PET scans show many Alzheimer’s patients may not actually have the disease
washingtonpost.com
washingtonpost.com
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3823377/pdf/nih...
> Results: The mean odor detection distance of AD patients’ left nostril (5.1 cm), and not their right (17.4 cm), was significantly less (F(3,90) = 22.28, p < 0.0001) than the other groups. The mean, standard error, and 95% Confidence Interval of the L R nostril odor detection difference (cm) for AD was −12.4 ±0.5, (−15.0, −9.8); for MCI was −1.9 ±1.2, (−4.2,0.4); for OD was 4.8 ±1.0, (2.6,6.9); and for OC was 0.0 ±1.4 (−2.2,2.1).
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4167392/pdf/nih...
But we'll also have machines that measure out the dosages. And possibly a few controls. Plus we'll have to adjust for folks that have an exceptional sense of smell. And come to think about it, we'll need to make sure we have baseline sensitivity levels at different ages to base the test result on. We'll have to account for folks that have sensitive sense of smells, which could be a large problem for controls. Not only that, but we'll need to check for signs of a stroke and the many other things that can cause one to lose one's sense of smell.
On second thought, I'm much more likely to support the more expensive test and hope they invent a simple blood test as it seems to narrow things down further.
Yet, as long as the errors are overwhelming at the false positive side, it can be used to reduce the number of the more expensive test.
Drink enough, sleep enough, eat well, do some sports, meditate. If that doesn't help, good luck with going to the doctors.
Any clinically proven benefit of meditation though? Don't throw it together with sleep and exercising...
I see "may" for some things, and "uncertain" for others. Nothing on that page says that it's been "thoroughly proven to be beneficial".
(mindfulness being a form of meditation)
"This study is limited by the lack of a control group or active comparison clinical intervention that would provide a basis for making a stronger inference about how MBSR might modify the behavioral and neural bases of different types of emotion regulation."
So while MBSR may help some people, this tested one specific method and did not include a control group or test against any other treatment methods.
Now, I'm not suggesting that meditation - MBSR or other - can't be helpful for some people (possibly even the majority of people under certain conditions), but it certainly has not been studied enough to show clear benefits compared to other treatment methods.
Actually, if you read recent studies (go through Pubmed), you'll find that it should in fact be lumped with sleep and exercise.
>In 2013, researchers at Johns Hopkins identified 47 studies that qualify as well-designed and therefore reliable. Based on these studies, they concluded that there is moderate evidence that meditation reduces anxiety, depression, and pain, but there is no evidence that meditation is more effective than active treatment. [1]
You can throw PETs, CSF tests etc at it but I never really have a high level of confidence calling it.
Basically people lose memory and certain cognitive functions...but anything could really do it.
At the moment the hodgepodge way I fudge it is: if it is a clearly progressive syndrome year over year, with an amnestic memory syndrome (vs. poor attentional state/registration), with language/naming involvement, and evidence of visuospatial neglect/apraxias, I tell them it may "likely" be AD. Otherwise I can't say if it is AD vs. vascular dementia.
There is a paper looking at accuracy of how we call things vs. post-mortem, and it is about 50/50 eyeroll. Sad but this is the limitation of science vs. mother nature at this state in time.
At one point, the article says "A positive test for amyloid does not mean someone has Alzheimer’s... But a negative test definitively means a person does not have it". To me, there seems to be a hint of "these patients' condition does not fit the dictionary definition of Alzheimer's, so clearly it would be wrong to treat them as if they had it", yet the article seems to leave open the door to the possibility that it is the progression of Alzheimer's that is not fully understood. I hope an expert can chime in and set me straight.
The amyloid hypothesis (that the cause of Alzheimers is the buildup of beta amyloid plaques) seems pretty weak at this point. The drugs that remove or reduce amyloid buildup don't seem to stop the progression of the disease. The current best guess seems to be that the amyloid plaques are a symptom of whatever the underlying cause is. And the key takeaway is that we have NO IDEA what the actual cause is. We've got a bunch of guesses. One of them might even be right. Or possibly multiple, there are probably several diseases that cause the same symptoms.
