This weeks edition of ALZForum carried an interesting article regarding the effects of exercise protecting the brain from neurodegenerative disease. The article reported information presented at the recent Alzheimer's Association International Conference in Los Angeles. It cited several studies of exercise and brain health. These included a large, important study (7,800 participants, 50 yrs and older -- part of "The English Longitudinal Study of Ageing") that found after 12 years, exercise reduced the risk of dementia by 40%. The article was "Physical Activity May Shield the Brain from the Onslaught of Aβ."
What was specifically interesting about the information was that it made a differentiation of positive effects on brain health of exercise and positive effects of a healthy cardiovascular system.
Neurologists and researchers are fond of saying "what's good for the heart is good for the brain," and so it is. Autopsies of the brains of people who had displayed evidence of dementia often find the plaques and tangles that signal AD, but too often they also find evidence of coexisting cardiovascular disease capable of having produced the dementia. We usually refer to this as mixed dementia.
As we discuss in Beating the Dementia Monster, the article acknowledges that physical exercise aids brain health by promoting generation of the brain-derived neurotrophic factor (BDNF) protein, but it also promotes a healthy cardiovascular system. This makes it difficult to determine the relative effectiveness of physical exercise and maintaining good cardiovascular health on brain health. The article acknowledged this difficulty, but concludes the effects are approximately equal.
We have discussed before the ambiguity in the amyloid hypothesis -- while the presence of plaques typifies AD, it's not clear what the role of amyloid is and if removing it will affect the progress of the disease. The article noted few studies have examined how physical activity modulates the
relationships between Aβ deposition, brain volume, and cognitive
decline. But the article highlights one study that is helpful here. It is the Harvard Aging Brain Study (HABS), which followed 182 cognitively normal participants who averaged 73 years of age at baseline. The outcome was that, for subjects with amyloid deposition in their brains, physical activity was strongly correlated with less cognitive decline and brain atrophy.
I don't know how much amyloid I have deposited in my brain. I had a lumbar puncture ("spinal tap") for the insulin study, but (consistent with their protocol) they never shared the results with me. This was likely done to measure beta amyloid in my cerebrospinal fluid. The way to do that now would be a PET scan targeting beta-amyloid, but the insurance company would never pay for it. If I wanted to pay out-of-pocket, the cost would likely be over $5,000. My guess is that I have a lot, but, consistent with this study, physical exercise has significantly impeded the advance of dementia. Every morning when I wake up I am so grateful for this!
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.
Monday, July 29, 2019
Sunday, July 28, 2019
A Fascinating Lecture
I have been on the East Coast for a while, and I've been trying to catch up on a lot of stuff. But something came up in the AD world yesterday that I want to share.
On July 27, 2019, UC San Francisco uploaded the video of a lecture from April 30, 2019. Click here. The core of the video was a presentation by Dr. Geroges Naasan, a neurologist at the UCSF Memory and Aging Center. The title was Diagnosing Alzheimer's Disease. Much of the focus was on biomarkers used to diagnose AD, which required considerable knowledge of the brain and AD to understand them. Some of what he presented was the result of very recent research.
It runs an hour and a half, but, depending on your interest, it may be worth your while. I learned a lot, and it changed my understanding of several things.
Recall that the diagnosis of AD begins with measurement of memory/ cognition loss, but you can't conclude anything about the cause of the loss without looking at biomarkers. The three biomarkers he discussed in the lecture were analysis of cerebrospinal fluid, PET scans, and MRI scans.
Something new I learned was that science has identified four different clinical syndromes that define how the disease will first be expressed. It is not clear whether all will express as a case of the disease progresses to its end. MRIs show that different parts of the brain are atrophying with the different syndromes. They are:
I had always read that elevated beta amyloid in cerebrospinal fluid is a biomarker for AD. (Why I got a spinal tap during the insulin study.) But they said that the biomarker is a decrease in amyloid in CSF because amyloids are being retained in the brain to form plaques.
Of course, the final diagnosis of AD is normally in the autopsy, but (as we said in Beating the Dementia Monster) very, very rarely a biopsy of brain tissue from a living subject may be performed.
