One cause of<unk>  is due to a genetic mutation in the FOLR1 gene. It is inherited from a person's parents in an autosomal recessive manner. The mutation of the FOLR1 gene causes an inability to produce the FRA protein. More commonly, CFD involves the malfunction and disruption of the folate receptor alpha (FRA). One way the FRA can be disrupted is by the attachment of the autoantibodies, causing dysfunction in the receptor. Also, a mitochondrial disease can impact the functioning of the folate receptor alpha. In order for the receptor to function properly, energy from the mitochondria is required. Folate must be actively transported into the brain, so ATP from the mitochondria is essential. If the individual has a mitochondrial disease, the FRA could be lacking adequate energy, resulting in the deficiency of folate in the brain. Other causes appear to be Kearns–Sayre syndrome and autoantibodies to the folate receptor. Furthermore, secondary<unk>  can develop in patients suffering from other conditions. For example, it can develop in AADC deficiency through the depletion of methyl donors, such as SAM and 5-MTHF, by O-methylation of the excessive amounts of L-dopa present in patients.
Cerebral folate deficiency
Hereditary folate malabsorption
Vitamin E deficiency
Fluorine deficiency
Iron deficiency
Folate deficiency
Boron deficiency 
Selenium deficiency