This morning, the Washington State/Northern Idaho chapter of the Alzheimer's Association extended to me an offer to join the board of directors. They had been vetting me for the role for a month or so. (This will be on top of the role that I already have as "Ambassador" to our congressional representative.) This, of course, was very flattering.
(So where did the term "to vet" come from in this sort of context? Before you buy a race horse, you want to know that it is in good health before you sign the check. So have the vet check it over first. Or, you may need to vet the horse before a race.)
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.
Thursday, June 25, 2020
Tuesday, June 23, 2020
For Nerds Only -- Why does Alzheimer's disease advance more quickly in some than others?
I get different feedback on my blog content from different people. Some are interested in the details I have about new research, but others are interested in my progress and in stories about living with dementia. This post will be more interesting to the former ... the nerds. But I'll be relatively brief.
A question is, why does Alzheimer's disease advance so much more quickly in some people than in others -- sometimes by a factor of 10? One answer seems to be in the tau protein.
A little refresher. Tau protein is essential to holding the "microtubules" together. The microtubules act as a skeleton in the cell to give it shape, among other functions. (We discuss this in Beating the Dementia Monster, complete with a little picture.) If an abnormal form of tau protein is present and it fails, the microtubules collapse into the tangles that Alois Alzheimer saw in the brain autopsy of Auguste Deter in 1906.
You will also recall that Alzheimer's disease probably advances for 15 or more years before the first symptoms appear. During that time, beta amyloid is leaving brain cells to eventually accumulate as plaques on brain cells. Alzheimer saw these plaques as well. But there is a tipping point in the advance of the disease that coincides with the first evidence of cognitive decline.
It is at this point that abnormal tau protein is expelled from cells to "seed" in other parts of the brain. It's also a point in which the beta amyloid begins to agglomerate as plaques. But it's this spread of tau protein in the brain that is under increasing scrutiny to explain how the disease advances.
There was an article in the June 22 issue of Nature Medicine that evaluates how different species of tau protein could be involved in more or less rapid propagation of tau in the brain -- and more or less rapid advance of dementia. The article is not yet available on line, but it was reviewed in this week's ALZForum. I won't try to go into detail about the research, but you can read all about it here.
The article points out one practical application of this knowledge in regard to trials of therapeutics. In a trial, you want to know how rapidly the disease can be expected to advance so you can know if your therapeutic is a factor. If the disease is advancing at a slow rate, is it because the study therapeutic is slowing it down, or was it going to advance slowly anyway? There will be great variability among test subjects as to who will advance more quickly without the study therapeutic depending on which species of tau protein they possess. Fortunately, a person's tau can be typed, and in so doing researchers will be able to tell what speed of advance to expect without the study therapeutic.
A question is, why does Alzheimer's disease advance so much more quickly in some people than in others -- sometimes by a factor of 10? One answer seems to be in the tau protein.
A little refresher. Tau protein is essential to holding the "microtubules" together. The microtubules act as a skeleton in the cell to give it shape, among other functions. (We discuss this in Beating the Dementia Monster, complete with a little picture.) If an abnormal form of tau protein is present and it fails, the microtubules collapse into the tangles that Alois Alzheimer saw in the brain autopsy of Auguste Deter in 1906.
You will also recall that Alzheimer's disease probably advances for 15 or more years before the first symptoms appear. During that time, beta amyloid is leaving brain cells to eventually accumulate as plaques on brain cells. Alzheimer saw these plaques as well. But there is a tipping point in the advance of the disease that coincides with the first evidence of cognitive decline.
It is at this point that abnormal tau protein is expelled from cells to "seed" in other parts of the brain. It's also a point in which the beta amyloid begins to agglomerate as plaques. But it's this spread of tau protein in the brain that is under increasing scrutiny to explain how the disease advances.
There was an article in the June 22 issue of Nature Medicine that evaluates how different species of tau protein could be involved in more or less rapid propagation of tau in the brain -- and more or less rapid advance of dementia. The article is not yet available on line, but it was reviewed in this week's ALZForum. I won't try to go into detail about the research, but you can read all about it here.
The article points out one practical application of this knowledge in regard to trials of therapeutics. In a trial, you want to know how rapidly the disease can be expected to advance so you can know if your therapeutic is a factor. If the disease is advancing at a slow rate, is it because the study therapeutic is slowing it down, or was it going to advance slowly anyway? There will be great variability among test subjects as to who will advance more quickly without the study therapeutic depending on which species of tau protein they possess. Fortunately, a person's tau can be typed, and in so doing researchers will be able to tell what speed of advance to expect without the study therapeutic.
