Hi John, the level of aluminum in my brain was indirectly measured, as EDTA chelates metal in the rest of my body, unable to cross BBB, and when the body is cleaned, aluminum from the brain spreads in the rest of the body, for the diffusion phenomenon, and EDTA chelates again.
For this reason that my values ​​had a fluctuating trend.

Liposomal chelation, in my opinion is much less efficient. It's still very important as an aid to IV.

Have you watched the videos of the previous post, what do you think?

There is much interest at the moment in the role of alpha-synuclein in the pathogenesis of PD. I thought it would be interesting to go through my posts, most of which were based on epidemiological evidence, and see if there were any evidence of an involvement of alpha-synuclein.

Munishkina et al. [1] write:
"Certain metals lead to increased risk of Parkinson’s disease (PD) and the aggregation of α-synuclein is implicated in the PD pathology. Although α-synuclein fibrillation has been extensively studied in dilute solutions in vitro, the intracellular environment is highly crowded. We are showing here that certain metals cause a significant acceleration of α-synuclein fibrillation in the presence of high concentrations of various macromolecules mostly through decreasing the fibrillation lagtime. The faster fibrillation in crowded environments in the presence of heavy metals suggests a simple molecular basis for the observed elevated risk of PD due to exposure to metals."

Tag johnt:alpha-synuclein

References:

[1] "CONCERTED ACTION OF METALS AND MACROMOLECULAR CROWDING ON THE FIBRILLATION OF α-SYNUCLEIN"
Larissa A. Munishkina, Anthony L. Fink, and Vladimir N. Uversky
Protein Pept Lett. 2008
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2677187/

John