Think the odds are stacked against you? Here is a man with no arms and no legs, but armed with faith and humor, he has succeeded as an entrepreneur and motivational speaker. A must watch!
No Arms, No Legs, No Worries.
Despite scoliosis and Parkinson’s, man, 88, stays motivated with aerobics, cycling
John Mathews can't hold himself upright when standing. He walks hunched over and has a shuffling gait due to Parkinson's. But the physical ailments do not keep him from his love of fitness. Read article.
Agatha Christy Wrote Even With Alzheimer’s
A new study appears to prove that Agatha Christy wrote mysteries even after she began suffering from Alzheimer’s. Listen to this podcast.
Former teacher just graduated from university in Ghana–aged 99.
“Education has no end,” he told CNN. “As far as your brain can work alright, your eyes can see alright, and your ears can hear alright, if you go to school you can learn.” Read this article.
Alzheimer’s man to tackle around loch canoe trip
A 77-YEAR-old man diagnosed with Alzheimer’s disease intends to undertake a marathon canoe trip around Loch Ness. Read this article.
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 from the computer, slid my glasses down, and asked back, "Agenda for your physical therapy?"
"Agenda for life?" (I thought I’d go for the gusto).
"Yes." He smiled.
"Ah. Well. The agenda for life is to live more fully. You are going to get back to being more fully you. We are going to visit the local museum, go see the natural wonders around us, go to the big city to check out the OMSI exhibit."
He smiled more broadly. We're on the right track.
Shoot, this Parkinson's is going to be a nuisance, but we are going to live one shaky bite, one shuffling step, one tough lesson, one adventurous ride, one grateful day at a time.
The topic of fasting and Alzheimer’s has been on my mind lately because, well, Alzheimer’s is always on my mind and because recently a friend of mine got on this diet where you’re supposed to eat six small meals a day to trick your body into not storing fat.
Since intermittent fasting has been shown to slow body and brain aging, I wonder (the fat part aside) what this continual eating is doing to the brain.
From Psychology Today (2003):
It has been known for years that sharply restricting the calorie intake of laboratory animals increases their life span. But a new study by researchers from the National Institute on Aging found
Yesterday I finished reading Still Alice. I think the title is meant to be a loaded question. Can I, after losing all memory of others and self, still be considered to be myself? Am I still “me” if I don’t have a clue what that me is or was?
The fictional book answers the question affirmatively.
I found myself examining my perceptions of Mom–who obviously no longer knows herself–and thinking the conclusion was absolutely true. I still recognize Mom in this shell of a person. She still has the same mannerisms, exudes the same kind affection, displays the same funny reactions. She’s still Mom down to the core.
But not so much with Dad–a victim of Parkinson’s. It seems I recognize him less and less. But then, I suppose I’m holding a higher standard of “self” to Dad, giving that I’m assuming he’s more “there” than mom. If I were to strip him down to mannerisms alone, I would probably find him to be his old self too. It’s a tricky question.
At the very end of the novel, Alice has a moment of lucidy and says, “I miss myself.”
That statement struck me to the core. You know why? Because I miss being me too! There is this incredible longing inside me to be “more” or “better” or “fuller” or something. I fall way short of the me I want to be, and I long for (or miss) that. Yet I still want to be treated as though I were fully “me” even though I don’t meet my own standard for myself.
Why not, then, treat the Alzheimer’s victim as though they were fully themselves, regardless of how short they fall from the perfect version of that self?
Ultimately, our longing is for acceptance, love, safety. Let’s just make a pact to offer it unconditionally to each other regardless of where we are on this journey toward the perfect self.
Alzheimer’s and the Ego: the Power of No
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!
So I re-listened to the Fresh Air segment today, then did some quick digging through articles I’ve seen online on the brain, stirred it all around, let it simmer some more, and here is the reduction I got.
Maybe our addiction to the pursuit of happiness is contributing to brain aging. It’s not an umbrella cause, of course. You would never have been able to say that Mom led a hedonistic lifestyle. And Ronald Reagan pursued a lot more things than happiness. But still… The connection between what Dr. Linden was saying and what I’ve read makes me suspicious.
In David Linden’s Compass of Pleasure, he talks about the pleasure area of the brain as being that part that–in response to certain activities or substances–produces dopamine. Dopamine is the “feel good” neurotransmitter in the brain. It is activated when we engage in certain activities or thought processes, but it is also activated when we injest/inject food, alcohol, narcotics.
Some things that produce dopamine are completely healthy. Like a good run, the enjoyment of friends, reading a stimulating book.
Some things are borderline good. Like food. Everybody needs it. The pleasure of good food produces dopamine. But when pleasure is sought after for pleasure’s sake, “the brain’s dopaminergic circuitry gets blunted. In all cases of producing pleasure in the brain, it takes increasing levels [of a thing] to produce the same level of pleasure” (quoting Dr. L). So with food, you eventually get overweightness if the pleasure of food is pursued beyond the body’s need for it. Obesity is contributing to an epidemic of Diabetes, which is strongly linked to brain aging. By indirect means, then, the pursuit of a happy palate can lead to brain aging.
Then there are things that produce dopamine (or cause its production) that are not healthy. Like alcohol, nicotine, cocaine. This falls in with the acetaldehyde hypothesis I wrote about in Does Alzheimer’s Take Guts. Alcohol, cocaine, and especially cigarette smoke have–at some point in their metabolic breakdown–the toxic aldehyde acetaldehyde. Very destructive to the brain. Dopamine is produced as the end-process of breaking down harmful aldehydes into harmless acids. It’s the brain’s “Yahoo!” after saving the day from the bad guys. That “Yahoo!” may be a good thing, but again, in order to get it a second, third, and nth time, you have to increase the attack on the body. [Interestingly, Disulfiram's use to treat alcohol and cocaine addiction works by inhibiting ALDH2 (aldehyde dehydrogenase) which is the enzyme that metabolizes acetaldehyde. It lets the toxin do its full work rather than disabling it by metabolizing it into a harmless acid. So the brain does not get its "yahoo!" And if you get no yahoo, you don't repeat the action.]
The problem with focusing on happiness above all else is that we may end up using the short-cut and more harmful methods of getting that dopamine high.
Dr. Linden’s solution? “Try to take your pleasures broadly: exercise, meditate, learn, have moderate consumption of alcohol, moderate consumption of food.”
I would add: pursue friendships, do charitable work, tend a garden, read a good book (get more ideas at Changing Aging).
As Captain Kirk once said, “There are a million things you can have and a million things you can’t have. Choose the million you can.”
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.
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.
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.
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.
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.”
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.
A Compromised Gut and Aging
Suppose we throw out the acetaldehyde-in-the-blood-and-brain hypothesis. Even if the liver can keep up with the load, the process of breaking down acetaldehyde into a harmless acetate itself will upset the NADH/NAD balance.
NAD (nicotinamide adenoid dinucleotide) is the most important co-enzyme in the body. Aldehyde dehydrogenase depends on it to break down toxic aldehydes. SIRT1 depends on it to keep cells from committing suicide. It is the key to glucose metabolism. Etc.
A shortage of NAD is a normal part of aging:
Once pancreatic β cells and neurons start having functional problems due to inadequate NAD biosynthesis, other peripheral tissues/organs would also be affected through insulin secretion and central metabolic regulation so that the metabolic robustness would gradually deteriorate over age at a systemic level. This cascade of robustness breakdown triggered by a decrease in
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.
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.
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.
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