4.5 Article

Expression analysis of inhibitory B7 family members in Alzheimer's disease

Journal

METABOLIC BRAIN DISEASE
Volume -, Issue -, Pages -

Publisher

SPRINGER/PLENUM PUBLISHERS
DOI: 10.1007/s11011-023-01274-8

Keywords

Alzheimer's disease; B7 family; Biomarker; Expression analysis; Immune checkpoint

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Alzheimer's disease (AD) is a complex global health problem, and new methodologies are needed to investigate its pathophysiology and develop treatments. The interaction of immune modulation and neurodegeneration offers potential for discovering biomarkers and therapies. In this study, we compared the expression levels of inhibitory B7 family members in the blood of AD patients and healthy individuals, and found that certain members were significantly higher in patients. These findings suggest the potential of these molecules as diagnostic biomarkers for AD.
Alzheimer's disease (AD) is a global health problem due to its complexity, which frequently makes the development of treatment methods extremely difficult. Therefore, new methodologies are necessary to investigate the pathophysiology of AD and to treat AD. The interaction of immune modulation and neurodegeneration has added new dimensions in current knowledge of AD etiology and offers an attractive opportunity for the discovery of novel biomarkers and therapies. Using quantitative polymerase chain reaction, we compared the expression levels of inhibitory B7 family members (B7-1, B7-2, B7-H1, B7-DC, B7-H3, B7-H4, B7-H5, B7-H7, and ILDR2), as immune regulators, in the peripheral blood of late-onset AD (LOAD) patients (n = 50) and healthy individuals (n = 50). The levels of B7-2, B7-H4, ILDR2, and B7-DC expression were significantly higher in-patient blood samples than in control blood samples. Furthermore, we discovered a substantial positive correlation between all gene expression levels. In addition, the current study indicated that ILDR2, B7-H4, B7-2, and B7-DC might serve as diagnostic biomarkers to identify LOAD patients from healthy persons. The present work provides additional evidence for the significance of inhibitory B7 family members to the etiology of LOAD.

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