Replies

I found influenza encephalitis to be the most compelling, however not confirmed. The increase in PD now, including far younger onset is most disturbing.

My hypothesis (model) not including Huntingtons is the neurodegeneration is a metabolic process involving disruption of the sulfur cycle. We have confirmed it with miRNA testing. The primary disruption begins with PANK and involves cysteine, glutathione, cysteamine and hypotaurine. All are related to ROS scavengers. Taurine is secondary to hypotaurine and is causative to sarcopenia wasting and frailty. PKAN is the rosette stone of neurodegeneration.

I think they should have continued the Huntington's trials with cysteamine for longer (increased BDNF in the short trial), however I suspect Huntington's is genetic and not metabolic.

I disturb a few neurosurgeons when I suggest we can eliminate DBS in the near future.

Understand where I'm coming from now?

LOL. Not a bit. That’s probably why my daughter won’t talk neuroscience with me. “Sulfur cycle”? OK, I made “A”s in three semesters of Biochem but Lehninger was a pamphlet in those days.

Didn’t we know Huntington’s involves storage disease due to, can’t remember, funny, I used to know the chemical structure, a complex Hyaluronic something or other? If I recall sulfur was part of it which seemed unusual but maybe not for a glycoprotein.