The October 2018 issue of Scientific American includes an article, "How Exercise Might 'Clean' the Alzheimer's Brain." It begins by acknowledging how the major pharmaceutical companies have thrown their hands up over the search for a drug to cure AD. The most recent trials have failed to improve cognition in people with AD, and the drug companies are, at least temporarily, at a dead end. The recent drugs have sought to remove amyloid plaques from the brain, but that hasn't led to improved cognition. According to the article (and according to Beating the Dementia Monster) this is challenging the amyloid hypothesis. The amyloid hypothesis has been pretty close to the center of the search for a cure for AD. (I'm not sure where the study I cited in my July 13 post fits into this narrative.)
Recall that the amyloid hypothesis notes the accumulation of amyloid plaques on neurons, and is assumed to impede neural activity between the cells. The plaques also appear to play a role in the deaths of neurons. Therefore, removing the amyloids from the brain should stop the progress of AD and lead to improved cognition. But it doesn't.
The article cites research with mice that correlates mice getting exercise with encouragement of the generation of new brain cells (neurogenesis) in the hippocampus. To quote the Scientific American article, "The researchers found that exercised animals from a mouse model of Alzheimer’s had greatly enhanced memory." As has been noted before, the article cites the role of brain-derived neurotropic factor (BDNF) in this neurogenesis, and I struggled to find anything in the research report that we didn't discuss in Beating the Dementia Monster. What seemed new in the report was to look at exercise as creating an environment in the brain that encourages neurogenesis, but this just seemed to me to be looking at what we already know using different language. There was an implication, however, to think in terms of a drug that would create an environment similar to that created by exercise.
The article is relatively short, and interested people should read it. But there wasn't much new in it, and I was disappointed.
In my book, "Beating the Dementia Monster," I describe what has occurred since 2015 when I first knew I had memory problems. (You can find it on Amazon.com.) I have experienced remarkable improvement, and I’m certain that I can share valuable information with many others. In this second edition I continue my story to 2020 and provide greater understanding of how Alzheimer's advances and why what I did worked.
Friday, October 19, 2018
Tuesday, October 16, 2018
Intelligence, Education, and Alzheimer's Disease
This week’s issue of ALZForum included a fascinating article about the findings of two recent research projects correlating intelligence, education, and risk for Alzheimer’s disease.
It’s known that people with higher educational attainment have a lower risk of AD as do people with higher measured intelligence. As we discussed in Beating the Dementia Monster, higher intelligence in the context of dementia is referred to as “cognitive reserve.” Do both education and intelligence have independent influence? Or is it coincidental that persons of higher intelligence will acquire more education, and the correlation with risk for AD is purely a consequence of that?
In one of the studies, researchers correlated a set of scores from a test taken by almost 400,000 high school students in 1960 with current Medicare usage. The actual sample was about 43,000 men and about 43,000 women. (I’m not sure how they got around the obvious privacy issues.) The tests probed general cognitive ability, language skills, perception, visualization, and mathematics, as well as complex intellectual aptitudes such as creativity and abstract reasoning. Some students had done well, and some had done not so well. At the time of the study, these people ranged in age from 66 to 73.
The research found that 2.9% of the men and 3.3% of the women developed AD or “related disorders.” I’m not sure what the related disorders are, but there was a strong correlation between test performance and resistance to developing AD. For you statistics buffs, for every standard deviation disadvantage a boy had with mechanical reasoning skills, there was a 17% higher chance of developing AD in old age. For girls, trouble with novel word memory yielded a 16% higher chance of developing AD in old age with each standard deviation of disadvantage.
The other study sought to explore whether the well-known correlation between education and dementia was due to more schooling or because the better-educated people were more intelligent to begin with and just went farther in school. One finding of their analysis was that education can, to a certain extent, improve intelligence, although this has been established previously. This points to one question that had intrigued the researchers: can additional education serve to reduce the probability of developing AD.
This project also worked with a large cohort of test subjects, more than 17,000. The researchers found that, for each standard deviation increase in educational attainment, the risk of AD dropped 37 percent. For every one standard deviation increase in IQ, the risk of AD went down 35 percent. But their analysis found that the influence of educational attainment went away after accounting for intelligence. Nevertheless, increased schooling as a means of AD prevention is promising to the extent that it can raise intelligence. This should be a topic of further examination.
