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So, the music itself was great. Plus, Greg was a gem of an entertainer, weaving funny little stories throughout his performance, making us laugh and shout out responses. Very audience-attentive.
Which brings me to the point of this post.
See, when Greg first came out on the stage, he sat in front of a rickety old pump organ that was set up next to his keyboard (just two of about sixty eight instruments he played that night). And he told us the story of how he went out to buy a computer that day and ended up buying this antique organ instead. A 1911 organ to be precise.
Now, the whole time he was relating his organ-acquisition saga, I was thinking of Mom, because this was the exact kind of organ that Mom played in church down in Brazil for many years. And I was picturing Sunday afternoons when Mom would fold up the organ (or have one of us kids do it), hoist it into the van and drive it to one of the favelas around town for a Bible club. I pictured snotty little kids running to the van, touching the organ as it was set up, and singing their lungs out at the sound of Mom’s squeaky playing.
At the end of his story, Greg paused, looked at the organ, and said, “I’ll have to name her.”
Well. It didn’t take two seconds for me to think of the perfect name for that organ. So I shouted out “Ruth!”
And it didn’t take Greg two seconds to feel it in his bones that the name fit. He chuckled, muttered something about my timid voice (I thought I’d shouted), and agreed that the organ should be named Ruth.
It made my day. Made my niece’s day, cuz now her Greg Laswell has an organ named after her grandmother (hmm. Is there any good way to reword that sentence?).
But this story means even more to me for the irony in it. You see, Greg sings a lot about trying to forget. Trying to forget a love. Trying to forget the pain of a lost love. And here he is now, lugging around a little pump organ whose namesake–Ruth–wants more than anything else in the world to remember. Too weird. One is cursed by memory, the other by the loss of it.
Anyway. I have to thank Greg for a fun night that will only grow in significance as I retell this story.
And you have to keep an eye out for Greg. In case, you know, he turns out to be somebody. Like Ruth.
All my life I considered myself an introvert, a private person, ungifted in the art of validating people.
In my early forties (a couple minutes ago), I bought a small restaurant, and all this changed. I grew by leaps and bounds in my fascination with people of all stripes and in my ability to dig beneath the surface and find the gold within. I grew in my ability to remember names, know faces, discover connections, and find new ways to validate people. I got high on it—on my ability to validate. It validated me in return.
Then one day this abruptly ended. I crashed. I had been working seven-day weeks for two and a half years, and my body and mind couldn’t take it anymore. The first scary sign of stress was when some of the music I played every day at the cafe lost its familiarity. I was evidently unable to learn new music. Then it was faces. New ones wouldn’t stick, and old but infrequent ones were a struggle to recall. I was filled with doubt when in conversation: what had we talked about the previous time? Did they just come from Europe, or were they going to Europe? I couldn’t remember.
Stress fried my brain, and my validation skills went with it. Nothing, but nothing hurt as much as having a newly-made friend appear and me not know who they were for ten or twenty seconds. The eager look on their face faded instantly, and nothing could bring it back. No amount of remembering in a few seconds would make up for my initial inability to validate them. I died a little bit every time it happened.
I wanted to resign from life. Retreat. Embrace my pre-cafe, introverted self. I wanted to be given a chance to explain (there is no such thing). I cried, prayed angrily, tried to bargain with God.
How do you love people when the principal organ of love—the brain—is shot?
I realized eventually that I was mourning my ego, not my lost ability to validate people—because I hadn’t lost the ability. I’d only lost the ability to do so in a way that would make me look good. There were and are plenty of opportunities to extend kindness and touch people’s souls even if we can’t immediately recall a face. It just takes an awful lot of something to give up the craving for reciprocity.This also showed me that validating was not my natural gift. To meet someone for whom it is, you must meet Jan Petersen. This afternoon I watched the video Jan’s Story: Love and Early-Onset Alzheimer’s again and re-discovered a true hero. Even with severe dementia, Jan knows how to seize each day and touch each person she meets. Jan’s is both a heart-wrenching and heart-warming story. Many people go through life mentally intact yet unable to see the goodness that surrounds them. Then you meet someone like Jan whose indomitable spirit sheds significance on everything and everyone she sees—regardless of her inability to name things.
