Here’s what happened: I’m not a “from scratch” web coder, so I installed what’s called a “theme” for my niece’s website and used it as a springboard to create a look that would capture her life and style.
A lot of work goes into designing the look of a website, but it has to pale in comparison to all the work that goes into creating themes, or “platforms” on which creative designs are based. By the time I get my hands on designing a website, all the hard prep work has been done, and I’m presented with a lovely spring board that allows me to jump and flip and fly wherever my creative juices lead. …read more
Yesterday I came across Lewis Carroll’s “Jabberwocky” poem in Alice in Wonderland (you can download the whole book for free at Gutenberg).
I’ve always loved how Carroll made nonsense words sound like language. But what got me this time around was Alice’s response, and the parallel of that with how I feel about “talking” to Mom.
‘Twas brillig, and the slithy toves
Did gyre and gimble in the wabe;
All mimsy were the borogoves,
And the mome raths outgrabe.
‘Beware the Jabberwock, my son!
The jaws that bite, the claws that catch!
Beware the Jubjub bird, and shun
The frumious Bandersnatch!’
As I was sitting listening to our various conversations around the table, something struck me as different this year. We’re all hovering around 50—give or take a couple years—and the aging process is beginning to take a more prominent seat at the table. Not only do conversation topics start with the premise of aging: declining health, the cost of health insurance, etc, but it seems that no matter what the topic, it eventually touches on something to do with aging. …read more
It’s a very painful fact that I miss Dad and that I wish I had spent more “being time” with him instead of dividing my time between being and being productive. As I’ve mentioned before, in hindsight, all you want is to be near the one you’ve lost just a few more minutes. Nothing else matters but being in the person’s presence and having them know you are there.
I want to do this with Mom, but Alzheimer’s presents a huge problem. Whenever I see Mom sitting alone, it kills me because she looks so terribly alone. So I go sit with her, and on a good day—most days—she is riveted with my presence. But the second I leave her sight—to fling clothes from the washer to the dryer; to use the bathroom; to make a cup of tea—she is completely alone again. And in those moments—from her perspective—she has always been and always will be alone. There is no memory of my having been in her presence all morning other than a few moments of necessary “productive time.”
I hate this disease. There is no sufficient quality time you can give someone with Alzheimer’s. As a caregiver, it feels like there is no neutral status for you as a human being: you are either benevolent or malevolent; sacrificial or selfish; worthy or worthless.
Alzheimer’s isn’t a one-man disease; it does a pretty good job of spreading the pain around.
Like the title of this blog says, there are things to be learned from all kinds of dementias. Here is a particularly astounding thing to learn: severe autism does not necessarily mean the sufferer is mentally retarded. This video will shock you into looking beyond the outward appearance of those who cannot communicate and into the soul.
Sometimes I wonder how much like this girl my mother is. How much does she really know about what’s going on around her?
Yesterday a social worker came to the house to evaluate Dad for possible in-home care assistance. It was a thoroughly humiliating experience for Dad.
The list of questions issued were designed to find out exactly what Dad can and cannot do for himself. The fact that Dad can’t do much at all for himself is something we try not to throw in his face even as it happens. Every time Dad can’t sit in the chair correctly and a struggle ensues to find the right verbal or physical cue to help him do so, Dad’s self-esteem takes a dive. Every time he can’t find a certain room in the house… can’t tell time… etc. So when a list of questions comes along and lays out each and every one of his deficiencies in one sitting, piling them up in front of him like so much garbage to be hauled around, well, it would be an understatement to say it was humiliating.
The further we got into the questionnaire, the more Dad’s countenance fell. It got to the point that I let Dad tell the social worker that he had no problem doing x or y or z, even though I knew the truth.
We ended up somewhere between the truth and Dad’s dignity, honoring neither.
At the very end, this wise social worker asked a question that was clearly not on the list. She asked, “Do you like to fish?”
You could see the dark cloud lift from over Dad’s beaten-down self! A tiny bit of affirmation in the midst of all that pummeling! Never mind that Dad can’t do it anymore; the question at least allowed him the pleasure of showing a positive side of himself. For once, he got to answer a very truthful “yes!”
And that made me wonder: why can’t we–in the pursuit of scientific correctness–remember the spirit of a man? Why can’t we sprinkle questionnaires with bits of affirmation for the sake of dignity alone? Would it hurt science or government to ask “what’s one of your favorite books?” to a woman applying for food stamps? Or “what superpowers would you most like to have?” to a veteran seeking disability assistance? Shoot, while I’m at it, can we change the the category from “seniors and people with disabilties” to “seniors and people with abilities”? There are always things we can still do; things we still like; things we still dream about.
