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

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 ne...

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Veröffentlicht in:Metabolic brain disease 2023-12, Vol.38 (8), p.2563-2572
Hauptverfasser: Sabaie, Hani, Tamimi, Parham, Gharesouran, Jalal, Salkhordeh, Zoha, Asadi, Mohammad Reza, Sharifi-Bonab, Mirmohsen, Shirvani-Farsani, Zeinab, Taheri, Mohammad, Sayad, Arezou, Rezazadeh, Maryam
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Sprache:eng
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Zusammenfassung: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.
ISSN:0885-7490
1573-7365
DOI:10.1007/s11011-023-01274-8