parkinsons is partly an auto-immune problem - Cure Parkinson's
parkinsons is partly an auto-immune problem
all very interestung but where does it leave us impoverished ones and what are we meant to do with this information in our poor everyday lives?
I think where it "leaves us" depends on a number of things, one of them being the stage of PD each one of us is at.
I'm at an early stage of the disease (diagnosed June 2015). Articles like this give me hope that I might be able to benefit from the results of this research some time in the future.
A person in a later stage of the disease might benefit from being reminded that hundreds of research scientists are working on finding ways to improve the lives of current and future PwPs.
And of course, those of us with an academic interest will appreciate the article in it's own right.
PS: I think you're overdue for a big hug.
One more reason to try mannitol.
does not sound like anything you can just try, unless you have water on the brain.
I do not get your point. Maybe you could have a look here :
youtube.com/watch?v=Z0mEkpJ...
(the mannitol story as told by the researcher who found it)
I googled it, and it didn't sound positive, at all.
beneficiaries were trying an untested, for humans, drug. we'll see in time if it has noxious side effects.
Mannitol is known since the ancient times though, and commonly used as a sweetener, for example in chewing gums. It's FDA approved under the classification GRAS (generally regarded as safe).
You are right about it's long term effects with 5 to 20g a day. I guess it's up to each of us to take the risk.
The last paragraph in Sulzer et al 2017 seems to suggest (I infer)
that among PwPs, a large subgroup may have autoimmune reactivity
against alpha-synuclein, and a large subgroup of PwPs will not have
(yet?) developed that autoimmunity. The first sentence is most
relevant here.
"Approximately 40% of the participants with Parkinson’s disease in
our cohort exhibited immune responses to α -syn epitopes, and these
responses may reflect variations in disease progression or
environmental factors. The fraction of patients who display these
responses in classic autoimmune disorders such as type-1 diabetes,
rheumatoid arthritis and multiple sclerosis is often around 20–50%
(31,32). As with type-1 diabetes, which features epitopes that are
derived from both preproinsulin and additional proteins, it may be
that epitopes related to Parkinson’s disease are derived from α -syn
and additional proteins. In classic autoimmune disorders, the MHC
class II response may precede MHC class I (ref. 5), and we note that
exposing microglia to α -syn triggers MHC class I expression by
dopamine neurons (10). The Parkinson’s disease-associated proteins
parkin and PINK1 may regulate antigenic presentation of
mitochondrial peptides (33), and it is possible that an autoimmune
presentation of antigenic epitopes unites lysosomal and
mitochondrial mechanisms of Parkinson’s disease pathogenesis."
ncbi.nlm.nih.gov/pubmed/286...
In Viartis news, there was a post about research contradicting the finding that Parkinson's is partly an autoimmune process. Not being adept at scientific stuff, I can't make much of the abstract, maybe someone else, here's the link:
22nd June 2017 - New research
AUTOIMMUNITY AND PARKINSON'S DISEASE
Researchers have claimed that they have found evidence that autoimmunity has a role in causing Parkinson's Disease. They suggest that fragments of alpha-synuclein, which can accumulate in people with Parkinson's Disease, trigger an immune response that kills the cells that produce dopamine. However, their theory is fundamentally flawed. When there is insufficient formation of L-dopa, which is what occurs in Parkinson's Disease, iron accumulation and superoxide anion can be formed. Both of these increase the formation and aggregation of alpha-synuclein. So it is Parkinson's Disease, due to low L-dopa that ultimately causes alpha-synuclein formation, not alpha-synuclein that causes Parkinson's Disease. For more information go to the : nature.com/nature/journal/v...
I suppose that has to be tested out........someone on this site commented that they find plenty of dopamine in pders brain, post mortem, I suppose.
I think the neuronal is a system and it has it's protective engine, appopsis engine, communication system, defensive mechanisms, much like our other systems and simplicity is a rule of law..
I like the phrase "etiologically significant factor" because it suggests that other factors (co-factors) may also be etiologically significant in a specific PwP.
If you suspect autoimmunity, first of all according to some experts people should go gluten- and dairy-free because those products can promote autoimmune responses.
hard to do, though.
think they would synthysis missing enzymes. there is also foods that provide enzymes.
For anyone who liked the NeuroscienceNews article, but found the research paper(s) a bit heavy going, there is another article about the Sulzer et al. paper, on the AlzForum website.
It's a slightly longer article, which goes substantially beyond the Columbia University press release, and also includes a significant comment from a couple of independent academics:
I think it's important to note that not all pders develop this folding/protirn with evidence of immune system attack. we might be talking about variable ailments as well as variable states of health/age. I think it's significant that it occurs primarily in aged, if i'm not mistaken.
immune system among unhealthy/or aged does not work. they cannot work up a fever, are ill and don't know it, because they don't have usual bodily manifestations. fever/phlem/etc. inflammation might be indicative of immune system action?