Just stuff I wonder.
And you? Do you have any beef with questionnaires?
This week I started wearing the monovision contact lens that I got three years ago. This is the lens that you wear in one eye to correct for reading while leaving the other eye free to focus on things in the distance.
I tried this lens years ago but found it unacceptable. Everything was at once blurry and sharp, and I couldn’t tolerate the tiniest bit of blur in my vision.
I realized it was a mental adjustment—I would have to learn to choose the sharpness of one eye over the blurriness of the other at any distance until all I saw was sharpness. But I was impatient and gave up on the adjustment period, resorting instead to donning and doffing reading glasses when in need.
Now my close-up vision has gotten so bad that when I tried the monovision lens this time, my mind was quite happy to accept the gift of semi-sharpness without the need to scout around for glasses. It took a very short time, in fact, for my brain to adjust and see all things in focus at all distances.
Remarkable how the brain can do that.
I learned a similar lesson in life with the attitude of gratitude. I was going through a very stressful, heart-rending period when nothing seemed to be “working” for me. One day I plopped down on the floor and began to say “thank you” for every part of my life. It was a turning point in my stress level. I began to see not problems but challenges; not curses but blessings. And what a difference it made!
Alzheimer’s and other devastating diseases, I’m noticing, can be lenses that change the way we see life; they change what we think is important; they bring into focal clarity the gift of family, friends, community, connection. I’m amazed as I surf the blogs written by sufferers and caregivers to see the softness that takes over when anger ends. I’m amazed, for example, with Michael J. Fox’s attitude toward his Parkinson’s, calling it a “liberating” gift. I’m touched by the may bloggers who share of the immense struggle of caregiving and the eventual gratitude it produces in them.
It’s always a choice the person makes to see disease differently. Or rather, to see the value of the person despite the disease.
In this season of Thanksgiving, it is good to see the change that Alzheimer’s and other diseases have brought to our self-centered culture.
So, thank you to all of you who write and share of your struggles, forming a new community that chooses to rise above bitterness and embrace even the bleakest, darkest days of life for the goodness they produce.
When dealing with Parkinson’s, sometimes one symptom can dictate behavior and end up causing a cascade of physical problems.
Symptom and consequence in point: hand tremors can lead to decreased liquid consumption (because the Parkinson’s patient is embarrassed to spill every time he drinks), and decreased liquid consumption can exacerbate constipation and possibly lead to impacted bowels in a Parkinson’s victim.
In dealing with Dad, we found that one solution to this cascading problem is a spill-proof sipping container. Dad used to spill everything on himself, the table, the floor. Now when his shaking is bad, we put all liquids in the spill-proof water bottle, and he is no longer embarrassed to drink.
The nice thing about the Camelbak water bottle is it’s sleek, sporty design which makes Dad feel like he fits in more with our physically active family.
So if you are having a hard time coming up with a Father’s Day gift for your Parkinson’s dad, this is my suggestion.
We already know that a Mediterranean diet helps stave off signs of dementia, but who wants to eat flavorless vegetables all the time?
If you think you have to sacrifice that deeply satisfying taste of butter and meat that you don’t typically get in a vegetable-rich diet, you don’t know Yum Sauce! This sauce is of Japanese origin and is full of protein, B-complex vitamins (B1, B3, B6, B12), and antioxidants—and best of all, it rounds out the flavor of anything you put it on with a “meatiness” that will satisfy the carnivore in you.
The dish pictured here is a prime example of a Mediterranean diet with a Japanese twist: a bed of baby spinach leaves with sauteed butternut squash, topped with Yum Sauce. Use this sauce on any steamed vegetable, over rice, or even on salad, and you’ll be on your way to fighting memory loss!
1/2 cup olive oil
1/2 cup water
1/2 cup nutritional yeast
3 packets of lemon or orange-flavored vitamin C
2 Tbsp soy sauce
4 Tbsp almond butter or peanut butter
2 cloves crushed garlic
1/2 cup black beans with juice
1 tsp cumin powder or curry powder
1 tsp white pepper
Throw everything in a blender and puree until smooth. Store in a refrigerator for up to one week.
After writing my last post regarding the stress of caregiving, I had to drive somewhere, and in the course of the short trip, I caught a clip of a Haydn symphony on the radio. I don’t know how, but there are sections in there that make me feel as though this exhausted, shriveling heart of mine is actually quite expansive and able not only to cope, but to bring beauty out of the brokenness around me. You know how sometimes you see a scene or a photograph that makes you certain that the universe is true and right and good? Well, music does that, but with thrice the emotion. Music can rewire a frazzled or finished outlook into one of hope. And hope can take you a looooooong way down a very dark road.
