Getting Old With a Sense of Humor
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.
When dealing with Parkinson’s, sometimes one symptom can dictate behavior and end up causing a cascade of physical problems.
Symptom and consequence in point: hand tremors can lead to decreased liquid consumption (because the Parkinson’s patient is embarrassed to spill every time he drinks), and decreased liquid consumption can exacerbate constipation and possibly lead to impacted bowels in a Parkinson’s victim.
In dealing with Dad, we found that one solution to this cascading problem is a spill-proof sipping container. Dad used to spill everything on himself, the table, the floor. Now when his shaking is bad, we put all liquids in the spill-proof water bottle, and he is no longer embarrassed to drink.
The nice thing about the Camelbak water bottle is it’s sleek, sporty design which makes Dad feel like he fits in more with our physically active family.
So if you are having a hard time coming up with a Father’s Day gift for your Parkinson’s dad, this is my suggestion.
Here’s a short section of a CNN interview of Michael J Fox done by Sanjay Gupta—about living with Parkinson’s:
“Liberating” is what Michael calls his Parkinson’s! A chance to do something significant with his life! The turning point? The diagnosis. The act of giving a name to his symptoms allowed him to take back control of his life. Wow!
I cried throughout, of course, because Dad’s Parkinson’s was nothing liberating. But the reason it was such a cage, I think, is that it went undiagnosed until the very end. His shaking was written off as “familial tremors” (like his father and brothers who likewise had hand tremors without Parkinson’s) for twenty years, so all his other symptoms—an expressionless face, shuffling gait, forward tilt, drooling, even dementia—weren’t blamed on a disease: Dad had to take the blame himself.
I’m sorry, Daddy. How freeing it would have been to know your body was beyond your control. I think it would have helped your mind to gain control over your brain.
I hope this will convince anyone out there who suspects they may have Parkinson’s to get a thorough neurological examination. Take control of your disease and don’t let it eat up the rest of your life.
A couple days ago a friend of mine called almost in tears: “I did such-and-such, and I’ve never done such-and-such before. Do I have early-onset Alzheimer’s?”
I laughed. “The thing about Alzheimer’s,” I said, “is that they say not to confuse normal aging with Alzheimer’s, and then they say Alzheimer’s hits long before any recognizable symptoms become evident, so you have to look for signs early on.”
So I want to know: are we to be concerned about Alzheimer’s as soon as we lose our keys for the first time, or should we just laugh it off and look at the bright side of life all through the aging process?
Recently, a new mini-test was developed for the easy detection of Alzheimer’s. It’s called the AD8. This 8-question test is supposed to bring a diagnostic tool into the hands of primary care doctors so that Alzheimer’s can be detected earlier and therefore treated more effectively.
The problem is, there is no effective treatment for Alzheimer’s yet. So what, pray tell, are we doing finding new ways to diagnose this disease when there is no treatment and when the disease itself is not even clearly defined?
When we first brought Dad to live with us, we set him up with a primary care doctor who ran him through the standard Alzheimer’s test: remember these three things; tell me the date; where do you live; what floor are you on; draw a clock that says three thirty; etc. Dad got every single question wrong, and the doctor proclaimed, “You don’t have Alzheimer’s.”
I wanted to laugh. I think it was relief that a doctor would buck the system and refrain from offering perhaps a true but useless diagnosis given the lack of any effective treatment.
Later, we took Dad to a neurologist who got through three of the standard questions and suggested he try Aricept.
We gave Dad the five-week trial supply. It profited him nothing.
I’m not saying that we should refrain from diagnosing diseases. From his neurologist Dad also got a diagnosis of Parkinson’s, and as I’ve pointed out in an earlier post, this diagnosis (though it came late in the progression of the disease) was tremendously helpful in understanding Dad’s behavior and in relieving his sense of guilt. The medication he took for Parkinson’s did him no good either, but the diagnosis itself was helpful—perhaps as much for us, his caregivers, as for him.
But Alzheimer’s is a tricky beast. There are some well-known Alzheimer’s victims like Richard Taylor and Dottie (of the Alzheimer’s Reading Room fame) who are now under fire as possible Alzheimer’s mis-diagnoses. How can anyone have Alzheimer’s for six or ten years and show no decline, or even show improvement over time? It is not the subject’s truthfulness that is questioned but the accuracy of the initial diagnosis (heaven forbid we should think Alzheimer’s can be stayed by sheer willpower—of the sufferer and/or caregiver. That would mean we don’t really need expensive meds).
Is diagnosis of value when there are so many causes of dementia that could result in a false positive? And are the statistics of any value when they are repeatedly misquoted? We keep using the phrase “there are 5.3 million Americans with Alzheimer’s” when the correct statistic is “5.3 million Americans with Alzheimer’s and other dementias“.
One last bit of datum against the usefulness of Alzheimer’s diagnoses: in the U.S., whites tend to get diagnosed and treated more frequently than Hispanics, African Americans, and Asians. Whites seek out professional medical care, while Latinos, African Americans and Asians with Alzheimer’s tend to stay home and be cared for by family. Yet whites with Alzheimer’s die sooner than their non-white counterparts.
