https://www.nature.com/articles/s41380-023-01979-3
Taken together, our findings could provide a rationale for testing iron-modifying interventions, such as deferiprone, with the aim to restore healthy cortical iron biology and improve cortical function in schizophrenia.
Full abstract:
Despite loss of grey matter volume and emergence of distinct cognitive deficits in young adults diagnosed with schizophrenia, current treatments for schizophrenia do not target disruptions in late maturational reshaping of the prefrontal cortex. Iron, the most abundant transition metal in the brain, is essential to brain development and function, but in excess, it can impair major neurotransmission systems and lead to lipid peroxidation, neuroinflammation and accelerated aging. However, analysis of cortical iron biology in schizophrenia has not been reported in modern literature. Using a combination of inductively coupled plasma-mass spectrometry and western blots, we quantified iron and its major-storage protein, ferritin, in post-mortem prefrontal cortex specimens obtained from three independent, well-characterised brain tissue resources. Compared to matched controls (n = 85), among schizophrenia cases (n = 86) we found elevated tissue iron, unlikely to be confounded by demographic and lifestyle variables, by duration, dose and type of antipsychotic medications used or by copper and zinc levels. We further observed a loss of physiologic age-dependent iron accumulation among people with schizophrenia, in that the iron level among cases was already high in young adulthood. Ferritin, which stores iron in a redox-inactive form, was paradoxically decreased in individuals with the disorder. Such iron-ferritin uncoupling could alter free, chemically reactive, tissue iron in key reasoning and planning areas of the young-adult schizophrenia cortex. Using a prediction model based on iron and ferritin, our data provide a pathophysiologic link between perturbed cortical iron biology and schizophrenia and indicate that achievement of optimal cortical iron homeostasis could offer a new therapeutic target.
See also: a Wikipedia page – Neurodegeneration with brain iron accumulation
By the way, I have keratoconus, and recently a hypothesis arose that the Fleischer ring, which consists of iron deposits and forms inside the cornea in this disease, may arise due to decreased levels of lactoferrin, which usually sequesters excess iron. Thus, this excess iron may deposit inside the cornea.
But lactoferrin works in the whole body. And in a different recent study they found decreased lactoferrin levels even in the blood of people with keratoconus. I went googling and found that it could be bought as a supplement, which got me thinking that maybe I should try it out. What if my anxiety somehow interlaps in its mechanisms with keratoconus, since the latter has been found to affect levels of molecules in the whole body, and not in the eyes only.
Just musing aloud to myself.
This is fascinating to me. I have thallasemia, which causes poor iron absorption and a higher level of free-floating iron in the blood. I have always had to be careful not to get too much iron, and I knew about acute iron toxicity, but didn’t realize it might also be linked to gray matter loss.
My MRIs have shown gray matter loss.
My daughter has thalassemia too. Do you have major thalassemia or minor?
Minor. If I had major, I would be a lot sicker, I think. Major requires blood transfusions.
My daughter has minor too. Her hemoglobin is usually only 9.0. They said if it drops below 9, they’ll do a blood transfusion
Holy cow! Mine has never been below 10.1
I’m glad yours has been no lower than 10.1.
I know how dizzy I get at times. I can’t even imagine.
Yeah. Her vision sometimes just goes black. And she suffers severe fatigue
Does she drink loads of gatorade? That is what helps me the most.
No. She mainly only drinks water and green tea or chai. I’ll tell her about Gatorade helping though for sure. Thanks for the tip @supernova!