So if we can detect the non-presence of amyloid plaques but detect symptoms that would be good as a way to distinguish between the different diseases. Of course there might be more than two variants...
[1] http://blogs.sciencemag.org/pipeline/archives/category/alzhe...
>"Of all the myriad way a protien can fold, it happens to find one that induces the same malformation when it interacts with another protein."
It doesn't really "just happen", amyloids consist of peptides folded into beta-sheets and aggregates of these seem to be the most thermodynamically stable structures it is possible for polypeptide chains (regardless of sequence) to form:
"From a wide range of in vitro experiments on peptides and proteins we now know that the formation of amyloid structures is not a rare phenomenon associated with a small number of diseases but rather that it reflects a well-defined structural form of the protein that is an alternative to the native state — a form that may in principle be adopted by many, if not all, polypeptide sequences
[...]
These observations, therefore, have led to the remarkable conclusion that, at the concentrations present in living systems, the native states may not always represent the absolute free energy minima of the corresponding polypeptide chains — the native form of a protein could in some cases simply be a metastable monomeric (or functionally oligomeric) state that is separated from its polymeric amyloid form by high kinetic barriers" http://www.ncbi.nlm.nih.gov/pubmed/24854788
A family member just had a stroke... the entire system is designed around maximizing billing. If someone is in a longer term situation and a Alzheimer's diagnosis makes a buck, you'll get that diagnosis.
Never mind the mental condition is probably a result of the institutional environment and drugs.
Our entire world is built that way, it isn't unique to medicine.
In that $3-5k cost of running a PET scan, I wonder how much of that is paying professional operators and physicians to interpret the results?
Could ML be applied to this problem to reduce the cost of a PET scan?
I want professional operators and physicians to look at my details.
What I don't want is dozens of layers of middlemen or ticket clippers (or healthcare driven by profit).
It doesn't outside of the US.
In fact, manufacturers are required to report such prices annually to the federal government, which bases Medicare payments on the average national price plus 6 percent. The limit for one liter of normal saline (a little more than a quart) went to $1.07 this year from 46 cents in 2010, an increase manufacturers linked to the cost of raw materials, fuel and transportation.
http://www.nytimes.com/2013/08/27/health/exploring-salines-s...
(which implies that manufacturers aren't the primary beneficiaries of the price that the hospitals charge)
"Hartmanns IV Solution AU$2.73 ex GST
Baxter 0.18% SODIUM CHLORIDE & 4% GLUCOSE IV SOLN 500ML AU$3.72 ex GST " https://www.medshop.com.au/consumables/intravenous-solutions...
The lack of quality health insurance means that a substantial number of people finance healthcare via bankruptcy. That's all priced in. As an insured person or private payer, you pay dramatically more as a result -- it's a hidden tax.
The high dollar cost may also be related to newer, more sensitive machines that don't require as much radiation exposure to the patient.
[1] https://www.betterhealth.vic.gov.au/health/conditionsandtrea...
I believe the way it works is that the injected source emits positrons as it decays (having swiped them from the vacuum), shortly thereafter, these annihilate with the electrons of your body, and the scanner looks for the signature pair of gamma rays thus created, using the relative time of arrival to determine their common origin in 3-space. That reduces the problem of scanning to arranging for the decaying source to accumulate in the place we wish to scan which apparently can be done.
That we scan ourselves by annihilating antimatter with our bodies in targeted ways just seems so awesome to me.
But an important distinction is whether medication is a choice, or is imposed by caregivers with legal authority, psychological influence, or whatever. I mean, I chose to take SSRIs for many years. And it made me crazy. Which I eventually realized.
But a ten year old kid who gets put on SSRIs inappropriately? They are screwed, and perhaps permanently.
I am eternally grateful my parents took me to a psychiatrist when they saw some aspect of my behavior wasn't normal and that it was affecting my quality of life, even if I was far too young to know or understand that. I think it was the humane thing to do, 100%.
People talk a lot about how terrible it is that 5 year olds are put on this shit, but extreme cases like mine are out there and they are legitimate. Sometimes things show up early because they're severe enough. It'd be fucked up if 10 year olds on SSRIs was the norm, but I have no doubt that there are rare cases where it'd almost be cruel /not/ to do it. Bipolar can absolutely be diagnosed in children. If you can diagnose it that early, why wouldn't you start treating it? Isn't that what you SHOULD do as a parent?