Only humans develop AD. Dogs may accumulate some beta amyloid, but there is no progress of dementia. Rodents are studied when their genes have been edited to unnaturally develop a disorder that is an analog for AD.
I had (correctly) understood that PET scans are used to image the metabolism of glucose in the brain. What I didn't know is that different tracers can be used to separately image tau protein and beta amyloid.
I'm going to watch it again and see what I might have missed the first time.
On July 27, 2019, UC San Francisco uploaded the video of a lecture from April 30, 2019. Click here. The core of the video was a presentation by Dr. Geroges Naasan, a neurologist at the UCSF Memory and Aging Center. The title was Diagnosing Alzheimer's Disease. Much of the focus was on biomarkers used to diagnose AD, which required considerable knowledge of the brain and AD to understand them. Some of what he presented was the result of very recent research.
It runs an hour and a half, but, depending on your interest, it may be worth your while. I learned a lot, and it changed my understanding of several things.
Recall that the diagnosis of AD begins with measurement of memory/ cognition loss, but you can't conclude anything about the cause of the loss without looking at biomarkers. The three biomarkers he discussed in the lecture were analysis of cerebrospinal fluid, PET scans, and MRI scans.
Something new I learned was that science has identified four different clinical syndromes that define how the disease will first be expressed. It is not clear whether all will express as a case of the disease progresses to its end. MRIs show that different parts of the brain are atrophying with the different syndromes. They are:
- Memory syndrome. This is our most familiar, but it is not universal, at least at the outset of the disease. Learning and short term memory are impaired.
- Language syndrome. This manifests as someone forgetting words and substituting other words that sound similar. They showed a video of an interview with someone with this form of the disease in which the subject used words that sounded like the word he wanted to use but conveyed different meaning. He seemed unaware he was substituting words.
- Visual syndrome. He said that the eye can be considered an extension of the brain (my very bright ophthalmologist would agree), and symptoms of AD can express in changes in vision -- changes in the processing of information gathered through vision. His description led me to believe this may explain the problem I had with driving in 2015 and early 2016. I would look to see if there was a car or pedestrian where I wanted to go, but I would not see them. (Fortunately nothing like this has recurred.) I wonder if this explains the correlation of glaucoma with AD.
- Frontal syndrome. This involves atrophy of the prefrontal cortex (a feature of the brain peculiar to primates) which does a lot of things for humans. Most notable for our purposes is its role in executive function. Executive function is what orders your behavior. Erosion of executive function may be reflected in inappropriate social behavior. The distinction from frontal-temporal dementia (not usually considered AD) is ambiguous.
I had always read that elevated beta amyloid in cerebrospinal fluid is a biomarker for AD. (Why I got a spinal tap during the insulin study.) But they said that the biomarker is a decrease in amyloid in CSF because amyloids are being retained in the brain to form plaques.
Of course, the final diagnosis of AD is normally in the autopsy, but (as we said in Beating the Dementia Monster) very, very rarely a biopsy of brain tissue from a living subject may be performed.
Only humans develop AD. Dogs may accumulate some beta amyloid, but there is no progress of dementia. Rodents are studied when their genes have been edited to unnaturally develop a disorder that is an analog for AD.
I had (correctly) understood that PET scans are used to image the metabolism of glucose in the brain. What I didn't know is that different tracers can be used to separately image tau protein and beta amyloid.
I'm going to watch it again and see what I might have missed the first time.
Saturday, July 13, 2019
Nuts and Brains
I came across a study of older Chinese people relating brain health to consumption of nuts. The study was conducted by researchers at the University of South Australia, and it focused on a population of 4,822 Chinese people, age 55 and older. The study was published in Journal of Nutrition, Health & Aging.
What did it find? It found that consuming more than 10 grams of nuts per day led to improved mental functioning and thinking, and better memory and reasoning.
A couple of things I noted:
I felt good about this, because I ate a bunch of peanuts today. I snack on almonds and Walnuts all day, but I normally avoid peanuts. I didn't think they helped my brain, and they seemed to add more weight on me than tree nuts. So I was feeling guilty about it...
