Of what I understand.
They make a supposition.
Ovarian removal operation (OVX) induces a lack of estrogen, like in age-old-years, pretending it induces a decline and a neurodegenerative process.
They make a correlation: iron accumulates with time. Excess iron is creating ROS.
Female rats have showed decreased dihydroorotate dehydrogenase (DHODH) expression when getting under OVX.
However DHODH supports a vital role in neuronal ferroptosis.
But E2 alleviates ferroptosis induced by erastin and ferric ammonium.
So, if we try to link:
a) OVX + neuro-decline + lack of estrogen
b) Excess iron in menopause + lack of estrogen
=> If A induces B, and if C induces B, A should equal C.
If excess iron induces ROS and lipid peroxidation, take the way back and get estrogen to cancel the decreased DHODH induced by ovarian removal operation (OVX).
How does iron cause ferroptosis?
Taken together, excess iron in both the cytosol and mitochondria significantly contributes to the development of ferroptosis in neurodegenerative diseases, and this occurs primarily through its promotion of oxidative stress and lipid peroxidation.
Note1: One correlation seems to give an analogy but not an equivalence. Expressed differently, pharma tries to find positive effect to supplementing E2, event by arranging or inventing improvements.
Note2: Estrogen is not directly linked to ROS. Iron is linked to ROS and ROS induce membrane peroxidation.