Aricept is an expensive drug and does about nothing. I dont even know why patients with AD are taking it.
http://www.alzforum.org/therapeutics/donepezil
> The effect size of donepezil's benefits is small and the drug does not modify the underlying pathophysiology of the disease
To understand what is going on, we have to see the problem that hit clinicians and families around 10-20 years ago. It seemed like an epidemic of confused elderly patients landing on wards without a specific diagnosis, very little ability to describe what is wrong with them, and causing disruption to other patients, either directly, or because they required a nurse to attend them continually.
Explaining to the family why their mother/father had gone from being someone who was independent at home to someone confused and unable to tend for themselves was difficult. Usually the blame would be attributed to infections (especially urinary tract infections, which are very difficult to diagnose in a confused patient), but doctors were reluctant to start using the term 'dementia' initially, particularly since there wasn't a good test for it.
In retrospect, what was happening was that we were seeing the success of treatment for cardiovascular disease. Many patients who would normally have died in their 50s and 60s of heart disease we now making it to their 70s, 80s and 90s, albeit with arteries that were still far from ideal.
Every organ in the body degrades with age. We tolerate and compensate for it up to a point. At the age of 20 our hearts can increase output from 5l/min to 20l/min, sometimes this is necessary to survive a particular bad infection. If your heart is unable to do this, we say it has decompensated. At the age of 60, even without a diagnosis of heart failure, this is not possible, but thankfully we are rarely in a position where 20L/min is necessary. The brain is no exception. An old brain with loss of volume can handle a daily routine in a familiar environment, but throw in a cold, or another infection, then make it worse by starting drugs and abruptly changing their environment, and we end up with an acute confusional state which can take weeks to resolve, if it ever does completely.
My suspicion is that most cases of dementia (and mild cognitive impairment) is due to a general decrease in function as we get elderly, exacerbated by vascular insufficiencies. Alzheimer's is a specific histological diagnosis - it doesn't give us a cause, it's more of a histological finding. Since we don't really have any good treatments for dementia caused by Alzheimer's or vascular causes, and we don't have a way of telling them apart, you could argue whether this histological finding matters..
Except that Alzheimer's is a term the public are familiar with, and will donate to.
NB I am not a neurologist nor a dementia expert. I've worked a lot in elderly care and have had to deal with patients and their families on many occasions. I have some amusing memories including overhearing a conversation between a confused patient on a ward who had picked up the ward phone at around 1AM - it was the bed manager calling to see if their were any beds, but the patient she was still at home so was quite confused at the question.
Heart is just one example - our kidneys get worse as we get older too (see figure 4 of this paper - it's a straight line pretty much [2]). In practice, it doesn't cause us problems in day to day life, but give it a really big insult (like sepsis) and it can decompensate. The difference with kidneys is that we can support kidney failure with dialysis or filtering (if their heart can support that), whereas with cardiac failure this is not so simple.
Brain failure is probably one of the worst forms of failure. Most causes have no cure, and they often require 24hr care.
[1] http://ajpregu.physiology.org/content/246/3/R331.short
[2] https://www.spandidos-publications.com/10.3892/mmr.2015.3292
Valscular dementia is also common and Dementia with Lewy bodies are also possible. Is it possible that many of these were misdiagnosed other dementia's?
"one of a variety of silver impregnation staining techniques, such as the modified Bielschowski or Gallyas technique, or the fluorochrome dye thioflavin S is typically employed to visualize neurofibrillary tangles
Because these techniques require either specialized equipment (the thioflavin S stain requires the use of a fluorescence microscope with specialized excitatory and barrier filters) or experienced histotechnologists (in the case of silver impregnation stains), most anatomic pathologists in general practice lack the capability to properly evaluate brain specimens submitted for the diagnosis of Alzheimer's disease. Such specimens are best referred to specialized neuropathology laboratories where the necessary experience and facilities are in place."
It's an old joke, but fitting for the title.