T.-S. Elliott

[stepan13]

"We used correlative light and electron microscopy and other advanced light microscopy methods to take a closer look at the brain of deceased Parkinson's patients and discovered that the Lewy bodies consist mainly of membrane fragments from mitochondria and other organelles, but have in most cases no or only negligible quantities of protein fibrils. The discovery that alpha-synuclein did not present in the form of fibrils was unexpected for us and the entire research field." Prof. Henning Stahlberg, University of Basel

news-medical.net/news/20190...

"And the end of all our exploring

Will be to arrive where we started

And know the place for the first time"

T.-S. Elliott

[Icequeen10]

Is this possibly good news?

[John_morris71]

No doubt that the focus is now narrowed down on to the the gut-brain axis and the microbiome. May be the origin of the cure lies hidden in the microbiome.

[jeffreyn]

Also discussed recently here:

healthunlocked.com/parkinso...

[ElliotGreen]

Huh.

I love peering into the glass and seeing what there is to be seen.

Imagined blobs of alpha-synuclein are replaced by something else.

Nature

You are the real Michelangelo

Oh mystery and wonder!

[Tribselyov]

“The gods laugh in their sleeves...”

[ElliotGreen]

There is still plenty of alpha-synuclein here. In fact, they detected these Lewy Bodies by sensing their high alpha-synuclein content. We are not dealing with homogenous globs of alpha-synuclein, but it still likely to be instrumental.

From the article: “[A]ll 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.”

The authors suggest that the alpha-synuclein may be sticking to mitochondrial membranes and causing the mitochondria to malfunction and stick to one another. Or they may disrupt membranes and pull apart organelles:

"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"