It wasn't clear to me if the Chinese government participated in the study at all. However, I heard at a seminar I attended that China is spending almost as much as the US on Alzheimer's research. Aside from an unhealthy lifestyle common in its population (smoking, high blood pressure, obesity), China's population policies have left aging Chinese citizens with very few children to care for them in their old age. So China has a huge stake in the search for effective treatments for AD.
What did it find? It found that consuming more than 10 grams of nuts per day led to improved mental functioning and thinking, and better memory and reasoning.
A couple of things I noted:
- The study did not attempt to correlate the memory improvements with AD.
- Change in cognition was measured during telephone interviews. (4,822 is a lot of people, and China is a big place.)
- I looked at the raw data and saw that the controlled for sex, urban/non-urban living, education, obesity, income, hypertension, and smoking. They did not control for exercise, which I think is important.
I felt good about this, because I ate a bunch of peanuts today. I snack on almonds and Walnuts all day, but I normally avoid peanuts. I didn't think they helped my brain, and they seemed to add more weight on me than tree nuts. So I was feeling guilty about it...
It wasn't clear to me if the Chinese government participated in the study at all. However, I heard at a seminar I attended that China is spending almost as much as the US on Alzheimer's research. Aside from an unhealthy lifestyle common in its population (smoking, high blood pressure, obesity), China's population policies have left aging Chinese citizens with very few children to care for them in their old age. So China has a huge stake in the search for effective treatments for AD.
On Sleep
Google seems to be tracking me and noting my interest in sleep. So it recommended this YouTube video for me on sleep. It was well worth the watch.
The lecture was by Dr. Matthew P. Walker, researcher and director of the Center for Human Sleep Science at Berkley. He spoke about all of the problems being caused by our chronically sleep-deprived culture, notably with respect to its influence on AD. He emphasized the importance of deep sleep, which I'm not getting much of. But he also said that REM sleep is valuable.
I hate the change from standard time to daylight saving time. You probably do too. He said that, the day after the change, we experience a 24% increase in heart attacks and traffic accidents. The opposite occurs in the fall when we change back. I believe that we're doing away with DST in Washington Sates sometime soon.
Another thing he noted is that sleep induced by chemical sedatives is not natural sleep and does not convey the benefits of natural sleep. For me, that means forgetting the antidepressants my doctor was (unenthusiastically) talking about and focusing on getting normal sleep. Things he said to do:
His recommendations are consistent with the classic book No More Sleepless Nights, by Peter Hauri (Mayo Clinic).
The lecture was by Dr. Matthew P. Walker, researcher and director of the Center for Human Sleep Science at Berkley. He spoke about all of the problems being caused by our chronically sleep-deprived culture, notably with respect to its influence on AD. He emphasized the importance of deep sleep, which I'm not getting much of. But he also said that REM sleep is valuable.
I hate the change from standard time to daylight saving time. You probably do too. He said that, the day after the change, we experience a 24% increase in heart attacks and traffic accidents. The opposite occurs in the fall when we change back. I believe that we're doing away with DST in Washington Sates sometime soon.
Another thing he noted is that sleep induced by chemical sedatives is not natural sleep and does not convey the benefits of natural sleep. For me, that means forgetting the antidepressants my doctor was (unenthusiastically) talking about and focusing on getting normal sleep. Things he said to do:
- Keep bedroom temperature low at night
- Keep regular hours, even on weekends
- Don't lie awake longer than 15-20 minutes, because you're training your brain that the bed is a place to be awake. Get up and read a book or something, then go back to bed when you feel sleepy.
His recommendations are consistent with the classic book No More Sleepless Nights, by Peter Hauri (Mayo Clinic).
Thursday, July 11, 2019
My Annual Evaluation
On July 1, I had my annual evaluation with my neurologist. Normally my evaluations are preceded by a couple of hours of intensive psychometric testing, but she had decided to forego it this year. She made that decision last year because I had been tested so frequently and intensely for the SNIFF (insulin) study. Taking a year off seemed to be a very good idea. The purpose of the testing is to track progress (or decline) and it would be unlikely that any particular results would change what I've been doing or change any treatment plan.
