The diagnostic significance of the chemokine CXCL12 in Alzheimer's disease

다국어 초록 (Multilingual Abstract)

A complex relationship between the stromal cell‐derived factor 1 (CXCL12) and dementia, including mild cognitive impairment (MCI) and Alzheimer's disease (AD) has been described in the literature. The chemokine CXCL12 regulates many functions of bone marrow‐derived stem cells and has been implicated in neurogenesis as well as with the recruitment of brain resident and non‐resident circulating cells towards sites of a lesion in the central nervous system. It has been suggested that dysregulation of the CXCL12/CXCR4 signaling pathway is involved in the pathologic process of cognitive impairment. Moreover, significantly changed expressions of the CXCL12 and CXCR4 were observed in AD patients' brains compared to the normal brain tissues of the healthy non‐demented subjects. The purpose of the study was to evaluate the concentration of the CXCL12 in patients with early stage of dementia (MCI) and compare it with classical biomarkers for AD.
The study group included 34 subjects: 18 patients with AD and 16 controls without cognitive impairments. The cerebrospinal fluid (CSF) concentrations of tested proteins were measured with the use of ELISA method.
The CSF concentrations of CXCL12 were elevated in AD patients in comparison to non‐demented controls. The increased levels of CXCL12 correlated with all CSF biomarkers (Aβ‐42, Aβ‐42/Aβ‐40, Tau, pTau181), age and MMSE in the whole study group. Moreover, significant negative correlation between CXCL12 and MMSE in AD and control group was observed.
It was established that CXCL12 might play role in the development of AD, although the question, whether this protein can be useful in diagnostic of dementia requires further examination on larger study group. Acknowledgment: The study was conducted with the use of equipment purchased by Medical University of Białystok as part of the RPOWP 2007‐2013 funding, Priority I, Axis 1.1, contract No. UDA‐RPPD.01.01.00‐20‐001/15‐00 dated 26.06.2015.