But, there’s always a spoilsport. At the end of the article, there was an interesting comment by a research reviewer from Massachusetts General Hospital. She said that it may simply be that educated people are just more likely to eat more nutritious food, exercise more, and get treatment for cardiovascular disease, and this accounts for a lower risk of AD. Hey—maybe she read Beating the Dementia Monster!
It’s known that people with higher educational attainment have a lower risk of AD as do people with higher measured intelligence. As we discussed in Beating the Dementia Monster, higher intelligence in the context of dementia is referred to as “cognitive reserve.” Do both education and intelligence have independent influence? Or is it coincidental that persons of higher intelligence will acquire more education, and the correlation with risk for AD is purely a consequence of that?
In one of the studies, researchers correlated a set of scores from a test taken by almost 400,000 high school students in 1960 with current Medicare usage. The actual sample was about 43,000 men and about 43,000 women. (I’m not sure how they got around the obvious privacy issues.) The tests probed general cognitive ability, language skills, perception, visualization, and mathematics, as well as complex intellectual aptitudes such as creativity and abstract reasoning. Some students had done well, and some had done not so well. At the time of the study, these people ranged in age from 66 to 73.
The research found that 2.9% of the men and 3.3% of the women developed AD or “related disorders.” I’m not sure what the related disorders are, but there was a strong correlation between test performance and resistance to developing AD. For you statistics buffs, for every standard deviation disadvantage a boy had with mechanical reasoning skills, there was a 17% higher chance of developing AD in old age. For girls, trouble with novel word memory yielded a 16% higher chance of developing AD in old age with each standard deviation of disadvantage.
The other study sought to explore whether the well-known correlation between education and dementia was due to more schooling or because the better-educated people were more intelligent to begin with and just went farther in school. One finding of their analysis was that education can, to a certain extent, improve intelligence, although this has been established previously. This points to one question that had intrigued the researchers: can additional education serve to reduce the probability of developing AD.
This project also worked with a large cohort of test subjects, more than 17,000. The researchers found that, for each standard deviation increase in educational attainment, the risk of AD dropped 37 percent. For every one standard deviation increase in IQ, the risk of AD went down 35 percent. But their analysis found that the influence of educational attainment went away after accounting for intelligence. Nevertheless, increased schooling as a means of AD prevention is promising to the extent that it can raise intelligence. This should be a topic of further examination.
But, there’s always a spoilsport. At the end of the article, there was an interesting comment by a research reviewer from Massachusetts General Hospital. She said that it may simply be that educated people are just more likely to eat more nutritious food, exercise more, and get treatment for cardiovascular disease, and this accounts for a lower risk of AD. Hey—maybe she read Beating the Dementia Monster!
Saturday, October 6, 2018
News on Exercise and Young Onset Alzheimer's Disease
If you read Beating the Dementia Monster you know science has established that physical exercise is a powerful weapon in the battle to stop the progress of Alzheimer's disease. But so far, this has only been shown to be true for "sporadic Alzheimer's disease." It has not been shown to be helpful for "familial Alzheimer's disease," sometimes called "younger onset Alzheimer's."
In familial Alzheimer's, symptoms appear when the person is in their 50s or even 40s. It is genetically determined, so there is a pretty well defined population of people carrying the gene. And if you carry this gene, the probability is quite high that you will develop the disease. Fortunately it's pretty rare. I read once that there may only be 300 or so families in the whole world carrying the gene. The most famous family is in Columbia, and they are studied carefully.
Sporadic Alzheimer's is all other Alzheimer's disease. It's sometimes called older-onset or late onset Alzheimer's. You may be at increased risk of Alzheimer's because you carry the ApoE4 gene, but that's not familial Alzheimer's, and it's far from certain that the gene will cause you to develop the disease. So I have sporadic Alzheimer's disease.
In this past week's edition of ALZFourms there was an article about a study of exercise and familial Alzheimer's. It found that there was, in fact, improvement in patients who got regular physical exercise. In fact, the researchers were surprised by the strength of the correlation between exercise and cognitive function.