However, I told her that I believed I had a marked "hiccup" in my cognition during the first two weeks in May. While my brain seemed to have adjusted some, I doubted that I had regained more than 85% of what seemed to have been lost. I prefaced that by saying I believed that, had I been tested in April, I would have done at least as well as I had done for Harborview's testing last summer -- 2018. But not after early May.
Concurrently with that, I seemed to have a new balance problem on top of the original one, but my perception of it is subjective. Also, I've been having increasing difficulty with sleep. I get little more than 5 hours per night, often significantly less.
I had prostate surgery in January in the hope I'd be able to sleep all night without trips to the bathroom, but that hasn't worked out. It's not unusual for me to get up 5 or more times/night, and it's a struggle to get back to sleep after each one ... a struggle I often lose.
She was very concerned about the sleep, and she may have connected it with the renewed cognition problem. We discussed Tamsulosin, and I told her I had stopped using it when the correlation was found between Tamsulosin and dementia. She said that the research on Tamsulosin was inconsistent, and I needed to put priority on getting better sleep.
Regarding the balance, she said that my vestibular system should be tested again. The previous two times the tests found nothing, suggesting to me that the balance problem is in my brain, not in my ear. My primary care provider went ahead and ordered some new testing for my vestibular system.
Sleep is important, but sedatives to aid sleep, like Ambien, are very much contraindicated with AD. She said, however, that I should consider getting a prescription for Trazodone when I got home -- but only if Tamsulosin doesn't correct my sleep problem. Trazodone is an older antidepressant used in cases of serious depressive and other psychological disorders. In recent years it has rarely been used for anything other than insomnia, and it appears to be the go-to sedative for elderly people, especially with AD. Or so I've read.
For a while, there was excitement that Trazodone had actually improved cognition in mice with AD-type disease, but I read a recent study from the UK that correlated Trazodone more strongly with dementia than other sedatives. So I definitely want to see if the Tamsulosin doesn't help before more seriously considering Trazodone.
But, one way or another, it will be really great to be able to consistently get a good night's sleep.
However, I told her that I believed I had a marked "hiccup" in my cognition during the first two weeks in May. While my brain seemed to have adjusted some, I doubted that I had regained more than 85% of what seemed to have been lost. I prefaced that by saying I believed that, had I been tested in April, I would have done at least as well as I had done for Harborview's testing last summer -- 2018. But not after early May.
Concurrently with that, I seemed to have a new balance problem on top of the original one, but my perception of it is subjective. Also, I've been having increasing difficulty with sleep. I get little more than 5 hours per night, often significantly less.
I had prostate surgery in January in the hope I'd be able to sleep all night without trips to the bathroom, but that hasn't worked out. It's not unusual for me to get up 5 or more times/night, and it's a struggle to get back to sleep after each one ... a struggle I often lose.
She was very concerned about the sleep, and she may have connected it with the renewed cognition problem. We discussed Tamsulosin, and I told her I had stopped using it when the correlation was found between Tamsulosin and dementia. She said that the research on Tamsulosin was inconsistent, and I needed to put priority on getting better sleep.
Regarding the balance, she said that my vestibular system should be tested again. The previous two times the tests found nothing, suggesting to me that the balance problem is in my brain, not in my ear. My primary care provider went ahead and ordered some new testing for my vestibular system.
Sleep is important, but sedatives to aid sleep, like Ambien, are very much contraindicated with AD. She said, however, that I should consider getting a prescription for Trazodone when I got home -- but only if Tamsulosin doesn't correct my sleep problem. Trazodone is an older antidepressant used in cases of serious depressive and other psychological disorders. In recent years it has rarely been used for anything other than insomnia, and it appears to be the go-to sedative for elderly people, especially with AD. Or so I've read.
For a while, there was excitement that Trazodone had actually improved cognition in mice with AD-type disease, but I read a recent study from the UK that correlated Trazodone more strongly with dementia than other sedatives. So I definitely want to see if the Tamsulosin doesn't help before more seriously considering Trazodone.
But, one way or another, it will be really great to be able to consistently get a good night's sleep.
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