Today a nice physical therapist came to assess a treatment program for Dad—to help him regain his balance and mobility and in so doing help him milk the summer ahead of us. A couple hours later, while sitting at the table Dad asked me in an unusually clear voice, "What's the agenda?" I looked up […]
Well, if this isn’t the best gift to buy for someone with early stages Alzheimer’s, I don’t know what is! Probably the one symptom that scares Alzheimer’s victims the most–and turns them into instant hermits–is geographic memory loss. Going out for a walk or a drive and suddenly not knowing where you are or how […]
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 […]
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?
In my research on Alzheimer’s and glucose metabolism, I ran across a fascinating article about the brain’s default system–that part of the brain that is affected in Alzheimer’s Disease; that part of the brain that hogs glucose like no other part of the brain.
In The Secret Life of the Brain, Douglas Fox brings together research on the default network beginning with Dr. Sokoloff who, in his attempt to find out why the brain uses so much glucose (20% of the body’s supply), discovered that the brain uses as much energy while “at rest” as it does while performing tasks.
Later, a neuroscientist named Marcus Reichle discovered a kind of “brain within the brain” that works its butt off when it’s supposedly in “idle mode.”
Raichle and Shulman published a paper in 2001 suggesting that they had stumbled onto a previously unrecognised “default mode” – a sort of internal game of solitaire which the brain turns to when unoccupied and sets aside when called on to do something else. This brain activity occurred largely in a cluster of regions arching through the midline of the brain, from front to back, which Raichle and Shulman dubbed the default network (Proceedings of the National Academy of Sciences, vol 98, p 676).
It was found that some parts of this network devoured 30 per cent more calories, gram for gram, than nearly any other area of the brain. Since part of this default system is in constant communication with the hippocampus (which records every day memories), Reichler speculated that its function was to sort, evaluate, and categorize memories in such a way that would allow the brain to use the past as an “inner rehearsal” for considering future actions and choices.
Brilliant. Just when you think daydreaming is a waste of time, it turns out it’s crucial for living.
Raichle now believes that the default network is involved, selectively storing and updating memories based on their importance from a personal perspective – whether they’re good, threatening, emotionally painful, and so on. To prevent a backlog of unstored memories building up, the network returns to its duties whenever it can.
In support of this idea, Raichle points out that the default network constantly chatters with the hippocampus. It also devours huge amounts of glucose, way out of proportion to the amount of oxygen it uses. Raichle believes that rather than burning this extra glucose for energy it uses it as a raw material for making the amino acids and neurotransmitters it needs to build and maintain synapses, the very stuff of memory. “It’s in those connections where most of the cost of running the brain is,” says Raichle.
Reichler later attented a lecture by an Alzheimer’s specialist and was shown a map of beta amyloid plaques (those clumps found in Alzheimer’s autopsies) in the brain. The picture looked exactly like the default network!
Raichle, Greicius and Buckner have since found that the default network’s pattern of activity is disrupted in patients with Alzheimer’s disease. They have also begun to monitor default network activity in people with mild memory problems to see if they can learn to predict who will go on to develop Alzheimer’s. Half of people with memory problems go on to develop the disease, but which half? “Can we use what we’ve learned to provide insight into who’s at risk for Alzheimer’s?” says Buckner.
That got me thinking…
Maybe one reason we lose memories is that our lifestyle doesn’t allow for much rich idle time like when we would sit on the porch sipping sweet tea on a hot afternoon. So the default network can never do its work of sorting and categorizing memories, and consequently we lose them.
And if this is a problem with the present generation, how much moreso for the upcoming generation. We are consumed with having something to pay attention to all the time. Just look at TV screens these days: not only do you have the main screen, but there’s the pop-up ad for the “next show,” a caption for what’s going on on the screen, and a ticker at the bottom of the screen for what’s happening elsewhere.
Maybe part of the solution for AD is the “quiet space” to be incorporated in school, at work, and at home. Hmm, come to think of it, I offered this very solution in a comment to an article in Time Magazine back in 09 (Turn Off, Tune In, Log Out):
I predict that the twitterification of our society is going to lead to an exponential increase in early-onset Alzheimer’s. We’re increasing the rate of input to our brains and decreasing the time for processing information, and our brains are going to revolt. That, in turn, will lead to the next big industry: de-twitterification rooms where you can sit alone and unconnected, with nothing but a giant aquarium and a beanbag. -Marty
The following describes the knowledge gained by Sharlene in the course of caring for both her parents with Alzheimer’s. It is not necessarily a reflection of my views, but I thought it good to publish the research of someone who has an insider’s view of Alzheimer’s dementia.
