Editing More:Molybdenum deficiency

[[Potentially Actionable Research]]

Molybdenum deficiency is more likely to be associated with upper motor neuron disease.

The paper, "Molybdenum deprivation, purine ingestion and an astrocyte-associated motor neurone syndrome in sheep: assumed clinical effects of inosine," {{#pmid:27014182|bourke2015}} describes the  "Mo-containing enzyme xanthine oxidase-dehydrogenase, which facilitates the final two steps in the catabolism of the endogenous purines to uric acid."

Molybdenum deficiency is affecting iron which then affects glutamate:

Immunohistochemical studies are required to differentiate the two. However, neither is characterised by the presence of cytoplasmic pigmented granules, which would indicate that the degenerate astrocytes associated with inosine and xanthosine are not Alzheimer-type cells and, consistent with this, the treated sheep displayed
no evidence of either liver disease or encephalopathy. In the brain, the conversion of ferrous to ferric iron takes place in astrocytes and if ferrous iron accumulates in an astrocyte it will cause rupture of the cell membrane. In the affected sheep, the pigmented granules that were formed in the astrocytes’ cytoplasm had a blue-green reaction to Lillie’s Fe2+ ion uptake stain. This stain is positive (green) for melanins; however, if Fe2+ is present and the pH is acidic the colour reaction becomes blue-green,15 as in the present case. If Fe2+ had accumulated in the affected astrocytes, that may explain why they underwent degeneration and as a consequence ended their
normal contribution to glutamate uptake and release. The effect of this on neuronal transmission would be to reduce glutamatergic excitation and by default increase the dominance of GABA-ergic inhibition.

== References ==