If earlier diagnosis is helpful, where is the evidence?
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.
Yesterday I asked my sister—who is visiting from abroad—what signs of Alzheimer’s she sees in herself. She rattled off some memory problems such as forgetting names of acquaintances or not being able to place someone’s face when out of context. Nothing particularly Alzheimersy, just decreased mental sharpness.
She then asked me if I was experiencing any unusual mental hyperabilities and went on to explain how she seems to have gained a fantastic ability to call up words she didn’t even know she knew.
Funny, I told her. I had this post saved as a draft when she asked me the question. The answer is yes, I’m experiencing this very same thing, and am curious to know if there is a name for it.
Is there such a thing as hyperphasia—the flip side of aphasia? The term hyperphasia exists, and it’s defined as an uncontrolled impulse to talk. But that’s not what I’m referring to. I’m referring to the mind’s sudden ability to pull up obscure words when common words won’t present themselves. Words so obscure that we had no idea we knew them.
I’m well acquainted with aphasia—the “tip of the tongue but it just won’t come” nature of language loss. I’m also familiar with another embarrassing result of gradual mental decline: the mind’s tendency to call up words similar in shape, but wholly different in meaning from the one the user wants. Try Googling “fairy schedule” next time you want to cross the Puget Sound to see what I mean.
But what is it called when the mind calls up unknown words that perfectly fit the context they were intended for? Does neurology study mental surfeits as well as deficits?
I told my sister that I’ve had arguments in my head over this new ability. One night, for example, I went to bed, and as I lay my head on the pillow a picture of our living room doorway came to mind, and with it the word “transom.” I immediately questioned myself:
“Transom? What’s that?”
“It’s the big piece that spans the top of the doorway, dummy.”
“How’d you know that?”
“I don’t know. I just know that it is.”
“You’re probably thinking of Hansom. And I think that’s a horse carriage, not a doorway.”
“No, I know hansom is a carriage. Transom is the door thingy.”
With that, I got out of bed and looked the word up in the dictionary: a horizontal crossbar in a window, over a door, or between a door and a window or fanlight above it
“OK, you were right.”
My sister laughed and said, yes, that’s exactly what goes through her brain.
So my question is, what is this newly acquired hyper-phasia called? And is it common to everyone as their minds begin to deteriorate?
I took Dad for a walk tonight. It wasn’t a long walk. Dad was tired and didn’t really want to go. But he acquiesced to my prompting, and we walked to the end of the 50-yard driveway.
The whole time we walked, I supported Dad’s right arm. And the whole time we walked, Dad’s arm shook violently. By the time we got back, my arm was buzzed and aching.
Then it occurred to me that if Dad’s energy gets passed onto me in this bad way, perhaps we could harvest the energy in a good way. I suggested to him that we design something like the soccer ball recently invented by those Harvard girls—you know, the ball that stores the energy of a game’s worth of kicking into a battery that can then be used to light up the Third World.
But hey, why not harvest the energy generated by Parkinson’s tremors? Maybe we could even wire the energy back into the brain for deep brain stimulation therapy.
There’s got to be an up side to the down side of this energy-depleting disease!
Here is something frustrating about clinical trials of Alzheimer’s drugs: the FDA requires that such trials show an almost immediate improvement in memory tests of participants in order for the drug to get approval, disregarding improvement in other symptoms, and consequently derailing a possible cure for this dreaded disease.
Here is why I think there is an inherent problem with this guideline:
If you go the the Alzheimer’s Association website and take the interactive tour of a brain with Alzheimer’s (a fantastic tool!), you will notice that there is a general pattern to the progression of Alzheimer’s and its accompanying symptoms. Specifically, looking at slide 13 you will see that the first part of the brain to be affected by Alzheimer’s is the inner core where the hippocampus resides—that part of the brain responsible for short-term memory. From there, damage spreads outwards to the cortex of the various lobes. As the second image in slide 13 shows, the Frontal Cortex is affected in mid stages of Alzheimer’s. This area is responsible for attention, social skills and intelligence (or wit). It is associated with “personality.”
Now, if an effective drug for Alzheimer’s were to be developed, you would expect to see the least damaged areas respond first, followed by the most heavily damaged areas.
Such were the preliminary results of the clinical trial of Dimebon. In reading the various anecdotal accounts of the Dimebon trial (see Bob DeMarco’s piece on the Alzheimer’s Reading Room), the results seemed to show precisely this initial response: Alzheimer’s sufferers reported increased alertness, social skills, and wit. Here is a sample quote from the various testimonials:
The major drug companies are focusing on memory. Are they after the right target? I’ll tell you this, in weeks 6 through 18 in the Dimebon clinical trial my mother was more engaged with me, more aware of her surroundings, more interesting, and more like her “old” self then she had been in six years.