Sharlene Spalding is a naturopathic consultant in the village of Casco, ME. She is a former primary caregiver for two parents with AD. She holds a master’s degree in natural wellness. Sharlene is an excellent resource in natural healing and a hound dog when it comes to research. Because of what she knows now, she is committed to a pharmaceutical-free home that revolves around organic foods and herbs. You can visit her website at The Village Naturopath.
John Thorndike’s The Last of His Mind is a work skinned in the devastating story of Alzheimer’s, but shows what an unexpected gift caregiving can be for a child who longs to understand the one who shaped so much of his own understanding of life and relationships.
In these pages, John Thorndike gives up the comforts of his normal life in Ohio to care for his father in the last year of his battle against Alzheimer’s. John takes this time to examine himself in the light of the two people who shaped him most—his proper, emotionally absent New England father and his passionate, dissatisfied mother. “No wonder I study my parents,” he says. “Within the compass of their lives, everything is foretold.”
More than anything, the author wants a peek at his father’s heart, but finds it impossible to reach through the shining armor that encases him. In the end, though, he finds that it’s not his father’s armor that shines, but his character. And in the end, the year of loneliness and frustration yields the sweetest of fruit: a softer, mended heart.
John Thorndike brings out the True by exposing the Fraud, and it’s contagious. I feel wholly exposed after reading this book, yet more able to forgive myself, to love Dad—imperfections and all, and to accept the inherently flawed but courageous effort we all make in loving those closest to us.
True, this book is about the beastliness of Alzheimer’s, but it should be read by anyone who hungers to know a parent and to find themselves healed in the acceptance of an imperfect knowledge.
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.
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.
In continuation of Alzheimer’s and Glucose Metabolism: The Niacinamide Experiment Part 1
This post is simply me mulling over things I’ve read in light of Mom’s dementia and my own experience with stress and mental short-circuiting, with the conclusion that in some cases of Alzheimer’s, intestinal flora could be greatly to blame. My conclusion also points to the possible way niacinamide could function in correcting one of the malfunctions in the gut-brain axis.
The Gut-Brain Axis
In-depth studies of human intestinal microbes are just now coming into maturity. The Human Microbiome Project is fueled by the increasing belief that the population of bacteria and yeasts that inhabit the human digestive tract is greatly responsible for how the body and mind develop and how they continue to function or malfunction as we tinker with the balance of flora in our gut:
Visionaries are hoping for cures for some forms of obesity and anorexia along with various forms of cancer, asthma, multiple sclerosis, Alzheimer’s, lupus, and most of the major psychiatric diseases. In the future, Blaser [of the infectious-disease research lab at New York University] says, pediatricians could help prevent these diseases by infecting babies with a starter kit of friendly bacteria. “Bottom line, humans and our fellow animals have been colonized by microbes for a very long time, going back a billion years. The microbes that we carry have been selected because they are helpful to us. They participate in human physiology. They are a compartment of the body, like the liver or the heart.” (1)
When the BP oil spill happened in the Gulf of Mexico, we were all
How much time is enough time? We know we are mortals and we know life is but a breath. In light of eternity, we calculate that 100 years passes as quickly as twenty. Yet, given anything less than 100, and we say we’ve been “cut off.”
My big, strapping brother-in-law lays in the hospital right now, fighting for each new minute after a two-year battle with brain cancer. He is tired, and he is ready to rest. We would prefer the doctors find a cure and make him bounce back, but we want to let him go.
Throughout this whole battle, Ken’s mind worked around his brain to bring humor and gratitude to his situation. He firmly believes God’s purposes can be worked through the worst tragedies, and it is amazing to hear how his concerns were always for the eternal perspective he could bring to the waiting room, the surgery room, the recovery room.
Ken’s life may be cut short in our view, but it has been a life well-lived, and that’s more than a lot folks can say. Socrates said that an unexamined life is not worth living; an anonymous person added that an unlived life is not worth examining. I can vouch for Ken that he’s had a life worth examining.
April 26, a.m.: Ken had a brain hemorrage last night and is on life support. Awaiting a family gathering to let him go.
April 26, 7 p.m. Goodbye Kenny. From someone who was present at his bedside: ” just wanted to write and let you know that Ken’s passing was beautiful in the midst of family and hymns and Scripture. The more that Daniel read and Ruth recited the easier his respirations…and soon he just passed on.”
