OMF: New Metabolomics Study Begins (Davis, Naviaux)

[JaimeS]

Gene- and cell type-specific demethylation of histones is stimulated by oxidizing conditions of the CDR by the Jumonji histone demethylases, increasing expression of pro-inflammatory cytokines like TNFα (Kruidenier et al., 2012).

...now they're just making stuff up.

Pathological persistence of the CDR can occur after the inciting agent has gone. This can be the result of hormesis and metabolic memory, somatic epigenetic changes (Blumberg et al., 2013), or both. Purinergic signaling appears to play an important role in sustaining the multifaceted metabolic features of the CDR. This observation led to the successful correction of all 16 of 16 multi-system, autism-like features in a classic animal model of ASD using antipurinergic therapy (APT) (Naviaux et al., 2013).

Boldface mine in both cases, o' course.

An example of APT would be suramin, an antiparasitic still used in African Sleeping Sickness, or this drug. Suramin has some significantly creepy side-effects including a 50% chance of serious adrenal damage, which may require corticosteroid replacement therapy ; some of the other purine-blockers don't look half so scary, but that may just mean less research has been done on them.

-J

 

[JaimeS]

I can barely dream of something like that!

Piece will be on #MEAction tomorrow AM. This is the best news we've had in a long while.

Waiting on a quote from Naviaux now....