The least damaged areas of the brain were affected in the 12-week trial! Then the trial was stopped because the inner (most damaged) area of the brain showed no marked improvement.
Would it not make sense to glean from the trial that a logical reverse course of the disease was set in motion and to continue it to see if the pattern held?
Pfizer et al, could you give us another 12 weeks when studying Alzheimer’s please?!
[Note: this analysis is mine alone. It may not be true that the least affected areas would show improvement first]
Definitely my pick for the most practical gift you can give yourself or a loved one suffering from Alzheimer’s.
What’s your pick?
Trying to follow Alzheimer’s research sometimes feels like walking through an Escher exhibit: the contradictions can border on the absurd.
Take the new findings on SIRT1 and its relation to Alzheimer’s. Research after research shows that SIRT1 apparently protects against Alzheimer’s:
25 July 2010. The sirtuin protein SIRT1 is emerging as an important player in learning and memory, and may have potential as a therapeutic target in Alzheimer disease. Fresh on the heels of a July 11 Nature paper that demonstrated a crucial role for SIRT1 in memory (see ARF related news story on Gao et al., 2010), two new papers add to the growing body of evidence that SIRT1 helps keep brains healthy. In a paper appearing July 21 in the Journal of Neuroscience, researchers led by Valter Longo at the University of Southern California, Los Angeles, show that a SIRT1 knockout mouse has numerous defects in learning and memory. This finding implies that SIRT1 could have a protective role in AD, and indeed, in a July 23 Cell paper, researchers led by Leonard Guarente at the Massachusetts Institute of Technology, Cambridge, report that overexpression of SIRT1 can decrease Aβ production and the number of amyloid plaques in a mouse model of AD.
You’d think, then, that more SIRT1 is better for Alzheimer’s and less is worse. But:
Michán and colleagues also examined a transgenic mouse that overexpressed SIRT1 16-fold in the brain. On this normal mouse background, the authors found that this massive SIRT1 overexpression conferred no improvements in learning or memory, and that synaptic function was unchanged except for a slight increase in neuronal excitability.
And though less is worse, vitamin B3 in the form of niacinamide has been shown to “cure” Alzheimer’s in mice by decreasing the expression of SIRT1: Nicotinamide Restores Cognition in Alzheimer’s Disease Transgenic Mice via a Mechanism Involving Sirtuin Inhibition and Selective Reduction of Thr231-PhosphotauWe evaluated the efficacy of nicotinamide, a competitive inhibitor of the sirtuins or class III NAD+-dependent HDACs in 3xTg-AD mice, and found that it restored cognitive deficits associated with pathology. Nicotinamide selectively reduces a specific phospho-species of tau (Thr231) that is associated with microtubule depolymerization, in a manner similar to inhibition of SirT1. Nicotinamide also dramatically increased acetylated -tubulin, a primary substrate of SirT2, and MAP2c, both of which are linked to increased microtubule stability. .
When asked about this contradiction, Dr. Greene, one of the researchers on this paper says,
You are correct – there are contradictions between the role of Sirt1 in AD. Regardless of these, nicotinamide has good effects in the preclinical models, and has been shown to now be effective for other neurodegenerative diseases as well. Sirt1 may be beneficial at some stages of the disease, and not others – we cannot [reconcile] these differences at this stage, but our research says that nicotinamide is highly effective in preclinical models and that inhibition of Sirt1 plays a role in these effects.
My mind wants to hyperventilate with the contradictions, but then I remember the story of the three blind men describing an elephant and realize the contradiction exists only because we do not yet fully understand.
And that’s what drives research onward.
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.
Because it’s Fall and crisp out and a good time to sit down to a good movie, I’m posting one of my favorite suggestions for a movie that deals with Alzheimer’s.
How To Kill Your Neighbor’s Dog is an unfortunate title for a great movie about self-centeredness and the cure for immaturity. The story centers around a playwright with writer’s block who must exit himself in order to find inspiration. Alzheimer’s isn’t the main theme of the movie, but it is present in the background, and the most lucidly-spoken scene in the movie is between the mother-in-law with Alzheimer’s and her brilliant, unhappy son-in-law.
Thought I’d pass it on.
Here’s a fascinating animation superimposed over a lecture by psychiatrist and writer Iain McGilchrist on the two hemispheres of the brain. You may have to watch it 15 times to really get it.
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.
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.
- alzheimer's antipsychotics art award body-language book-review cancer caregiving causes coping cues cure death dementia diagnosis diet Dimebon disabilities drugs early-onset ego end-stages fear gadgets gut heredity humor images language lifestyle metabolism movies music parkinson's phenotype prevention progression research seniors slideshow stigma stress symptoms validation violence
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- The Hope of Alzheimer's - Mary Kay Baum and sisters with early-onset speak out
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- The Myth of Alzheimer's - A doctor’s perspective on Alzheimer’s
- The Tangled Neuron - A Layperson Reports on Memory Loss, Alzheimer’s & Dementia
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- Best of the Web Nomination
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