We already miss your booming laugh, your exhuberant living, and your unwavering faith. Save us a place at the banquet table, and we’ll see you in the morning.
Rose Lamatt recently sent me her book Just a Word: Friends Encounter Alzheimer’s—the true account of her best friend’s rapid decline after being diagnosed with Alzheimer’s, and of the author’s life as a caregiver. After reading (or should I say “crying”) my way through this book, I decided I had to recommend it to all my readers as well.
I read and liked Still Alice, but it doesn’t hold a candle to Just a Word when it comes to describing the wretchedness of Alzheimer’s and of caregiving and of life in a nursing home after home-based caregiving is no longer an option. Just a Word may not be as polished a work as Still Alice (my editor’s eyes kept making corrections until the story sucked me in), but this book will give you the real thing: Alzheimer’s with poop and bruises and the constant anguish of those trying to love and care for its victims (unlike the sanitized version in Still Alice).
In all my reading on Alzheimer’s, I have not found anything so powerful as this book to stir a desire to rid this disease from the face of the earth!
A curious thing happened to me on my way to finding the cure for Alzheimer’s all on my own: I gained more respect for drug research companies, for neurologists, for folks who are obsessed with theories and practically live in their labs trying to prove their theories. More specifically, I gained greater respect for drug companies that fail colossally, then dust themselves off and try again.
After Eli Lilly revealed that their latest trials of the Alzheimer’s drug semagacestat resulted in greater dementia in their subjects, the response from the public was overwhelmingly angry. Adding to Lilly’s revelation, a recent report on Alzheimer’s drug company stocks by NeuroInvestment painted a bleak picture of the effectiveness of Alzheimer’s drug development across the board, giving the impression that research in the field is pretty much a crap shoot.
If you follow the very well-attended Alzheimer’s Reading Room online, you will see an interesting reaction to these reports. Richard Taylor (who suffers from Alzheimer’s) is one of many who feel crushed and devalued by the repeated failures of Alzheimer’s drug trials. Imagine trying to live with hope, then seeing over and over again that no matter how much money and time is spent on Alzheimer’s research, reality refuses to sustain any hope.
No matter the good intentions, Alzheimer’s research seems a recipe for failure.
This week I got a wee taste of what things might look like from the inside of these drug companies. For the past few years, I’ve been building a theory of Alzheimer’s of my own and keeping my eyes peeled for evidence that would support my suspicions. More recently, I decided to take a serious look at my hunch and see if a) I could gather legitimate scientific data that would shed light on my “theory,” and, b) see if this data had any kind of flow to it—if it had a “storyboard.”
My motives were twofold: I like to discover truths; and I very much want to avoid getting Alzheimer’s (like my mother). Curiosity and Fear fed my research. When I finally thought I had an airtight storyboard, excitement at the implications led to action: I shot off my “storyboard” to a leading researcher in the field.
Sobriety set in the next day. I took another look at what I’d written, then re-checked my sources and found not just one, but several really weak extrapolations in my thinking, and one particularly week substantiation of the evidence. I should have waited. I should have spent another eight weeks (I know, right?) researching before putting it out there and risking embarrassment.
But think about it: the possibility of being right on something so devastatingly urgent will make people take risks. And I’m not talking only about the drug companies; people signing up for drug trials are equally taking risks, knowing that the outcome is not certain at all. When you consider that it takes years and years and years to move inches in the direction of a safe and effective drug release (such as the six years it took to find how a fine-tuned alternate to semagacestat About a decade ago, Dr. Greengard and his postdocoral students made their first discovery on the path to finding the new protein. They got a hint that certain types of pharmaceuticals might block beta amyloid. So they did an extensive screen of pharmaceuticals that met their criteria and found that one of them, Gleevec, worked. It completely stopped beta amyloid production. That was exciting, until Dr. Greengard discovered that Gleevec was pumped out of the brain. Still, he found that if he infused Gleevec directly into the brains of mice with Alzheimer’s genes, beta amyloid went away. ‘We spent the next six years or so trying to figure out how Gleevec worked’ on gamma secretase, Dr. Greengard said. He knew, though, that he was on to something important.functioned in mice), the urgency for a cure leads all sides to gamble on a shortcut. And we’re not interested in companies that aim to keep the Alzheimer’s victim home “three months longer.” We want a cure.
Colossal goals risk colossal failures.
Can you just imagine what went through the minds and guts of Lilly’s leaders when they realized they’d failed? When they had to go out there and tell their shareholders of their failure?
