Lactoferrin in cerebrospinal fluid and saliva is not a diagnostic biomarker for Alzheimer's disease in a mixed memory clinic population

Publikation: Bidrag til tidsskriftTidsskriftartikelForskningfagfællebedømt

Background: The pathological changes in Alzheimer's Disease (AD) and other neurodegenerative disorders begin decades prior to their clinical expression. However, the clinical diagnosis of neurodegenerative dementias is not straightforward. Lactoferrin is an iron-binding, antimicrobial glycoprotein with a plethora of functions, including acting as an important immune modulator and by having a bacteriocidic effect. Two previous studies indicated that salivary lactoferrin could differentiate between neurodegenerative dementias. Methods: A total of 222 cerebrospinal fluid (CSF) and saliva samples from a consecutive, mixed memory clinic population were analysed for lactoferrin. In addition, the association between lactoferrin in CSF and saliva and the concentration of tau, phosphorylated tau (p-tau) and amyloid 1–42 (Aβ42) in CSF were addressed. Findings: CSF lactoferrin was assessed for the first time in a cohort of patients with neurodegenerative dementias. No significant differences were found in the levels of CSF or saliva lactoferrin between the diagnostic groups. In addition, no significant relationships were found between lactoferrin levels and tau, p-tau and Aβ42, respectively. Interpretation: Neither CSF nor saliva lactoferrin could differentiate between neurodegenerative dementias in this study.

OriginalsprogEngelsk
Artikelnummer103361
TidsskriftEBioMedicine
Vol/bind67
ISSN2352-3964
DOI
StatusUdgivet - 2021

Bibliografisk note

Funding Information:
Funding: The study was supported by Lundbeck Foundation, Grosserer L. F. Foghts Foundation, Augustinus Foundation, Frimodt-Heineke Foundation and the Foundation for Neurological Research. The Danish Dementia Biobank was supported by the Absalon Foundation of May 1 st 1978 and Simon Spies Foundation.

Funding Information:
The study was supported by Lundbeck Foundation, Grosserer L. F. Foghts Foundation, Augustinus Foundation, Frimodt-Heineke Foundation, and the Foundation for Neurological Research. The Danish Dementia Biobank was supported by the Absalon Foundation of May 1st 1978 and Simon Spies Foundation. The funders had no role in the conceptualization, study design, data collection, analysis, interpretation of data, in writing the paper or in the decision to submit the paper for publication.

Funding Information:
The authors are grateful to the clinical staff at the Copenhagen Memory Clinic, Copenhagen University Hospital, Rigshospitalet and the Dementia Research Centre, Zealand University Hospital. The study was supported by Lundbeck Foundation, Grosserer L. F. Foghts Foundation, Augustinus Foundation, Frimodt-Heineke Foundation and the Foundation for Neurological Research. The Danish Dementia Biobank was supported by the Absalon Foundation of May 1st 1978 and Simon Spies Foundation.

Publisher Copyright:
© 2021 The Author(s)

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