The validation breakdown begins with us who think Jan’s story is nothing but a tragedy. But I tell you, if I could pick one trait to take with me on the dark road into oblivion, I’d pick Jan’s ability to validate without requirement; to love without strings attached; to milk each moment and each encounter.
That is the validation breakthrough!
Here are four more of my current heros—people with early onset Alzheimer’s who put themselves in the crosshairs of the stigma-tazers so they can help the rest of us see a little bit of the road ahead:
If you click on the picture at left, you'll hear the loveliest little story about a nursing home in Germany that decided to install a fake bus stop in front of their facility for patients to go to and "de-stress." Folks would go out to the bus stop thinking they'd get on a bus and go home. But after a few minutes of waiting, they'd forget why they were there and go back inside, no longer agitated and afraid.
So, if lying achieves a good end, is it OK?
Looking at it another way, is the aim of interaction to be correct or to be kind?
In the bus stop story, think about what it is the patient really wants when he waits for the bus. He wants home and family. But why? He wants these things because they mean acceptance and love.
So if the bus stop allows a patient to calm down enough for a staff member to have a soothing, friendly visit with them, is it not giving them what they were after in the first place? And is this not Truth?
This is the same rationale for communicating with Alzheimer's patients even when they are home with family. The point isn’t to constantly correct your loved one ("no, it’s not morning, it’s evening;" or, "no, my name isn’t Mary, it’s Marty"). We’re not here to elicit factual correctness from each other, but to honor each other as full-fledged beings created in the image of God—regardless to what extent we are broken.
And, no, I'm not a post-modernist saying there are no facts, or that facts are what we want them to be.
Just saying, facts aren't the point. Love is.
e all know, even without reading research papers, that music has emotional benefit: it can excite and calm and induce a wonderfully cathartic weeping session. This applies whether you’re healthy or sick; whether you have Parkinson’s or autism or Alzheimer’s.
But studies have found that music can also be of cognitive benefit: it helps people remember things better.
What exactly does this mean, and what specifically does it mean for an Alzheimer’s patient? Does it mean that if you play the oldies station in the background all the time, your Mom will wake up one day and remember everything again?
Let’s look at the evidence:
First of all, "music" is a pretty general term. Are we talking about singing? Playing a guitar? Listening to Mozart? Listening to Bobby McFerrin’s improvisational jazz? Believe it or not, these are all different things.
According to a study reported by Time Magazine,("Music on the Brain")
Different networks of neurons are activated [in the brain], depending on whether a person is listening to music or playing an instrument, and whether or not the music involves lyrics.
In another study, quoted in Neuroscience for Kids,
researchers have recorded neuronal activity from the temporal lobe of patients undergoing brain surgery for epilepsy. During this study, awake patients heard either a song by Mozart, a folk song or the theme from "Miami Vice". These different kinds of music had different effects on the neurons in the temporal lobe.
Also, from Time'“Music on the Brain”
Experimental Audiology in Germany has shown that intensive practice of an instrument leads to discernible enlargement of parts of the cerebral cortex, the layer of gray matter most closely associated with higher brain function.
As you can see, different music affects different parts of the normal brain in different ways.
People are always studying the music-brain connection, trying to understand the mystery of it. There was a particular study done in 1993 that tried to see if music affected memory. The researchers used a song by Mozart for their experiment, and their results seemed to show that this composer’s music improved test-taking. This became widely known as The Mozart Effect, and people started playing Mozart to their unborn babies thinking it would give them a head start in learning.
Though later studies failed to duplicate the Mozart Effect (perhaps the only real effect is that Mozart helps relax the body right before a test), that original research sparked further research into music-as-memory-aid. A recent study, for example, found that Alzheimer’s patients can remember new information if it is sung to them much better than if it is spoken (as opposed to healthy people who can remember it equally well when sung as opposed to spoken).
We also know without reading studies that music helps trigger old memories. For example, when I hear the song "Dust in the Wind," I am immediately transported back to our family van as we drove across the country in 1977. I remember my oldest sister introducing this song to me, and how it resonated with the angst of my teenage years, etc. A whole cascade of memories brought on by a single song.