All to say that music—in addition to being a fantastic tool for treating Alzheimer's—is a very inexpensive way to get your groove back when you’re done in from caregiving. Or from living a regular life-is-pain-highness kind of life.
To prove this, I'm giving you a little tool in this post that some people may not know about. The tool is called Pandora—an internet service that lets you create your own radio station online.
The extra cool thing about this service is that you can create multiple radio stations, all with different moods—colored by different genres or artists—to suit your changing needs. Sometimes I don't even know what my need is or what it is that will trigger a brighter outlook, so having multiple "moods" to choose from is very useful.
Cutting to the chase, here are four stations I created to get you started. Click on any one of them and follow instructions to log into Pandora. From there, you can tweak the station by "adding variety" (a specific music piece or musician) to the station. You can also "thumbs up" or "thumbs down" any piece that you hear, and the station will remember to pick similar music or not to play that piece in the future. Talk about tailored just for you!
So here goes—four different flavors for your listening pleasure:
Jazz. You know, the good stuff with Stan Getz and Louis Armstrong and Bobby McFerrin and Michael Buble…
This is a fusion of old hymns and contemporary Christian pop. Nice, especially for Sunday mornings.
My personal favorite: spicy Latin mix. Makes you want to jiggle and dance and go crazy! A great stress-reliever.
Classical is music to transport the soul.
A couple more tips: if you want to play this music off your sound system without leaving the kitchen table, you can buy a $4 wireless FM transmitter and send the station to your main tuner. You can also "send the station" to the radio that sits on your mother's side table in the bedroom while you’re working on the laptop in the kitchen. Just a whole lot of things you can do with Pandora!
Do have fun, and come back and post a station of your own creation if you dare!
The Alzheimer’s Research Paradigm
If you’ve every studied philosophy of science, you’ll recognize that current research in the field of Alzheimer’s Disease is battling paradigms. The funny thing is, the Alzheimer’s field hasn’t even reached the level of robust theory, yet there is strife in the ranks of researchers fighting over the direction inquiry should take:
“Kill the amyloid plaque!”
“No, viva le beta amyloid!”
“Forget amyloid. It takes tau to tangle.”
“Ha! The biomarker emperor has no clothes!”
“Wait. Isn’t it all about insulin resistance?”
“Nix all the above. Just get quality sleep, and you’ll be fine.”
If you think this is funny, these basic statistics will sober you up:
* As of 2010, there are 5.4 million people in the US with Alzheimer’s
* Almost half the people over 85 have Alzheimer’s
* When the baby boomers come of Alzheimer’s age, the costs of care for this disease alone will cripple Medicare and Medicaid
* Federal funding for research into a cure is dropping fast
* YOU will be paying for either your own care or for that of a loved one if a cure is not found. And YOU will either be grossly neglected when this disease hits you, or you will die the slow death of stress from caregiving for someone else.
Bottom line: research into Alzheimer’s—its cause(s), treatment, and cure—is alarmingly urgent and terribly underfunded.
There are plenty of people out there who believe we shouldn’t put money into research at all, because so far nothing has been found to stay the course of “Alzheimer’s” dementia, and the whole drug industry is just a ploy to line the pockets of the pharmaceutical fat cats. If you’re in that group, you can stop reading this now. If, however, you would really like to see your Mom or Dad or Yourself able to have a meaningful conversation with your loved ones and know whom you’re talking to—hopefully for the rest of your life—read on, because the question isn’t whether or not to research. The question is where do we put our research dollars?
Not a simple answer when you consider that the reigning paradigm for Alzheimer’s research is serious question.
Let me explain with recent findings from my own readings:
A couple weeks ago I attended a Cure Alzheimer’s Fund webinar presented by Dr. Rudy Tanzi (of Massachusetts General’s Institute for Neurodegenerative Disease) on Alzheimer’s research and drug development.
Beta Amyloid: Clues From Our Genes
Dr. Tanzi’s group is in the “clues from our genes” pool (looking at the genes as a starting point rather than, say, looking at diet first). The dominant belief in this pool up until recently is that beta amyloid plaque accumulation in the brain, followed always by tau tangles, are the two main biomarkers for Alzheimer’s Disease. That is, where there is Alzheimer’s, there is an overabundance of beta amyloid plaque and destruction caused by tau in the brain. Also, a higher load of plaque correlates with a higher degree of dementia (see slide from webinar). Plus, as this accumulation progresses and moves to different parts of the brain, there is a parallel manifestation of symptoms.