Friday, June 19, 2020
Loneliness
In Beating the Dementia Monster, we discussed the role of social activity in fighting Alzheimer's disease. Studies have found that, for whatever reason, lonely people decline faster than people with rich social lives. It's not clear that lonely people are more likely to develop Alzheimer's disease, but the evidence is that one's capacity to oppose neurodegeneration, once it has begun, is impeded by loneliness.
In May, I posted about a friend with dementia who died in a senior living facility. The lockdown had been in place for a couple of months, and he would have been very lonely. His dementia was serious, but he still responded strongly to me when I visited him. He was very much an extrovert, and we enjoyed time together -- I as much as he.
The Lancet is perhaps the oldest medical journal publishing peer-reviewed medical research. In February 2018 they published some research on the physiological effects of loneliness -- "The Growing Problem of Loneliness." The research found a 26% increase in the risk of premature death among lonely people, although they acknowledged difficulties in measuring who is lonely. And it expressed alarm with how pervasive loneliness is becoming in our culture.
I was directed to the Lancet by an article in c|net regarding how loneliness affects us physiologically -- "How loneliness could be changing your brain and body." The article explored several aspects of loneliness and the brain, including its relationship to Alzheimer's disease. It's well known that sources of stress, such as loneliness, change the chemistry of the body, usually in negative ways.
According to the article, loneliness and the hormones it promotes do not appear to initiate events leading to the plaques and tangles of Alzheimer's disease. Nevertheless, chemistry changes resulting from loneliness can change which genes are "expressed," meaning which genes will be used to produce different proteins. Some of the proteins promoted by the chemistry of loneliness may be involved in inflammation. As we have said so often before, inflammation can encourage an existing case of Alzheimer's disease to proceed more rapidly.
In May, I posted about a friend with dementia who died in a senior living facility. The lockdown had been in place for a couple of months, and he would have been very lonely. His dementia was serious, but he still responded strongly to me when I visited him. He was very much an extrovert, and we enjoyed time together -- I as much as he.
The Lancet is perhaps the oldest medical journal publishing peer-reviewed medical research. In February 2018 they published some research on the physiological effects of loneliness -- "The Growing Problem of Loneliness." The research found a 26% increase in the risk of premature death among lonely people, although they acknowledged difficulties in measuring who is lonely. And it expressed alarm with how pervasive loneliness is becoming in our culture.
I was directed to the Lancet by an article in c|net regarding how loneliness affects us physiologically -- "How loneliness could be changing your brain and body." The article explored several aspects of loneliness and the brain, including its relationship to Alzheimer's disease. It's well known that sources of stress, such as loneliness, change the chemistry of the body, usually in negative ways.
According to the article, loneliness and the hormones it promotes do not appear to initiate events leading to the plaques and tangles of Alzheimer's disease. Nevertheless, chemistry changes resulting from loneliness can change which genes are "expressed," meaning which genes will be used to produce different proteins. Some of the proteins promoted by the chemistry of loneliness may be involved in inflammation. As we have said so often before, inflammation can encourage an existing case of Alzheimer's disease to proceed more rapidly.
White Noise Machine for Insomnia
My insomnia probably became chronic when I was in my mid-60s. I used to look forward to the peace that would come from lying down and closing my eyes after a busy day. But suddenly every night was a battle. I could normally get to sleep relatively easily, but staying asleep was another matter. And I didn't sleep well. I got some help from zolpidem (Ambien), but the doctors and insurers became increasingly reluctant to prescribe it. And for good reason.
One of my providers recommended the book No More Sleepless Nights. I didn't get it, but I found similar advice on line. Experts recommend techniques like keeping your room dark, keeping room temperature low, avoiding caffeine after noon, spending your last hour before bed in non-stimulating activities, and such like. The book originated in the 90s, before we had all these device screens, but we are now advised to avoid screens in the evening. Most are juiced with extra blue light, which reminds our brains of the mid-day sun.
Still frustrated, I recently read an article that recommended using a white noise machine. I was trying to do everything else I'd read about and thought this might be worth a try. Amazon suggested the Dohm Classic, so I picked one up.
When I started it, the first thing I noticed was that it sounded just like my CPAP machine with the hose pulled off. A steady whooshing noise. It had two speeds, so I started with the lower speed, since I was afraid the noise would keep me awake. But I fell right to sleep, and I had an insomnia-free night! So I ran it the following night with the same results. But the third night was like before -- quick to fall asleep at 10, but awake at 2 or 3. And it continued this way for several days.
So by a brilliant stroke of genius, I moved the speed up to the higher level. Wonderful! Two nights of great sleep -- better than I'd had in a year or two. But then back to normal. I took it to Seattle, and it didn't help at all the two nights before my tests.
