Analyze the binding of amyloid beta 1‐42 to specific regions of the TREM2 gene

We showed that Aβ interacted with the regulatory DNA regions of the TREM2 gene, including the enhancer located upstream, intron 2, and non-coding exon 5. The signal from the enhancer region was higher than that from the others. (Fold enrichment values above 3 were considered binding signals.) CONCLUSION: Our results showed that Aβ interacts with the regulatory DNA regions of the TREM2 gene. The data obtained will contribute to the identification of a new mechanism, beyond the receptor-ligand relationship, involving Aβ and TREM2 in the pathological mechanisms of AD, and to the understanding of complex processes related to AD. Our study is also expected to provide insights into TREM2-related therapeutic approaches for AD. This study is supported by the Health Institutes of Türkiye (TUSEB) (Project ID: 37319).

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Publication Details

Journal
Alzheimer s & Dementia
Published
2025-12-01
DOI
https://doi.org/10.1002/alz70855_106314
Primary Topic
Neuroinflammation and Neurodegeneration Mechanisms
Type
article
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article

Analyze the binding of amyloid beta 1‐42 to specific regions of the TREM2 gene

Tugay Çamoğlu, Zuhal Yurttaş, Erdinç Dursun, Duygu Gezen‐Ak et al.
Alzheimer s & Dementia
Neuroinflammation and Neurodegeneration Mechanisms
article

Analyze the binding of amyloid beta 1‐42 to specific regions of the TREM2 gene

Tugay Çamoğlu, Zuhal Yurttaş, Erdinç Dursun, Duygu Gezen‐Ak, Seçil Dülger
article en

Abstract

We showed that Aβ interacted with the regulatory DNA regions of the TREM2 gene, including the enhancer located upstream, intron 2, and non-coding exon 5. The signal from the enhancer region was higher than that from the others. (Fold enrichment values above 3 were considered binding signals.) CONCLUSION: Our results showed that Aβ interacts with the regulatory DNA regions of the TREM2 gene. The data obtained will contribute to the identification of a new mechanism, beyond the receptor-ligand relationship, involving Aβ and TREM2 in the pathological mechanisms of AD, and to the understanding of complex processes related to AD. Our study is also expected to provide insights into TREM2-related therapeutic approaches for AD. This study is supported by the Health Institutes of Türkiye (TUSEB) (Project ID: 37319).

Alzheimer s & DementiaVol. 21(S1)
Istanbul University-Cerrahpaşa (TR), Istanbul University (TR)
Openalex Percentile: Top 38%
Neuroinflammation and Neurodegeneration Mechanisms
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