The connection seems pretty obvious. And Dr. Tanzi certainly has the credentials: back in the 80’s when he was studying Down’s Syndrome, he realized they had isolated the gene responsible for amyloid “plaque” deposits in the brain, and—given that all Down’s Syndrome sufferers end up with Alzheimer’s—thought to make a link between this gene and other cases of Alzheimer’s. From there it was one success after another, with Dr. Tanzi participating in the discovery of three of the four known gene mutations causing early-onset Alzheimer’s (these are the genes that guarantee you will get Alzheimer’s). Granted, early-onset AD accounts for only 5% of Alzheimer’s cases, but it does give weight to the conviction that Alzheimer’s has a genetic link. More recent studies looking at family history suggest that up to 80% of Alzheimer’s cases are genetically influenced (see slide from Tanzi’s presentation).
The presentation is convincing enough until you start reading the commentary in the field and start learning that current direction of research into the causes of Alzheimer’s is highly questioned.
Researchers coming on the scene today, for example, would argue that the plaque theory is circular reasoning. You can’t say that plaque leads to Alzheimer’s if you first define Alzheimer’s as “dementia with plaque.” And when your theory states that plaque accumulation leads to Alzheimer’s, the automatic null hypothesis is that where there is plaque (in copious amounts) you will always find dementia, and when plaque is cleared, dementia will go away.
But this has not born out. It is now known that “roughly one-third of all elderly adults have such plaques in their brains yet function normally.” It has also been proven that the elimination of beta amyloid plaque (achieved by the “Alzheimer’s vaccine”) does not cure dementia.
Thus the paradigm shake-up. Why continue with the biomarker research when the facts don’t bear an airtight connection? Is the “clues from our genes” group too heavily invested financially and psychologically in this line of research (as some suggest) to give it up as dead?
Dr. Tanzi responds to these fears in his recent presentation. He didn’t use the word per se, but nuance was the main come-back. All theories undergo refinement, and this plaque-causes-dementia theory is no exception. Looking at the genes may have lead to wrong conclusions in the past, but there are still some pretty interesting clues to follow going forward.
Here is a crude rendition of the protein-level pathology in Alzheimer’s:
Beta amyloid (Aβ) is cut off from its precursor protein; Aβ links to other ab in small clusters; Aβ kills nerve synapses; Aβ accumulates into plaques
For the past twenty years, research has focused on improving the symptoms of dementia by eliminating the final clusters of beta amyloid (plaques). Looking at the little diagram above, different drugs targeted the beta amyloid at different points on the linear progression toward plaque: Flurizan targeted the process that snipped the Aβ off its precursor protein; Alzemed tried to block the aggregation of Aβ; Dimebon was designed to protect the neurons from Aβ; one drug successfully immunized the brain against Aβ (resulting in clearance of plaque from the brain, inflammation in the brain, and progressive dementia); and finally, drugs were developed (Aricept and Namenda) to act at the symptomatic level.
None has had any significant effect on the brain’s function in memory tests.
Tanzi’s response? Perhaps the reason drug trials fail is that the potency of the drug is off—either too weak or too strong—and funding for a subsequent trial is cut off. Or perhaps researchers need to stare at the diagram a little longer and find out whether beta amyloid needs to be left to do some mission, then cleared before it wreaks havoc on the synapses.
Which is exactly what happened with Dr. Tanzi—a little stroll through the lab, a light-bulb moment, and Tanzi discovers that beta amyloid kills bacteria and yeast like nobody’s business. Beta amyloid is a good guy? The plaques themselves are just “a field of bullets” left over from some major battle?
Definitely worth an investigation. A new direction.
To Fund Or Not to Fund
So it turns out that looking at clues from the genes is not a paralyzing avenue of research after all. Is the paradigm really dead, or just needing refinement? In the new direction of Alzheimer’s research, Dr. Tanzi’s findings have lead to a more recent drug (PBT2) that takes the “antibiotic” role of beta amyloid into account as it tries to clear its toxic leftovers. Do we pull the plug on funding just when the story is getting really interesting?
The competition out there is fierce. You would think from some of the stinging accusations aimed at the “old school” research that funding for groups such as Tanzi’s should be questioned. Yet, as the webinar pointed out, “the vast majority of our knowledge about AD and AD drug discovery has been based on studies of the four known AD genes over the past two decades.” That’s old school success.
On the down side, “about 70% of AD genetics is unexplained by the four known AD genes.” On the further down side, it’s going to take A LOT of funding to find the genetic culprits for the rest of Alzheimer’s cases. And genetics is still only one of several approaches to studying this disease! (Besides, paradigms don’t die until a better one supersedes it, and there is no airtight theory out there yet).
