"In conclusion, this study has demonstrated that even in early-stage PD brain metabolic alterations are evident and involved in all brain lobar areas of the cerebral hemisphere contralateral to the dominant side of disability. This result indicates that PD affects not only brain local regions by dopaminergic denervation, but also the brain network within the hemisphere."
I'm beginning to think I will not meet my target of having my situation sorted out by the end of the summer.
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Bolt_Upright
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Lewy bodies are discovered all over the place in PD post mortem brain analysis. It likely explains the great diversity in symptoms. The condition isn't simply about dopamine and the substantia nigra. It also means you should be rather guarded about how much stock you put in "recovery" stories.
Yes. PD seems to be a tough nut. If you give me a day I bet I could find at least 3 people that have been cured of MS using HSCT. People with names and stories.
I've been truly saddened by my inability to find one person (with a name) who has recovered from PD.
All I've found is that 72 YO case study who had REMSBD and early PD who took 2 or 3 mg of melatonin for 6 months and his RBD and PD cleared up. They had brain scans and tracked him over 4 years as his brain scans improved. Don't know his name though. (it seems odd that every time an alien lands on earth the entire US government sends out troops and tanks to capture and study the alien but nobody locked this guy up in a lab to study).
There was also that one person who recovered using Qigong.
PD is misdiagnosed frequently (ie false positives). Some of those people are subsequently dx with something worse (I.e MSA). Of those that actually had some more benign condition, most of them realise that and move on, but some of them decide to write books about (and seek other publicity around) their "recovery". I believe these people are sinceree, just mistaken.
You'll note that around these parts neurologists are largely considered valueless relentless drug pushers that exist solely to separate us from our money....until someone wants to believe a recovery story, at which point the neurologists involved are infallible and have never made a mistake in dx. Despite misdx being common and there being a number of non degenerative conditions that can mimic PD.
The great news for you is that you may not develop PD before something else gets you, which sounds morbid, but is actually good.
The most extensive detailed scientific discussion ever proposed about misdiagnosis when it comes to PD, can be found in Dr Hadlock's book and it is free:
I notice you mentioned Qigong. I received a partial healing via Qigong and have been stable ever since. It is not for everybody - takes a lot of dedication. My story here: healthunlocked.com/cure-par...
Logically, the cause must be proportional to the effect you want to cause.
If I had the aim of slowing down the progression of PD, I would address the aging process of cells which is influenced by four macro factors:
1) Contact and intake of toxic substances, radiation, pollution.
2) chronic nutritional deficiencies at the cellular level.
3) Insufficient body exercise.
4) Spiritual stress,
Each of these points is a world unto itself, (also here on HU CP), but if properly resolved, they could in my opinion slow down the progression and be, taken together, a cause proportionate to the purpose.
The birth of a new organism, growth, aging and death are the way chosen by "Nature" to procure a future that otherwise, without the death of organisms, would be a little crowded for this small planet.
This cycle allows the evolution of life towards more efficient forms of life, but it can be slowed down. The Human race longevity potential is estimated to be much higher as it is actually.
So the mechanisms that lead to this aging are written in the cells themselves, no doubt in the case of the Pd there must have been an error, the study of genes will tell us.
in the meantime we try to straighten the "toy" (body) without breaking it completely with harmful substances and medicines as in the first point.
".....it is not known when during the natural history of PD the first intracerebral α-synuclein pathology appears and whether there is a “point of no return” beyond which the damage to the neural systems affected by synucleinopathy can no longer be protected or revived, even with the most effective therapies. As mentioned earlier, it is currently believed that α-synuclein pathology begins to develop during the PD prodrome,20 and by the time motor symptoms have appeared the aggregates are widespread in the brain."
I put several snippets of it for reference into my digital file, but its Conclusion section alone could shed some light:
Conclusion
"It is believed that self-aggregation and transmission of α-syn contribute to the gradual spreading of pathological degeneration in PD.
Misfolded aggregates escape from clearance and are released into the extracellular space via synapse, exosome, vesicle, cell death, or tunneling nanotubes.
Afterward, α-syn aggregates are internalized by the recipient cells and induce endogenous α-syn to misfold and assemble in some unclear manner.
All the studies mentioned in this review support the fact that misfolded α-syn have much in common with prions in their mode of action:
(i) α-syn and prions both mainly exist either without a defined structure or in an α-helix, however, they tend to misfold when the conformation is rich in β-sheets under certain circumstances.
(ii) Misfolded proteins lead to further accumulation of normal proteins and acts as template to change their conformation.
(iii) Misfolded proteins are capable of being taken in by and transferred from cell to cell. [To me, this is the sad part.]
However, there are still plenty of unanswered questions regarding the pathogenesis of α-syn:
(i) the specific molecular mechanisms of misfolding, release, uptake, and transmission of the aggregates;
(ii) whether the misfolded protein in a cell can induce protein misfolding in the neighboring cells directly;
(iii) the physicochemical and environmental factors that affect the pathological process;
(iv) whether the diversity of species and conformations has an impact on clinical manifestations; and
(v) whether PD has the same infectivity as prion diseases.
By asking these questions, we are witnessing the beginning of a new field of research in PD and other neurodegenerative disorders.
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