In familial Alzheimer's, it's much easier to predict when someone will develop the disease. Therefore it was easier to study how the point of intervention with respect to age affected how effective the exercise is.
Participants were categorized by how much exercise they got. A minimum of 2.5 hours per week was necessary for participation, with the high end at 6.5 hours. Many exercised 5 hours per week, playing tennis, walking, and hiking. (I spend 5.5 hours per week on the treadmill.)
Peak cognitive improvement was at 6.7 hours. One odd thing was that exercising more that 8 hours per week may have actually caused decline in cognition. This was not seen in the control population, so it appears to be related to the disease. Of course, the worst decline was among those who got no exercise.
All non-control test subjects had familial Alzheimer's. Does this mean that the optimal exercise for us with sporadic Alzheimer's is also 6.7 hours (just shy of an hour per day)? Or if we go more that 8 hours per week we'll experience decline? I don't know, but I'm having great success with 5.5 hours per week.
In familial Alzheimer's, symptoms appear when the person is in their 50s or even 40s. It is genetically determined, so there is a pretty well defined population of people carrying the gene. And if you carry this gene, the probability is quite high that you will develop the disease. Fortunately it's pretty rare. I read once that there may only be 300 or so families in the whole world carrying the gene. The most famous family is in Columbia, and they are studied carefully.
Sporadic Alzheimer's is all other Alzheimer's disease. It's sometimes called older-onset or late onset Alzheimer's. You may be at increased risk of Alzheimer's because you carry the ApoE4 gene, but that's not familial Alzheimer's, and it's far from certain that the gene will cause you to develop the disease. So I have sporadic Alzheimer's disease.
In this past week's edition of ALZFourms there was an article about a study of exercise and familial Alzheimer's. It found that there was, in fact, improvement in patients who got regular physical exercise. In fact, the researchers were surprised by the strength of the correlation between exercise and cognitive function.
In familial Alzheimer's, it's much easier to predict when someone will develop the disease. Therefore it was easier to study how the point of intervention with respect to age affected how effective the exercise is.
Participants were categorized by how much exercise they got. A minimum of 2.5 hours per week was necessary for participation, with the high end at 6.5 hours. Many exercised 5 hours per week, playing tennis, walking, and hiking. (I spend 5.5 hours per week on the treadmill.)
Peak cognitive improvement was at 6.7 hours. One odd thing was that exercising more that 8 hours per week may have actually caused decline in cognition. This was not seen in the control population, so it appears to be related to the disease. Of course, the worst decline was among those who got no exercise.
All non-control test subjects had familial Alzheimer's. Does this mean that the optimal exercise for us with sporadic Alzheimer's is also 6.7 hours (just shy of an hour per day)? Or if we go more that 8 hours per week we'll experience decline? I don't know, but I'm having great success with 5.5 hours per week.
Still Another One Bites the Dust
For several years there has been excitement that some blood pressure medications can remove amyloids and treat Alzheimer's disease. Occasionally, people contact me with hopeful and promising stories about a blood pressure medication that might work.
This past week's edition of ALZForum reported on a study to determine if the blood pressure drug nilvadipine would slow cognitive decline. It was a great disappointment that the phase 3 trial showed no improvement in in the study population. Recall that a phase 3 trial is final stage with the largest study population. It's the one required for FDA approval of a treatment.
Not everyone is ready to abandon nilvadipine. Some suggested that there may have been problems with the design of the study. The dose may have been too low, the trial may have started too late in the progress of the disease, or inadequate screening of test subjects meant that the subject population included people who did not have Alzheimer's pathology. But, who knows?
This past week's edition of ALZForum reported on a study to determine if the blood pressure drug nilvadipine would slow cognitive decline. It was a great disappointment that the phase 3 trial showed no improvement in in the study population. Recall that a phase 3 trial is final stage with the largest study population. It's the one required for FDA approval of a treatment.
Not everyone is ready to abandon nilvadipine. Some suggested that there may have been problems with the design of the study. The dose may have been too low, the trial may have started too late in the progress of the disease, or inadequate screening of test subjects meant that the subject population included people who did not have Alzheimer's pathology. But, who knows?
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