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CSF ferritin in the clinicopathological progression of Alzheimer’s disease and associations with APOE and inflammation biomarkers
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    RE: CSF ferritin in the clinicopathological progression of Alzheimer's disease and associations with APOE and inflammation biomarkers

    Ayton et al. reported the association between ferritin, apolipoprotein E (APOE) and dementia-related biomarkers such as amyloid β42/total-tau and phosphorylated tau181 (p-tau181) in cerebrospinal fluid (CSF) (1). CSF ferritin and APOE were positively associated with p-tau181, which was most predominant in subjects without increase in amyloid β42/total-tau. I present information about the study.

    Pan et al. investigated the associations of CSF ferritin and CSF biomarkers of Alzheimer's disease (AD) (2). They found that CSF ferritin increased in subjects with more advanced categories of CSF biomarkers such as amyloid β42 and p-pau, although there were stronger relationships of CSF ferritin with p-tau and t-tau, rather than amyloid β42. This means that biological action of ferritin in the brain for AD may be more closely related to tau protein.

    Baringer et al. described brain iron homeostasis in Alzheimer's disease, Parkinson's disease, and other neurodegenerative diseases (3). They emphasized that endothelial cells of the blood-brain barrier were the site of iron transport regulation, and iron uptake, transcytosis, and release were mainly conducted. By controlling the excess of brain iron, neurodegenerative disorders may be improved. The mechanism that tau protein spreads through functionally connected neurons in Alzheimer's disease have been precisely reported (4), and it may be related to the excess of brain iron storage.

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    Conflict of Interest:
    None declared.