“Well, there’s good news, and there’s bad news. The good news is that our drug was more effective than the placebo…”
Of course drug companies are going to be motivated by the excitement of financial gain. But they’re also going to be motivated by the fear of getting it wrong. They know what failure can do to their reputations and their ability to fund further research.
Today, Indystar.com published a very thoughtful article on Eli Lilly’s semagacestat trial failure. You won’t have to wonder what it was like behind the scenes at Eli Lilly—the article gives you a pretty well-rounded look. You also won’t have to wonder what someone’s response would be after being given the drug and having it backfire. From the wife of one participant:
“I just hope the researchers dig their heels in and keep trying to find a cure,” Dianne said. “That’s the important thing.”
I know there’s the whole layer of marketing that plants diseases into people’s conciousness so drug companies can make money off their fears. For this there is a solution: TiVo (and the advice of a good doctor).
But we shouldn’t assume that everyone researching Alzheimer’s has only one goal in mind—to get into our pockets with random, pointless medications. Any rational company would avoid this particular field: the risk of failure is pretty much guaranteed.
I hope we can learn from Eli Lilly and other Alzheimer’s research companies to risk failure; to work even harder; to join forces in finding a cure.
I don’t know how much I’ll be able to write about Parkinson’s here. If I write about Parkinson’s, it’ll be about how it’s affecting Dad. And if I tell you the things this disease makes Dad do, you won’t have a pretty picture of Dad. And that ain’t fair.
Here’s just a little, white example. A couple days ago Dad had to go to the bathroom. He asked what direction the bathroom was, and I pointed it out. He walked to the bathroom door, then asked me again where the bathroom was. I told him he was standing at the bathroom door. He said, “And now what?” I explained that he had to walk over to the toilet. He was standing four feet from the toilet and asked, “Where?” I put pressure on his back and gently led him to the toilet. He said, “And now?”
I had to help him through the whole process.
The concept “how to back up” seems to be the biggest obstacle his brain has to overcome. He can’t figure out how to back up to the toilet before sitting, or once he’s in a chair, how to back up from the edge. The same when he goes to bed.
My sister and I try “scoot back, Dad.” He scoots forward even though he’s already on the edge of whatever. We try changing the cue. “Put your back here” (while patting the back of the chair). Nothing. “Lift your bottom and move it back.” Nothing. Yesterday I tried switching languages. I said, “Put your butt in reverse” in Portuguese. He couldn’t do it, but he did double over laughing. And that’s a huge gift.
But these gifts are hard to come by. So I probably won’t write much about Dad and his Parkinson’s. I’d rather you see the adventurous man who loaded up his wife and eight kids in a van and drove from New York to Bolivia in 1966. This man taught us all kinds of good things about nature and God, and I’d rather not leave you with a highly unbalanced picture of who he is.
This weekend I picked up and devoured Dr. Oliver Sacks’ The Man Who Mistook His Wife for a Hat—a fascinating collection of clinical tales of neurological aberrations accompanied by philosophical and social observations regarding the people affected by these aberrations.
One of the first things that hit me as I read these tales was remorse over my inadequate caregiving of Dad in the past three years. I mean, the very first case in the book reminded me very much of Dad—his inability to tell the difference between his foot and his shoe; to interpret a picture or the furniture layout of any room; to distinguish between his body and a chair across the room. But whereas Dr. Sacks’ response to these aberrations was fascination, interest, and kindness, mine was a struggle against exasperation, irritability, and impatience.
Why couldn’t I marvel at (instead shake my head at) Dad’s description of his back pain as an imaginary horizontal tube about a foot in front of his abdomen? Why did I only nod in shame when doctors asked, “Is your father’s mentation… always… this… shot?” instead of pushing the observation beyond the superficial to the interesting? If I’d only read this book or studied neurology before taking care of Dad! I feel like a parent looking back on her inadequate parenting skills and feeling remorse over the damage it may have caused.
Dr. Sacks laments the tendency of neurology to focus on “deficits,” leaving the soul out of the doctor’s concern. This echoed my own feelings expressed in the post Regarding Disabilities and Questionnaires. We are so concerned in medicine and social services to define what’s wrong with the patient that we miss seeing the desperate starvation in front of our eyes: the individual’s need for affirmation—for having someone notice what’s right with them. Thus, the simplest of all medicines or disability benefits is left completely out of the picture in professional delineation of care: making use of what’s left of the damaged self to make positive human connections.
