Over the last 60 years or so going all the way back into the 1960's, researchers and drug companies have examined and proposed multiple theories relating to PD and have spent $millions in doing so. Unfortunately, this research has led to very few true breakthroughs. Perhaps things will changes; perhaps they won't. Hopefully they will.
Here's a classic example: mercury is know to cause both low thyroid and PD, but statistics shows little difference in low thyroid between people with and without PD. The reason: it is estimated that at most only 6% of PD is caused by mercury. This also says anything that only affects PD caused by mercury will not show up if tested in the general PD population without considering sub-groups.
I hate to disagree with you and some of the PD blogs, but PD is PD if the datscan confirms sufficient neurodegeration in the brain's dopaminegeric neurons. Whether some blog or "pop science" publication wants to call it primary PD, secondary, tertiary, etc. it is PD...you have lost the "function" of a sufficient amount of your neurons, which are in limited supply in the brain to begin with.
"Manifestations" of PD may vary from person to person for a variety of reasons, but no evidence exists that it represents a specific "type" of PD that is different than another as we researchers in cancer consistently differentiate between lung, beast, etc. cancers because of its organ origination.
Can we make or should we make a distinction between "motor" and "cognitive" PD? Don't think so IMO because almost all long term PD patients have "lewy body" dementia in the autopsy studies on PD patients. We can then split hairs if you want by saying PD dementia is really LBD, or is it the other way around? Or is LBD really CBD and both simply PD in the final analysis?
Splitting hairs IMO leading back to square one...almost always.
..."how do you explain...?" I don't know if the use of the term "PD" when induced isn't prematurely defining it as PD, meaning the presumption that induced PD is really PD might be premature, meaning that is how to explain apparently successful trials in mice "induced" PD...apples assumed to be the same to oranges, but really maybe they are not the same. So how do you explain deciding in the first place that they are the same, what warrants such as assumption in the first place?
Like saying the brakes on a lorry are the same as an elevator because they both cause something to stop, without noting whether the two mechanisms really are the same or just apparently so on the surface, but not shown instead how they couldn't be completely different.
Some of the same symptoms and some (perhaps, or perhaps only via hypothesis) similar features as PD, yes, but that is not proving the same thing as PD in humans, any more than "phenotype" is the same thing as "genotype." The similarity might well be only superficial. Or they may be essentially similar, such as an internal combustion automobile and an electric vehicle, but really, also different in significant ways. Petrol is not going to work in a Tesla, though it will in a hybrid. Is that enough to call the two the same?
One needs a demonstrated mechanism in both subject (mouse) and eventual subject (human), and for that mechanism to be demonstrably similar if not identical or chemically equivalent. Is that true in these mouse induced cases and, I suppose, "natural" PD in mice?
sharoncrayn defines "PD is PD if the datscan confirms sufficient neurodegeration in the brain's dopaminegeric neurons." The mice fit this definition. Thus, if you say the disease of the mice is different, then you have to say there is more than one type of PD.
The evidence suggests that there is more than one mechanism. But I don't know what "type" means or what you mean by it. If that is a medical term, medical terms are not always specific or scientific, though many times they are, you might have to check with WHO. If type is a chemistry term (IUPAC), then it may or may not be the same thing.
I don't know the medical terms. What I'm trying to say is all the mechanisms may not have the same cure. Thus, research needs to attempt to consider all the mechanisms. This is difficult since we don't know all the mechanisms, but must look at symptoms, genetic markers, and other possibly related diseases for comparison.
In the case of restoring neurons, an overall solution such as stem cells may be possible. However, when it comes to stopping the progress of PD, one may need to address the causes, which can be many and all are not identified. Stopping one cause might be different than stopping another.
I totally agree, which is why I favor finding a "holistic" neurologist who specializes in PD and isn't tunnel minded. Difficult to find in some locations, but worth it if you can find one.
These novel PD subtypes are significantly influenced by disease duration and staging, which might suggest that they do not represent mutually exclusive disease pathways. This should be taken into account when attempting correlations with putative biomarkers of disease progression.
"These novel PD subtypes are significantly influenced by disease duration and staging, which might suggest that they do not represent mutually exclusive disease pathways. "
I agree since this concept is what I have said occurs, which leads to the mistaken belief that PD sub-types exist. They really don't .
Basically, replacing or fixing the dopamine producing neurons is likely a universal fix for PD. However, progression of PD depends on the cause and may need a fix determined by the cause.
"Basically, replacing or fixing the dopamine producing neurons is likely a universal fix for PD. "
How would you suggest doing so on a broad scale basis (given the numbers of PD cases in the US let alone in China). DBS and FUS are extremely limited surgical options with sometimes questionable outcomes.
Right now the most hopeful is using a person's own stem cells from fat or skin to replace the dopamine producing neurons, assuming they can finally get this perfected. Any method that replaced the dopamine neurons should be universal for PD. However, PD progression will likely start over again unless it is stopped.
Please provide a better way other than a brain autopsy. I would really like to learn about your research observations that led you to your conclusion. The accuracy of the Dat/Spec scan done correctly is pretty high.
--- Datscan is not entirely successful in diagnosing "early" PD, which is to be expected because nothing really is. Otherwise, it is the best we have because it is somewhat systematic (IMO) rather than influenced by the individual practioner's experience, etc.
My take is that if the scan shows a loss, you have a problem. Granted, reading the scan is not always systematic. Just like a pathologist examining a cancer biopsy.
My understanding is a normal DATscan would mean a significant number of dopamine producing neurons are responding symmetrically from left to right. In many cases PD starts on one side (left hand tremor expected to show less producing neurons on the right). By the time PD progresses to the other side, both sides may have low enough activity to show up on the DATscan. A good DATscan for a PD patient would seem to mean that both sides are degrading symmetrically, but with enough active neurons to make it difficult to detect degradation.
"A good DATscan for a PD patient would seem to mean that both sides are degrading symmetrically, but with enough active neurons to make it difficult to detect degradation."
#1) I personally don't think sufficient, validated research has been done on the accuracy of Datscans to draw too many specific conclusions, such s yours. The UK meta analysis was pretty weak. really weak.
"Four systematic reviews were found on the
accuracy of DaTSCAN. All four were limited
in terms of their search methods: all were
susceptible to publication bias, and one used
a single bibliographic database, raising the
probability that important studies might have
been missed."
#2) PD autopsy research suggests that PD patients lose up to 80% of the dopminergic neurons before being diagnosed with PD. If so, Datscans will generally be unable to detect anything unless sufficient neurons show up to plot them on a scale, not the other way around.
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