Do we put all our eggs in one basket? What if there aren’t enough eggs to spread around to the different baskets?
Frankly, I don’t know the answer to this question.
There are a couple good reasons I think the Cure Alzheimer’s Fund group is worth supporting, though. One reason is the Cure Alzheimer’s Fund website itself. The Internet has plenty of faults, but it also has the advantage of open criticism. If you look at the comments sections of one of the papers put out by Tanzi’s group on the Alzheimer’s Forum, you’ll see an open debate. It’s free collaboration. It’s crowdsourcing at its best. I think it multiplies the value of your funding dollar.
Another reason is that I’ve suspected my own mother’s caseStay tuned for a post on this topic to be of possible bacterial/fungal origin and am dying to see what this group finds in their new line of research. The only thing I fear is the psychological barrier to this new approach.
A Taboo Research Project?
To be specific: the two agents being considered by Tanzi’s group as possible aggressors in the beta amyloid battle are Chlamydia and Candida Albicans. But looking at Candida Albicans as a possible cause of anything is TABOO in mainstream medicine. Just browse the comments section of a recent article in the New York Times about Candida Albicans, and you’ll see what I mean.
Will Tanzi’s group have the courage to fight all the enemies of research at the same time: tainted motives (the desire for personal glory), psychological entrapment (continuing in a line of research simply because it’s been going on for so long), and mainstream opinion about what is acceptable research (we do not look at X)?
I guess it’s going to take a lot of money to find out. Which brings us back to the basket issue.
Do we have to duplicate Alzheimer’s research at the Federal and State levels? The state of Texas, for example (being one of the top three states that will go broke paying for Alzheimer’s care in the future), is spreading its research egg money into several baskets:
* Prevention and Brain Health
* Disease Management
Why repeat this with every state, plus private groups on the side? Is there a way to get more collaboration between research groups? The well of needed funding is infinitely deep, so why are we digging multiple wells?
I guess part of the answer is that individual motivation for research (even if it is for personal glory) is the strongest kind you can find, and therefore the best engine for finding a cure. And likewise, education plus individual conviction will drive donations. There is certainly enough information available at one’s fingertips to give no one who is interested in a cure an excuse to sit on the sidelines!
So what will you do?
Because where there is a will, there will be a way to end the increasingly long goodbye.
For further reference:
Beta-Amyloid: An Antibiotic? (with a slew of interesting comments)
Alzheimer’s Brain Tangles Offer Clue To Worsening
Alzheimer’s Disease: No End to Dementia
New Potential Cause of Alzheimer’s Disease Detected
Alzheimer’s Scary Link to Diabetes
Follow the Alzheimer’s Breakthrough Ride journal
An video report on several intriguing theories of Alzheimer’s.
Memory can be wonderful and cruel all at once.
It’s been almost a year since Dad died, and I’ve discovered that it takes a year to fully recover from the exhaustion of caregiving. It takes a year to recover fully enough to crave the chance to do it a second time over—to do it right this time.
Last Thursday was one of those gorgeous days that make your spirit soar. It was just warm enough, just breezy enough, just relaxing enough, just full enough of good plans that I wanted Dad here to enjoy it with us. I was in the middle of a supermarket parking lot when that thought came to me, and it was the beginning of a four-day breakdown.
Why can’t I be given a second chance? I’ve got all my energy back now, and I swear if I’m allowed, I’ll show Daddy all the tenderness that I had no time or energy to give him before. Why did he have to die before I recovered my ability to love him?
It was a catch-22 I battled with all weekend.
That Thursday evening I drove over the mountains to attend the licensing of a young preacher. I took advantage of the lonesome drive to listen to a book on tape my niece lent me. The title was “My Life in the Middle Ages.” It was supposed to be funny. Turns out the first two CDs were all about this guy’s father’s declining months. It was about death; about tying up all those messy loose ends.
Of course I bawled my way through that. When I couldn’t take it anymore—when I thought I’d better get my face in shape for the licensing ceremony—I popped in an Ingrid Michaelson CD. Quirky, upbeat Ingrid. Problem is, I’d never really listened to some of those songs before. About the fifth song on the CD is about the inevitability of death. “We are all snowmen, and we’re going to melt one day.”
The same message is being pounded into me over and over.
We’re all snowmen, and were are going to melt one day. It’s the norm. It’s not a devastating tragedy.
But the point of it? The point of living and dying and leaving others behind to bawls their eyes out?