From his chapter, “The President’s Speech,” I learned one way to use what’s left of Mom’s mind to connect more effectively with her. Like the patients in the aphasiac ward, Mom too has lost all language while retaining extraordinary function in the area of intonation, body language, inflection, and facial expression. I’ve always sensed that she could “read our body language.” Dr. Sacks’ confirmation of this ability has made me more aware of how I use those meta-verbal cues in communicating with Mom. The smile I get in response is more valuable than any drug-induced ability to tell what date it is.
One of the most fascinating passages in Dr. Sack’s book tells of a man with Tourett’s who, when given Haldol in the smallest of doses, ceased to exhibit the excesses of Tourett’s and became disastrously dulled—both physically and mentally—causing him as much distress as had his Tourett’s dysfunction. It took three months of counseling and “preparation for healing” before the man was again willing to try a tiny dose of Haldol. As Dr. Sacks put it, “The effects of Haldol here were miraculous—but only became so when a miracle was allowed.” Scandalous! Was Dr. Sacks milking the placebo effect for all its worth? I’ve always wondered why doctors don’t deliberately incorporate the placebo effect into the real medication to multiply its effect. Now I know: some do (what’s wrong with spending three months preparing a patient for healing?).
It’s easy to see why Dr. Sacks is considered an exentric. His methods go beyond the cut and dry. They touch the soul. I think I like this.
AC6BTV7AQCKPToday I stopped at a light and to my right was a truck hauling what looked like a small, complete house all wrapped in white plastic. I wonder if it was one of these “Granny Pods” that are becoming a hit all over the country. I don’t know what people are bellyaching about. I think these are a great idea! It would be like playing house and you wouldn’t have to put up with any teenagers blaring music from their room as you would if you lived in the real house. Think I’ll order one with a Japanese soaking tub when I get around to needing one.
The other day my sister saw a note I had written on a sticky pad. It was a list of things I needed to do, one of them being to order a refill of Mom’s Seroquel. Except my sister read “Mom’s sequel” and thought I had written a book about Mom and was now working on a sequel. Not a far-fetched idea, as I’m always writing some book or other under the covers with a flashlight (so to speak).
Turns out I’m not writing a sequel about Mom.
Unless I’m writing it with my life.
In my last post I expressed fear that I might be following in my mother’s footsteps. Who wants to inherit Alzheimer’s? But the more I think about it, the more I would be proud to be called my mother’s sequel. I’m certain that anyone who knew Mom would give their right arm to be compared positively to her. She was the most selfless person I’ve ever known. The prayingest person I’ve ever known. The best cook, the best artist, the most humble…
I can remember a couple tizzy fits Mom threw right in the middle of menopause. But dang, other than that it’s hard to think of anything bad coming from Mom.
So I have to say that it is with great pride that I would love to be able to say “I am my mother’s sequel.”
I saw an old friend yesterday and we caught each other up on our families. I told him I recently lost my brother-in-law to brain cancer. He said he was about to lose his sister to the same. Then he shared how his sister—who has a month or two left to live and is tired as can be—blurted out a couple days ago that “There are just so many fun things left to do.” No self-pity; no giving up despite the shortness of time. Her mind is winning over her dying brain.
I am deeply humbled by this woman’s attitude. I want to think like her—to take what’s left in the glass and drink it! Yet here I am with probably years left to live, claiming to be getting the upper hand on this Alzheimer’s caregiving business, but feeling devoid of creative ideas for living, for laughing, for loving.
I need help making a list. I have to have a bunch of small stuff, because the big stuff like going to a play or out to dinner or hang gliding don’t work with both parents. I just want some ideas for bringing laughter into our home.
To start, here are some little things that make Mom laugh:
Dancing for her with a feather boa.
Episodes of “I Love Lucy.”
Singing raucous songs loudly.
Pretending to eat her up.
Laughing babies (like this youtube one):
Here are some things that make Dad laugh:
Pretending to eat him up.
Episodes of The Colbert Report.
Mom when she’s in a funny mood.
And here are some new things I’m going to try:
Wear a fake mustache to the dinner table.
Spray whipped cream on Dad’s nose.
Put a fake snake or tarantula in the bathroom before Dad goes in.
Find a DVD of Victor Borge (like this youtube):
I’d love to hear your ideas, and I’ll leave you with this fun project: make a muppet like the one in the introductory picture above to add some fun to your Alzheimer’s caregiving.
Wait, here’s another idea: make these funky glasses. They crack everybody up!
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