Prompted by a new Blaylock paper
and discussion, I browsed the PD glutamate literature and
found Van Laar et al reference describing NAC, parkin, and
Read Van Laar 2015 at: "NAC facilitates Parkin translocation and
mitophagy in neurons following excitotoxic insult – a possible
unexpected role for oxidative stress".
Also read at: "Glutamate exposure causes mitochondrial
depolarization and delayed loss of ATP".
Glutamate excitotoxicity in neurons triggers mitochondrial and
endoplasmic reticulum accumulation of Parkin, and, in the presence
of N-acetyl cysteine, mitophagy.
Van Laar et al 2015,
An update on the potential role of excitotoxicity in the
pathogenesis of Parkinson's disease.
Mutant LRRK2 enhances glutamatergic synapse activity and evokes
excitotoxic dendrite degeneration.
Neuroprotective and symptomatic effects of targeting group III mGlu
receptors in neurodegenerative disease.