But I'm still using it, and I'm doing better. Quite a bit better, in fact. Anxiety over the tests may have been a factor with my experience last weekend, but that's behind me now. So the last three nights have gone very well. An important thing is how I feel when I wake up. Part of my experience with insomnia is being awake when I want to sleep, but also just not sleeping well. Usually, when I use the white noise machine, I wake up feeling quite rested.
So if you have issues with insomnia, you should consider a white noise machine like the one I tried.
One of my providers recommended the book No More Sleepless Nights. I didn't get it, but I found similar advice on line. Experts recommend techniques like keeping your room dark, keeping room temperature low, avoiding caffeine after noon, spending your last hour before bed in non-stimulating activities, and such like. The book originated in the 90s, before we had all these device screens, but we are now advised to avoid screens in the evening. Most are juiced with extra blue light, which reminds our brains of the mid-day sun.
Still frustrated, I recently read an article that recommended using a white noise machine. I was trying to do everything else I'd read about and thought this might be worth a try. Amazon suggested the Dohm Classic, so I picked one up.
When I started it, the first thing I noticed was that it sounded just like my CPAP machine with the hose pulled off. A steady whooshing noise. It had two speeds, so I started with the lower speed, since I was afraid the noise would keep me awake. But I fell right to sleep, and I had an insomnia-free night! So I ran it the following night with the same results. But the third night was like before -- quick to fall asleep at 10, but awake at 2 or 3. And it continued this way for several days.
So by a brilliant stroke of genius, I moved the speed up to the higher level. Wonderful! Two nights of great sleep -- better than I'd had in a year or two. But then back to normal. I took it to Seattle, and it didn't help at all the two nights before my tests.
But I'm still using it, and I'm doing better. Quite a bit better, in fact. Anxiety over the tests may have been a factor with my experience last weekend, but that's behind me now. So the last three nights have gone very well. An important thing is how I feel when I wake up. Part of my experience with insomnia is being awake when I want to sleep, but also just not sleeping well. Usually, when I use the white noise machine, I wake up feeling quite rested.
So if you have issues with insomnia, you should consider a white noise machine like the one I tried.
Wednesday, June 17, 2020
Insomnia and testing
This past weekend we went to Seattle and I had neuropsychological testing on Monday. I had been tested annually, but I also had a lot of additional testing for the insulin trial from 2017 to 2018. So they gave me a break in 2019. This was the first test I've had since June 2018.
Monday was a fairly difficult morning. The testing ran about 3-1/2 hours, one test after another. I could ask for a break, but I only took breaks to go to the restroom. I've complained before about insomnia, and so I had four hours of sleep Saturday night and four hours of sleep Sunday night. So I wasn't at my best on Monday morning.
Nevertheless, I think I did OK. I was disappointed with my performance on some recall tests, but I think I did OK on problem solving tests. Would I have felt better if I had slept better? I don't know, but this my assessment. I'll hear from the neurologist on the 30th with the official results and the neuropsychologist's assessment.
Monday was a fairly difficult morning. The testing ran about 3-1/2 hours, one test after another. I could ask for a break, but I only took breaks to go to the restroom. I've complained before about insomnia, and so I had four hours of sleep Saturday night and four hours of sleep Sunday night. So I wasn't at my best on Monday morning.
Nevertheless, I think I did OK. I was disappointed with my performance on some recall tests, but I think I did OK on problem solving tests. Would I have felt better if I had slept better? I don't know, but this my assessment. I'll hear from the neurologist on the 30th with the official results and the neuropsychologist's assessment.
Friday, June 12, 2020
Sleep, Research News, My New Book, and Testing ... in no particular order
For several reasons, I haven't posted recently. For one thing, with the covid lockdown, there has been very little news on research findings. The most recent issue of a magazine from a research center that I follow featured an article on how the researchers were spending their time now ... working in the garden, doing artwork, reflecting on all they have to be thankful for, etc.
But my big focus has been on the new book. I have uploaded a manuscript that I hope is final, but my co-author still needs to finish her review. We also need to finalize the cover. But it's really close, and I'm really excited. After all, it's been two years since I started.
I have neuropsych testing at Harborview in Seattle on Monday. You may recall that I was doing so well in 2018 that they decided to skip 2019. I went in for my regular evaluation last year, but it was without tests. But I did not feel well about how things were going at the time, and my neurologist attributed it to sleep problems. After that I worked hard on improving my sleep, and my intuitive sense was that I'd have done as well earlier in 2020 as I did in 2018
But I've been struggling with sleep again, and I don't think I can do as well now as I did in 2018. I blame sleep. I go to bed at 10, and I try to sleep until 5. I usually fall asleep pretty easily, but I'm wide awake at 3:00. Trying to go back to sleep is futile. So I've learned to get up then and do the things I would normally do when I get up normally -- takes about an hour to an hour and a half -- and then go back to bed. Often, but not always, I can then sleep until 6:30. When this works, I feel well, but we'll need to see the results of my cognitive tests next week to see if this is helping.
