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Robust and accurate measurements of these underlying pathological accumulations will be a critical part of applying new interventions in PD, as well as other synucleinopathies

Seneff S, Davidson RM, Lauritzen A, Samsel A, Wainwright G (2015) A novel hypothesis for atherosclerosis as a cholesterol sulfate deficiency syndrome

Co-immunoprecipitation mass spectrometry and CRISPR KO in cells identified that mitochondrial m -AAA protease AFG3L2 is responsible for degrading SLC25A39 through the matrix loop 1

The activation process is complex and continues to be elucidated 9,14,15,16,17