Here I was, the daughter of a preacher, going to the licensing ceremony of a young, vibrant, new preacher, and I wasn’t getting it.
The point of living and dying, it slowly sunk in, is to pass on the baton. The best thing we can do is to spend ourselves living, then die and offer the lessons of our lives as rich mulch for the next generation.
It made me think of all the lessons I absorbed from Dad’s life. Like:
– Nature is awesome
– Don’t spend what you don’t have
– Prayer changes things
– God is gentle
– Invest in people on the fringe of society; they’re the ones who will remember you
It was a good weekend to mourn and know that there is good in all of this.
From now on, when mourning strikes, I will try to add to the list of lessons learned.
And I will think about how my life will have an impact after I—like all of us will—eventually melt.
Here’s what happened: I’m not a “from scratch” web coder, so I installed what’s called a “theme” for my niece’s website and used it as a springboard to create a look that would capture her life and style.
A lot of work goes into designing the look of a website, but it has to pale in comparison to all the work that goes into creating themes, or “platforms” on which creative designs are based. By the time I get my hands on designing a website, all the hard prep work has been done, and I’m presented with a lovely spring board that allows me to jump and flip and fly wherever my creative juices lead.
Today the world has been given the very bad news that there is nothing that can help prevent or slow the progression of Alzheimer’s. The disease is a thief and a murderer, and nothing can stand in its way.
I say the folks who did these studies need to study Mom. Round out the evidence of all that hopeless progression with a little taste of surprising regression.
I wrote the rest of this post a week ago, but only got around to publishing it today:
Mom is going backwards. She’s regressing, it seems to us, and that’s a good thing when you have Alzheimer’s.
How? What? When? Where? Why? Is it wishful thinking that we’re seeing marked improvement in Mom’s cognition, or is this real?
Exactly what I’m asking myself these days. Granted, being a highly motivated observer may make my observations suspect, but I feel it would be irresponsible not to report what appears to be clear evidence of improvement in Mom’s condition. It would be irresponsible of you not to suspect my findings, but dumb not to take a look at all.
So here goes.
A few weeks ago, we who have been taking care of (or been around) Mom for the past three years noticed that we were telling people Mom was having a good month. We were used to telling people that Mom was “having a good day” every now and then. A good day once a week was a good thing. But the entire month of March of this year seemed to be “a good day.” It came to the point that we were scratching our heads saying, “Hmm. Maybe Mom doesn’t have Alzheimer’s. Maybe this was all stress, and now that she’s been de-stressed for three years, she’s coming back.”
So I decided to take inventory of the new signs of cognition (and physical improvement) coming from Mom these days. What exactly is she doing that she wasn’t doing before? This is what I have:
- Mom has gained weight. Exactly a year ago Mom weighed 85 pounds and was bed-ridden with pneumonia. Hospice pronounced her a week from the grave. Today Mom weighs 95.5 pounds. No sign of physical sickness (OK, an occasional night fever and drippy nose).
- Mom sucks from a straw. For the longest time, we were having to “prime the pump” to get Mom to suck from a straw. A year ago, when we put a straw in her mouth, nothing would happen. So we’d plug the straw with our finger, then release the contents into her mouth, and, voila, she’d start sucking. Now Mom sucks as soon as the straw hits her lips.
- Mom opens her mouth at the sight of food. Again, for the longest time we’d just get a pleasant stare when we lifted a fork to her mouth. Two years ago, it would take us a good hour and a half to get through breakfast because it was only one time out of ten that Mom’s lips would part when we brought food to her mouth. Now, six-seven times out of ten, her mouth opens like a baby bird’s. Breakfast time has been cut in half.
- Mom swallows. Up until (this is where I wish I’d kept an exact diary) about four months ago, Mom had a permanent sore on the right side of her mouth. This was caused by the fact that Mom leans to the right when she sleeps, and food that remained in her mouth (because she wasn’t aware enough to swallow) dribbled out and ate at her skin. No matter how well we brushed her teeth and how much Vaseline we slathered around her lips, the sore was there off and on for the last three years until–a few months ago. The sore has not returned.
- Mom watches TV now. Meaning, she actually turns to it, focuses on it, and laughs on cue–sometimes for a 10-15 minute stretch. This hasn’t happened at all in the past three years until this “awakening.”
- Mom stops at the photo gallery in the hallway, looks at individual family photos and “comments.” For the past three years we’ve been walking through the hallway with Mom–past a 4 foot x 4 foot photo gallery–occasionally stopping to show Mom the family photos in hopes of getting a response. She wouldn’t even look where we were pointing. And if she focused at all, it would just as likely be on a knot in the wood frame as on a photo. Now Mom takes the initiative to stop and look from frame to frame, pointing, jabbering, looking at us and back at the photos. Sometimes getting teary-eyed at our description of the photos.
