Significant breakthrough in search for Parkinson's biomarker

https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3762356/

Another study: https://pubmed.ncbi.nlm.nih.gov/26505466/

> Conclusions: Administration of parenteral high-dose thiamine was effective in reversing PD motor and nonmotor symptoms. The clinical improvement was stable over time in all the patients. From our clinical evidence, we hypothesize that a dysfunction of thiamine-dependent metabolic processes could cause selective neural damage in the centers typically affected by this disease and might be a fundamental molecular event provoking neurodegeneration. Thiamine could have both restorative and neuroprotective action in PD.

This experience report of halting Parkinson's: https://youtu.be/iuSOQOTyB9w

This actually seems pretty significant.

1) It gets us closer to understanding the pathology:

>> It also suggests that alpha-synuclein aggregation in spinal fluid is not a life-long trait but rather acquired as part of a disease biology process that ultimately gives rise to symptoms.

2) It gives us a higher resolution of detection.

>> αSyn-SAA can distinguish Parkinson’s from control volunteers with a stunningly robust sensitivity of 88 percent and specificity of 96 percent.

3) It shows different disease subtypes or mechanisms:

>> These results suggest that not all cases of clinical Parkinson’s symptoms are associated with the accumulation of alpha-synuclein aggregates as detected by this assay, and that LRRK2 variant carriers, in particular, may not show this pathology.

4) It gets us earlier signal:

>> This finding suggests that synuclein pathology could be detectable by this assay earlier than dopamine dysfunction is seen with DAT imaging, extending the window in which it may be possible to intervene with preventive therapies.

This is a valuable tool that will shed light on the entire disease pathology and guide further research and investigation into treatments.