I have not been able to let these two anecdotal experiences of PWP rest.
** As early as the 70's PWP have reported improvements during in flight travel.
**More recently, MJF tells the world in an interview that his symptoms improved to point of not needing meds during a stay in the mountains of Bhutan.
I have been wondering if hypoxia, or reduction in oxygen, helps us somehow and why? The research points to a big yes, so makes you wonder if PD has a vascular component which is overlooked. Results are quite interesting. There is a new hypothesis out there that PD, ALS, AD may start with oxygen transcription factors know as Hypoxia Inducible Factors (HIF-1a). Generally speaking they regulate release of oxygen from blood stream into our cells. All of our cells.
I could list different ways this hypothesis explains many seemingly trivialities in PD but would take too long. The gist of it is, we underexpress HIF-1a (note cancer is now thought due to over expression of this). In PWP, this underexpression is linked to excess iron accumulation, unchecked Reactive Oxygen Species, resulting in cell loss. This explains BOTH the loss of Dopamine and Norepinephrine because these specialized areas are high in neuromelanin which is a known iron regulator. These cells are the main losses in PD, so iron homeostasis and metabolism must be key to the pathology of PD. The big questions left are what is the role of alpha-synuclein clumping, where do prions fit in, and why is our immune system triggered? Oh, and the biggie- why isn't iron being cleared out like it should?
Here is what hits home for many of us:
Hypoxia-inducible factor (HIF) plays an important role in cell survival by regulating iron, antioxidant defense, and mitochondrial function.
Pharmacological inhibitors of the iron-dependent enzyme class prolyl hydroxylases (PHD), which target α subunits of HIF proteins for degradation, have recently been demonstrated to alleviate neurodegeneration associated with stroke and hypoxic-ischemic injuries. Here we report that inhibition of PHD by 3,4-dihydroxybenzoate (DHB) protects against 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP)-induced nigral dopaminergic cell loss and up-regulates HIF-1α within these neurons
That DHB is an iron chelator. In fact there are numerous studies popping up showing iron chelation resulting in an increase in HIF-1a and...
A more recent study finds that placing cells in a mildly hypoxic state thus inducing HIF-1a promotes the change from neuronal stem cell to dopamine cells.
Iron chelation resulted in protection of dopa cells but also in their restoration. In fact when treated prior to inducing the MPTP model of PD, this treatment completely reversed the loss.
Hypoxia Inducible Factor-1 as a Target for Neurodegenerative Diseases