- Mom is using sentences. I wrote in a previous post that Mom’s language consists almost entirely of two syllable experiments in sound with an occasional word thrown in. We used to get so excited when she uttered a word that we’d call a family member and share the big news. In the past couple weeks, Mom has used short sentences. Like three days ago when I put her to bed, I said, “Mom, I love you.” She nodded and said, “For me, for me, for me too too.” The next morning at breakfast I tried to give her some juice while she was still chewing on her eggs and she shoved my hand aside and said “Put it down down.” I put her down for a nap in the afternoon, put on some Vivaldi, and did a farcical ballet dance (a la BodyVox). She nodded and said, “Yes. I do too too too.” Then that evening when I tried to give her her Seroquel (ground up in some juice), she shook her head. I kept bringing the juice to her mouth, and in exasperation she said, “Tsk! What what what do you do?” (Translation, “cut it out!”).
Four sentences in two days! Yesterday was a quiet day for Mom. No miraculous signs of anything. I’m dying to report more on this healing process, but Mom is not a science project, and I have to remember that she is worth all my love no matter what direction her mind and body take.
But I do think it’s worth mentioning that something has happened to Mom that has sent this Alzheimer’s into some sort of retreat. There is more than death taking place in her brain. Somewhere, somehow, regeneration is taking place as well.
Have any of you had the experience of watching a loved one with Alzheimer’s have a good month? I know Bob DeMarco recently reported an extraordinary event with his mother Dotty. Huge “regressive” step.
Next question will be, what could be causing these amazing regressions? We may have to rely on each other–the caregivers–to find the answer rather than on lab tests alone.
Yesterday Bloomberg Businessweek published an article titled Mouse Study Suggests Alzheimer’s-Linked Protein Can Migrate Into Brain.
The story is this: researchers took brain matter from mice that had beta amyloid plaque (were genetically modified to have such plaque), injected it into the stomachs of normal mice, and months later found beta amyloid plaque in the brains of the normal mice.
If all you read is the headline of this story, the conclusion is that the beta amyloid from the sick mice got into the bloodstream of the healthy mice and passed through the blood brain barrier to take up residence in the healthy brains.
But if you read to the end of this article, it is suggested that there could be all kinds of reasons the healthy mice ended up with beta amyloid plaque in their brains, such as maybe there is some chemical in the plaque brain sample that passes through the blood brain barrier and causes a chain reaction that produces beta amyloid plaque—which would negate the headline altogether.
Now, watch the news and see how many people with take only the headline of this story and pass it off as scientific fact.
The moral of the story: be careful what you read and how you read it.
Trying to follow Alzheimer’s research sometimes feels like walking through an Escher exhibit: the contradictions can border on the absurd.
Take the new findings on SIRT1 and its relation to Alzheimer’s. Research after research shows that SIRT1 apparently protects against Alzheimer’s:
25 July 2010. The sirtuin protein SIRT1 is emerging as an important player in learning and memory, and may have potential as a therapeutic target in Alzheimer disease. Fresh on the heels of a July 11 Nature paper that demonstrated a crucial role for SIRT1 in memory (see ARF related news story on Gao et al., 2010), two new papers add to the growing body of evidence that SIRT1 helps keep brains healthy. In a paper appearing July 21 in the Journal of Neuroscience, researchers led by Valter Longo at the University of Southern California, Los Angeles, show that a SIRT1 knockout mouse has numerous defects in learning and memory. This finding implies that SIRT1 could have a protective role in AD, and indeed, in a July 23 Cell paper, researchers led by Leonard Guarente at the Massachusetts Institute of Technology, Cambridge, report that overexpression of SIRT1 can decrease Aβ production and the number of amyloid plaques in a mouse model of AD.
You’d think, then, that more SIRT1 is better for Alzheimer’s and less is worse. But:
Michán and colleagues also examined a transgenic mouse that overexpressed SIRT1 16-fold in the brain. On this normal mouse background, the authors found that this massive SIRT1 overexpression conferred no improvements in learning or memory, and that synaptic function was unchanged except for a slight increase in neuronal excitability.