In a study reported by the Telegraph in 2009, researchers found that this recall effect is due to the fact that music is processed in the same area of the brain that forms vivid memories. They furthermore found that such memories appear to be immune to the ravages of Alzheimer’s. And this could lead to a unique kind of therapy:
Because memory for autobiographically important music seems to be spared in people with Alzheimer’s disease, …making a "soundtrack of someone’s life" before their mind is too damaged, and playing it back to them could help form a resistance to the disease.
Love the idea! Plus I have a variation on this idea from watching this next video of Bobby McFerrin (at a conference called "Notes and Neurons"), and from observing Mom as I play the piano. First, here’s Bobby:
What Bobby is doing here is getting the mind to go in a familiar direction (the pentatonic scale), then leaving an auditory blank and letting the mind fill it in. I mean, aside from jumping around, that's what he's doing. He’s giving the mind a puzzle to solve. He’s making the mind work. And working the mind is better than not working the mind if you want to keep it.
The next part of my idea came from playing the piano for Mom and watching her reaction. You should know Mom hasn’t spoken but a few words in a couple years, and she no longer sings intelligible tunes. You should also know that I don't play the piano. I used to when I was seven, but now my playing is reduced to guessing the notes with my right hand. I can play fast enough for the tune to be recognizable. Barely. Fortunately for Mom, the tune is always a hymn—something she is very familiar with. Unfortunately for Mom, I mangle the tune. And that's where the puzzle comes in.
See, when my finger's can't find the right note, Mom gets exasperated and sings it out loud to help me find the dang thing. I'm even wondering if this puzzle-solving exercise is a factor in Mom's recent awakening.
So here is my variation on the soundtrack idea. Try this exercise (for an Alzheimer’s patient) with the following video clip:
Play it once. It will probably be familiar to the listener already, but there are enough repetitions in this piece that parts of it will quickly become familiar if they aren’t already. Play the video again, but pause the video every so often. There are a ton of repeated theme snippets. Pause before a theme is repeated and see if the listener is prompted to supply the missing piece. If they do, you've got a good puzzle to use.
Then, if you do this with that "Life Playlist", you should be able to double the benefit in fighting that Alzheimer’s monster.
Music and Caregiving—Pandora to the Rescue
Alzheimer’s and Music: Stimulating the Brain into Action
Posit Science Blog, Your Brain on Jazz
American Music Conference, Music and the Brain
One thing Parkinson’s can’t take away from a man is all he has passed on in his lifetime. Here is Dad, rock-hounding Parkinson’s style. The fact that he can’t stand up on his own or kneel and claw through the dirt to get to the jasper or petrified wood doesn’t detract from the fact that he instilled the love of nature and science in his children. It’s in our blood now to visit all the national parks we can and to dig for fossils wherever there be beds.
He’s taught his children so many good things, and Parkinson’s can’t take that away from him.
The other night I watched the movie Limitless. I thought it was a typical heart-pounding thriller with a touch of fantasy—in this case about a guy who discovers a drug that turns him into a genius. I thought the plot was moving toward the inevitable crash he would suffer when his supply ran out (as happened to everyone else in the movie whose supply ran out).
Then came the twist at the very end that made me laugh out loud. OMG, what Pretty Woman was to prostitutes, Limitless is to drug addicts and the whole drug industry.
If you’re smart enough, it says, you can make the perfect brain drug; you can take the last dose of the perfect drug to a lab and figure out how to reverse engineer and reproduce it; and you can figure out how to tweak it downwards in a perfectly safe manner (all within very short time periods); then you can wean yourself from a phenomenally addictive drug; and finally, you can train your brain to retain all the benefits of said drug once you have weaned yourself off it.
HA HA HA HA HA.
I think the whole problem I have with the drug industry is that, except in this extreme pharmacofantasy, it is additive rather than subtractive. You add one drug to treat a condition, then you add another to deal with the side effects of the first drug, then you add an nth drug to deal with the side effects of the combination of all the previous drugs.
Why not start with subtraction?
What are we injesting that we should cut out? Sugar? Preservatives? Smoke? Alcohol? Pesticides?
How often/much are we eating that we should cut back? Are we inhibiting certain enzymes—such as the anti-aging SIRT1—that only activate during fasting hours?
