Thanks, Lurking for adding the calcium channel blocker connection; this is a biggie! I just learned that not only is the protein CACN1S (this is key in Isradipine therapeutics for PD) linked to schizophrena...and the other team of scientists and researchers who can't get past dopamine. In other words, schizophrenia, long touted as result of excess dopamine, and its opposite manifesting as PD, are both perhaps channelopathies.

Interestingly, only the "L Type" Calcium Channel blockers may be neuroprotective (this is Isradipine). Other old school channel blockers like Verapimil actually have induced Parkinsonism! I have no idea why only the L Type seems to be our friend.

Rick, I just ran across this morsel when researching L type calcium dealies. Apparently, a certain receptor protein is essential for proper function of L type. It is known impacted by the gene CLCNL1A3

From Wikipedia:
This gene encodes one of the five subunits of the slowly inactivating L-type voltage-dependent calcium channel in skeletal muscle cells. Mutations in this gene have been associated with hypokalemic periodic paralysis, thyrotoxic periodic paralysis and malignant hyperthermia susceptibility.[1]

Rick- if you have haven't run across the Thyrotoxic Periodic Paralysis info, please connect to a brief NYT article- it sounds alarmingly familiar! Even lists salty foods as a possible trigger.

Next up:

Moreover, rom the ER that consistently induced mitochondrial Ca2+ uptake, with a rise of mitochondrial matrix free Ca2+. In other words...too many free radical Ca2+ cells resulting in toxicity.

I sure wish we could put all these pieces together into actually beginning to make sense of how the substantia nigra ends up taking the biggest hit for us. I also wonder if this model of how PD might originate allows for potential autoimmune role and my hope for a vaccine.