Lewy bodies are just rubbish dumps

[wriga]

Extraordinary findings from a research group at Univ Basel. They expected to find alpha synuclein and just found fragments of cells and mitochondria.

unibas.ch/en/News-Events/Ne...

Fragments of mitochondria seem to be everywhere. Could it be that Parkinson's disease is due to excess damage and death of mitochondria. Vitamin B1 is said to revive mitochondria and certainly helps some PD patients, including me. Is this the first link between the two ?

[aspergerian13]

The finding seems to be an important advance.

[Gioc]

Now we will unleash hell, but as the Hubble telescope has unveiled us habitable planets, the electron microscope allows us to see the smallest organelle of the cell. As I have sometimes written the ability to observe not only depends on the instrument, but also on the personal integrity that is “to see something and not deny having seen it because we do not like it”.

It is a requirement for a good researcher.

It's not easy! Try it to believe!

Thank you Wriga for share.

[park_bear]

Good find.

Lest there be any misunderstanding, these researchers did find alpha-synuclein in these Lewy bodies in addition to the other debris.

[wriga]

I agree Park, but alpha synuclein is only part of the story. It's time to sort through the debris to find out which bit is the origin of the problem.

[ElliotGreen in reply to wriga]

From the scientific article:

“The precise form and location of αSyn within the LB and LN here observed by CLEM is not known. Since all Lewy pathology studied here were identified by their high content of αSyn, but primarily contained membranous material, αSyn must be present in these LB and LN in an alternate form besides filamentous; αSyn has been shown to be structurally polymorphic. One possible interpretation is that αSyn may be acting as membrane tether, bridging different mitochondrial membrane patches and leading to excessive adhesion between mitochondrial membranes, which could have led to mitochondrial damage, membrane disruption and formation of Lewy pathology—consisting of fragmented organellar membranes, each excessively decorated with αSyn. Alternatively, αSyn might have disrupted the membrane integrity, leading to fragmented organelles, which subsequently clustered into LB. Either way, our data indicate that αSyn may modulate the compartmentalization and function of membranes and organelles in LB-affected cells, prompting a new hypothesis about the role of αSyn in the formation of Lewy pathology in PD.”

[Gioc]

Stahlberg. “The big question for us now is: How does alpha-synuclein contribute to the formation of Lewy bodies, if not present in form of fibrils?”

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“Our finding indicates that in order to uncover the causes of a disease one needs to be more strongly guided by the exploration of the pathology in humans,” explains Stahlberg

end of research with mice?

I hope

[jeffreyn]

Simon wrote about this in a December 2017 SoPD blog post, when the research report was posted on the preprint website BioRxiv. It has taken a while to get published.

scienceofparkinsons.com/201...

[Gioc in reply to jeffreyn]

Exactly Jeffreyn, thanks for remembering it.

"Houston we have a problem": a problem of the disclosure of research / discovery, I.e., if the research is not functional to the marketing of some product to sell, it remains a little blurred by other things. As I said, it's not enough to have a powerful electronic microscope to see. Some will say that it is normal, but not me that I have the PD and I don't have all the time to wait for these things to run their course for profit reasons. I think that today we have the tools and the knowledge to solve neurodegenerative diseases, let's get to do!

[aspergerian13]

Speculation: Perhaps one role of intracellular alpha-synuclein is to corral excessive debris. Hence, Lewy bodies...