Maybe less is more?
Let’s start by removing the offending substances first, because once you start adding, it’s not you who benefit. It’s the industry that initially did have your brain in mind but now needs you to need them more and more.
As an artist whose artistic mother also has Alzheimer’s, this movie hit home for me. It was like watching my own mother lose all her nouns, then her knowledge of interpreting nouns on a canvas, and finally her knowledge of self.
In this film, the mother’s sorrow and fear are mitigated by the son’s desire to hang out with her. I only hope his desire lasted beyond the making of the film. For the sake of all those with Alzheimer’s, I hope love lasts beyond the time the disease is an interesting artistic or scientific curiosity. I hope it lasts beyond the time a diseased person has anything at all to offer.
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.
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.
Deep In The Brain is a cerebral self-examination written by a philosophy professor who was riding the top of a success wave when he was diagnosed with Parkinson’s. Talk about the relationship between mind and brain! Here is one who, thanks to his training, steps outside himself to make an objective assessment of his behavior even as he battles the attachment he has to that self.
In this book, Helmut Dubiel analyses his response to the personal and social implications of his Parkinson’s disease. He does not blame or excuse. Rather, he tries to put his and other’s reactions in context of the overarching laws of social interaction.
There is pain in this book. There are lies and pity and anger and judgment. But mostly, there is acceptance of the facts of disease and an acknowledgement of man’s irrepressible will to live and to thrive.
Yesterday as I read this book to Dad, I noticed him fidgeting more than usual. I stopped and asked him what was the matter. He said, “It seems like you’re reading about me.” I explained that this was a philosophy professor writing about himself. Dad calmed back down and listened with interest. Dad doesn’t talk about his inner battles much, so this would logically be painful for him. But good. I think this was one of Professor Dubiel’s hopes–that through his honest self-examination, others would feel released from the need to hide from their disease and, in so doing, find relief.
I’ve often asked people, “Which would you prefer: to lose your body or to lose your mind?” Given that I live with one parent with Alzheimer’s and the other with Parkinson’s, this question has personal weight. In his book, Professor Dubiel clearly expresses his preference for holding onto the self despite the ostracism brought on by the physical distortions of Parkinson’s. Knowing you are being unfairly rejected is still preferable to knowing nothing at all. On the other side, in Still Alice the protagonist affirms this appreciation for the self when–in a lucid moment–she acknowledges “I didn’t meant to get this way. I miss myself.” The mind is a far greater gift than the body.
Of course, in the end, Parkinson’s takes the mind as well.
My take-away? Pray for a cure for both diseases; forgive my and others’ shortcomings; enjoy today.
More on the brain’s default network:
The default network in the brain is considered a “second brain” because it turns on when the rest of the brain is at rest, and turns off when the rest of the brain is at work. Normally, that is. As people age, the default network is less and less capable of shutting down when the mind is concentrating on some difficult cognitive task as it would do in a younger adult’s brain. Since the default network uses 30% more resources than the rest of the brain, you can see how the resources available for cognitively challenging tasks decreases as we age.
In Alzheimer’s, you get the extreme case of this aging effect: the default network doesn’t shut down at all when it’s supposed to (same as in Schizophrenia–which is probably why they use antipsychotic drugs meant for Schizophrenia in Alzheimer’s patients) until that part of the brain eventually dies.
The default network is not very developed in children. It gets more active as we grow into adulthood. That makes me wonder if language is the software that runs the default network. Think about it: the default network is the part of the brain that sorts, categorizes, and edits/deletes memories, and language is the software that sorts, categorizes, and edits/deletes meaning. With language also comes prejudice, and prejudice does not exist in the very young. Also, in Alzheimer’s the default network eventually atrophies, and language ceases (just further argument that the default network is inextricably tied to language).
All of which brings me to the point of this post. Last week there were articles all over the news saying that having more than one language guards you against the worst of Alzheimer’s. Mom spoke four languages and fell prey to Alzheimer’s in her sixties–with no family history of early Alzheimer’s. Dad spoke three
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 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.
This site has been nominated as a Best of the Web in “Best Senior Living Blogs by Individuals 2012” category. If you agree, you can vote for me here!
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.
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