Multiple "kinds" of Parkinson's

[NanCyclist]

From my experience, I think this is the way Parkinson's works.

medicalxpress.com/news/2017...

[999---666]

CANCER IS A BEAST THAT SPRINGS FROM METABOLIC DISORDER, ONE OF WHICH REQUIRES EXCESSIVE SUGAR AND OXYGENE.THAT APPARANTLY CAN BE STARVED, ACCORDING TO LATEST INFO..PD IS THE RESULT OF IMBALANCE OR STARVATION OF BRAIN CELLS..POSSIBLY INDITING ENZYMES....COULD BE ELECTRIC PROBLEM ALSO

[Hikoi]

Totally agree Nan

Interesting comment on the approach to future research.

Slightly different approach but this is an interesting perspective too. Swedish research article I think.

perspectivesinmedicine.cshl...

[Hidden]

me too

[Juliegrace]

Interesting. New approaches are good.

[Bazillion]

Thanks for that .My wife a retired nurse has been saying for a long time ,that with all the money that has been spent on research we should be a lot nearer to a cure. If research was better co ordinated and less duplicated I'm sure the outcomes would be more promising.

Having taken part in several research projects I feel some are more interested in statistics than outcomes ,and we all know how stats can be manipulated to suit the outcome.

How many times have we be asked to take part in a 'survey' where the way the questions are asked definitely bias the outcome.

[PDConscience]

('aspergerian' provided a link to the same news in his/her "precision medicine in PD" post a couple days ago. It''s not about "the way PD works", it's about how to better treat it.)

[Motal]

Anyone have a sense of whether PD drug trials are set up to take note if the drug is more effective on one subset than another?

I hate to think of how many trials may have been done on drugs and supplements that may have been effective on say, those with tremors ... but were deemed failures because they were not as effective on the wider group.

It'd seem that viewing the trial subjects simply as PWP , positive outcomes for a subset would get lost in the sauce....

[Hikoi in reply to Motal]

By subsets are you thinking tremor dominant, stiffness dominant Motai? If not I dont know of any agreed on categorisations of PD. This would certainly be helpful and explain how some can claim results from a particular approach which others get no benefit from.

[Motal in reply to Hikoi]

Yes, HIkoi, my mind was going to those two major types of movement disorder - tremor dominant and non-tremor dominant - if only because they seem so different. With one, there's an involuntary movement, with the other a lack of movement - fast and slow, if you will.

Maybe if more research focussed on ways to stop the progression of symptom-specific types of PD , it might help crack the code that's been elusive so far.

[aspergerian]

Categories of premotor symptoms may point towards one way to define subgroups in PD.

See Table 2 in:

The

impact of nonmotor symptoms on quality of life in patients with

Parkinson's disease in Taiwan.

Liu WM, Lin RJ, Yu RL, Tai CH, Lin CH, Wu RM.

Neuropsychiatr

Dis Treat. 2015 Nov 11;11:2865-73.

ncbi.nlm.nih.gov/pubmed/266...

Table 2

ncbi.nlm.nih.gov/pmc/articl...

* * * *

See also:

The

Concept of Prodromal Parkinson's Disease.

Mahlknecht P, Seppi K, Poewe W.

J

Parkinsons Dis. 2015;5(4):681-97.

ncbi.nlm.nih.gov/pmc/articl...

[aspergerian]

I should have written:

Categories of premotor and non-motor symptoms may point towards one way to define subgroups in PD.

[NanCyclist in reply to aspergerian]

This is just a shot in the dark, but focus has been placed on defining by symptoms thus far. What if the divisions/distinctions are at the molecular or cellular level? They could certainly be quantified more readily.

I'm thinking about my experience with the young plasma for example. Is it or has it reached a tipping point in my blood such that the evil trash is being discarded and healthy blood is taking its place? For many years my body threw out the trash and generated new appropriate cells. Then the trash piles got so big I tipped the wrong way and got PD. Why are the young cells working? Does it have something to do with the amount of exercise I do? The food I eat? Meditation? Yoga? What is the molecular stamp in my body that is responding to the young plasma? Ruminations....

[PDConscience in reply to NanCyclist]

And then, of course, there remains the possibility that that "stamp" in your body merely reads "PLACEBO EFFECT" as you're still well within that particular post-treatment window...

[NanCyclist in reply to PDConscience]

I asked a Stanford doctor about that and he said that the type of changes i'm reporting, i.e., no dystonia, are not in the realm of things that would be affected by placebo. I'm interested in following up on. that.

[aspergerian in reply to NanCyclist]

NanCyclist,

Your ruminations point in worthy directions. Here are some molecular tidbits.

A recently published study provides a "cartoon" of alpha synuclein's

role (1). On a molecular level, pathological angiogenesis seems

important in the etiology of PD (2). Questions abound: For instance, how

and why does PD-like angiogenesis occur? Only in some individuals? Why

the inter-individual variation in which brain locales are initially and

significantly affected?

The last question above seems to point towards PD subgroups defined by premotor and non-motor symptoms.

As we try to identify initial events in the development of an

individual's PD, perusing Zarow et al 2003 can be helpful. Loss of

dopamine neurons in the substantia nigra may be secondary to

noradrenergic neurons in the locus coeruleus and to cholinergic neurons

in the nucleus basalis (3).

1. PD: Chemists from Konstanz prove what happens when selective mutations occur to alpha-synuclein protein

[see illustration]

sciencedaily.com/releases/2...

2. Angiogenesis (eg, 9 studies):

Increased CSF biomarkers of angiogenesis in Parkinson disease.

ncbi.nlm.nih.gov/pubmed/265...

Microglia-blood vessel interactions: a double-edged sword in brain pathologies.

ncbi.nlm.nih.gov/pubmed/267...

Melatonin and Other Tryptophan Metabolites Produced by Yeasts: Implications in Cardiovascular and Neurodegenerative Diseases.

ncbi.nlm.nih.gov/pubmed/268...

The fine balance of chemokines during disease: trafficking, inflammation, and homeostasis.

ncbi.nlm.nih.gov/pubmed/236...

Minocycline: far beyond an antibiotic.

ncbi.nlm.nih.gov/pubmed/234...

c-Abl Inhibitors Enable Insights into the Pathophysiology and Neuroprotection in Parkinson's Disease.

ncbi.nlm.nih.gov/pubmed/278...

Nilotinib Effects in Parkinson's disease and Dementia with Lewy bodies.

ncbi.nlm.nih.gov/pubmed/274...

c-Abl phosphorylates α-synuclein and regulates its degradation:

implication for α-synuclein clearance and contribution to the

pathogenesis of Parkinson's disease.

ncbi.nlm.nih.gov/pubmed/244...

Tyrosine kinase inhibition facilitates autophagic SNCA/α-synuclein clearance.

ncbi.nlm.nih.gov/pubmed/237...

3. Neuronal loss is greater in the locus coeruleus than nucleus basalis

and substantia nigra in Alzheimer and Parkinson diseases.

Zarow C, Lyness SA, Mortimer JA, Chui HC.

Arch Neurol. 2003 Mar;60(3):337-41.

ncbi.nlm.nih.gov/pubmed/126...

open access at:

jamanetwork.com/journals/ja...