And though less is worse, vitamin B3 in the form of niacinamide has been shown to “cure” Alzheimer’s in mice by decreasing the expression of SIRT1: Nicotinamide Restores Cognition in Alzheimer’s Disease Transgenic Mice via a Mechanism Involving Sirtuin Inhibition and Selective Reduction of Thr231-PhosphotauWe evaluated the efficacy of nicotinamide, a competitive inhibitor of the sirtuins or class III NAD+-dependent HDACs in 3xTg-AD mice, and found that it restored cognitive deficits associated with pathology. Nicotinamide selectively reduces a specific phospho-species of tau (Thr231) that is associated with microtubule depolymerization, in a manner similar to inhibition of SirT1. Nicotinamide also dramatically increased acetylated -tubulin, a primary substrate of SirT2, and MAP2c, both of which are linked to increased microtubule stability. .
When asked about this contradiction, Dr. Greene, one of the researchers on this paper says,
You are correct – there are contradictions between the role of Sirt1 in AD. Regardless of these, nicotinamide has good effects in the preclinical models, and has been shown to now be effective for other neurodegenerative diseases as well. Sirt1 may be beneficial at some stages of the disease, and not others – we cannot [reconcile] these differences at this stage, but our research says that nicotinamide is highly effective in preclinical models and that inhibition of Sirt1 plays a role in these effects.
My mind wants to hyperventilate with the contradictions, but then I remember the story of the three blind men describing an elephant and realize the contradiction exists only because we do not yet fully understand.
And that’s what drives research onward.
By now it’s not news that scientists at Case Western have successfully used a cancer drug to clear plaques from the brains of mice that were engineered to have Alzheimer’s, resulting in a reversal of rodent dementia. The hope is that this drug will do the same for humans.
Here is a more in-depth explanation of Bexarotene (“Drug Reverses Alzheimer’s Symptoms in Mice”):
Alzheimer’s disease arises in large part from the body’s inability to clear naturally-occurring amyloid beta from the brain.
In 2008, Case Western Reserve University researcher Gary Landreth, professor of neurosciences at School of Medicine, discovered that the main cholesterol carrier in the brain, Apolipoprotein E (ApoE), facilitated the clearance of the amyloid beta proteins. […] The elevation of brain ApoE levels, in turn, speeds the clearance of amyloid beta from the brain. Bexarotene acts by stimulating retinoid X receptors, which control how much ApoE is produced. …bexarotene improved memory deficits and behaviour even as it also acted to reverse the pathology of Alzheimer’s disease [and] worked quickly to stimulate the removal of amyloid plaques from the brain.
[T]he drug addresses the amount of both soluble and deposited forms of amyloid beta within the brain and reverses the pathological features of the disease in mice.
Another thing I got from Oliver Sacks’ book was a new notion of the power of music in dealing with dementia. My previous post on music and Alzheimer’s dealt exclusively with the notion of music as a memory stimulant. But Sacks’ book made me realize that music can be used as a tool to organize thought and action in the present—in the midst of neurological damage.
Yesterday as I lay down for a recuperative nap, I listened to a Scarlatti sonata in the background, and immediately got a visual sense of what goes on in the brain when music is played. The first picture that came to mind was an animation of DNA transcription: that funny little zipper head that makes a perfect copy of your DNA as it unzips the double helix. Nibble, nibble, nibble, copy, copy, copy. Then I saw Scarlatti’s sonata as doing the opposite with my thoughts: grabbing all the randomness in my mind and knitting it into a useful strand, or, if you want to be more esoteric, turning it into functional narrative.
In Sacks’ The Man Who Mistook His Wife for a Hat, the first clinical case is of a man who had lost all “sense of familiarity:” he could not recognize faces, body parts, food, clothing. Sacks wondered how the man (also a music professor) could function with this neurological deficit, so he went to visit him in his own home. It turned out the man had a very musical brain, and he functioned by humming a tune as he went about his daily business. He could eat as long as he sang, but if interrupted, would no longer recognize his food and would stop eating. He could dress by the same means. His wife would set out his clothes for the day, and he would only recognize them as clothes and dress himself once he started singing! His musical brain was compensating for his lost sense of recognition.
And now I remember a funny little entry by Bob Demarco on the Alzheimer’s Reading Room that is seriously brilliant. He talks about using music to stimulate his mother into action:
My sister was shocked when I told her on the phone that I finally “convinced” my mother to drink prune juice after years of trying and failure. Joanne was here and saw my mother refusing to drink and calling the prune juice poison. It was only after I introduced the “prune juice song” that my mother starting drinking the juice every day and the dreaded Poop-E problem was solved.
I also have the pee song, the poop song, and a long list of songs soon to be number one hits.
This is exactly what Oliver Sacks would have recommended! Music and Alzheimer’s (and Parkinson’s and most other dementias): stimulating the mind into action.
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