingly, this was not the case among the APOe4 non-carriers.

This was a small study and needs replication before we can conclude that physical exercise staves off amyloid accumulation in those with genetic risks for AD.  However, the study has a very intuitive finding and gives credence to a much larger body of work showing that good cardiovascular health may reduce the risk of Alzheimer's disease.

The suggestion from this study is very significant.  It could be that genetic risk for AD (usually considered to be an unmodifiable risk), could possibly be reduced by physical exercise.  If so, it will put a whole new spin on those old arguments against genetic testing.