We discussed the central importance of sleep in Alzheimer's disease in the first edition of Beating the Dementia Monster, but we'll get into it more deeply in the new edition.
What I'm interested in is trends. I am 100% fully functional, but I worry that my trend of improvement has stalled or even reversed a little. A question I'll have for my care team when the results are in (June 30) is whether a renewed decline is in line with normal aging from where I was in 2018. Recall that my trend in cognitive improvement from 2015 to 2018 was pretty powerful. Which is why I wrote Beating the Dementia Monster. I was told in early 2016 that I had bought 10 years with my lifestyle changes. Five of those years are now gone.
I recently purchased a white noise machine on Amazon, and I think it's helping a lot ... usually. Sometimes not so much, but usually. Basically it makes a steady whooshing noise, like a fan or something, that calms you. The first couple of nights I had it on low, and I slept all night for the first time in probably a year. But after the second night, I couldn't discern an improvement. Last night I ran it on high, and I slept through the night again.
When I say I slept through the night, I still got up frequently to visit the bathroom. After the third time I don't get back to sleep. But I'm sometimes up 5 or 6 times a night. I have an appointment to see a new urologist, and I want him to investigate the possibility of neurogenic bladder. You'll notice that Alzheimer's disease is listed as the #1 cause, and my symptoms track exactly. My previous urologist never talked to me about it as a possibility, but I saw recently that he wrote "neurogenic bladder?" a couple of times in his notes.
After my tests next week I'll be sure to post regarding how I think I did with my neuropsychologist and her tests, and I'll post again June 30 on the outcome of my visit with my neurologist.
But my big focus has been on the new book. I have uploaded a manuscript that I hope is final, but my co-author still needs to finish her review. We also need to finalize the cover. But it's really close, and I'm really excited. After all, it's been two years since I started.
I have neuropsych testing at Harborview in Seattle on Monday. You may recall that I was doing so well in 2018 that they decided to skip 2019. I went in for my regular evaluation last year, but it was without tests. But I did not feel well about how things were going at the time, and my neurologist attributed it to sleep problems. After that I worked hard on improving my sleep, and my intuitive sense was that I'd have done as well earlier in 2020 as I did in 2018
But I've been struggling with sleep again, and I don't think I can do as well now as I did in 2018. I blame sleep. I go to bed at 10, and I try to sleep until 5. I usually fall asleep pretty easily, but I'm wide awake at 3:00. Trying to go back to sleep is futile. So I've learned to get up then and do the things I would normally do when I get up normally -- takes about an hour to an hour and a half -- and then go back to bed. Often, but not always, I can then sleep until 6:30. When this works, I feel well, but we'll need to see the results of my cognitive tests next week to see if this is helping.
We discussed the central importance of sleep in Alzheimer's disease in the first edition of Beating the Dementia Monster, but we'll get into it more deeply in the new edition.
What I'm interested in is trends. I am 100% fully functional, but I worry that my trend of improvement has stalled or even reversed a little. A question I'll have for my care team when the results are in (June 30) is whether a renewed decline is in line with normal aging from where I was in 2018. Recall that my trend in cognitive improvement from 2015 to 2018 was pretty powerful. Which is why I wrote Beating the Dementia Monster. I was told in early 2016 that I had bought 10 years with my lifestyle changes. Five of those years are now gone.
I recently purchased a white noise machine on Amazon, and I think it's helping a lot ... usually. Sometimes not so much, but usually. Basically it makes a steady whooshing noise, like a fan or something, that calms you. The first couple of nights I had it on low, and I slept all night for the first time in probably a year. But after the second night, I couldn't discern an improvement. Last night I ran it on high, and I slept through the night again.
When I say I slept through the night, I still got up frequently to visit the bathroom. After the third time I don't get back to sleep. But I'm sometimes up 5 or 6 times a night. I have an appointment to see a new urologist, and I want him to investigate the possibility of neurogenic bladder. You'll notice that Alzheimer's disease is listed as the #1 cause, and my symptoms track exactly. My previous urologist never talked to me about it as a possibility, but I saw recently that he wrote "neurogenic bladder?" a couple of times in his notes.
After my tests next week I'll be sure to post regarding how I think I did with my neuropsychologist and her tests, and I'll post again June 30 on the outcome of my visit with my neurologist.
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