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白细胞端粒长度相关长链非编码 RNA NBR2 在阿尔茨海默病中的作用研究。

Study of the role of leukocyte telomere length-related lncRNA NBR2 in Alzheimer's disease.

机构信息

Department of Geriatrics, The First Affiliated Hospital of Ningbo University, Ningbo 315000, China.

Department of Geriatrics, Jiangsu Key Laboratory of Geriatrics, The First Affiliated Hospital of Nanjing Medical University, Nanjing 210000, China.

出版信息

Aging (Albany NY). 2024 Sep 16;16(18):12593-12607. doi: 10.18632/aging.206107.

DOI:10.18632/aging.206107
PMID:39287993
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC11466486/
Abstract

Alzheimer's Syndrome (AD) is a neurodegenerative disease that is prevalent in middle-aged and elderly people. As the disease progresses, patients gradually lose the ability to take care of themselves, which brings a heavy burden to the family. There is a link between leukocyte telomere length (LTL) and cognitive ability. To search for possible pathogenic mechanisms and potential therapeutic agents, we demonstrated a causal link between LTL and AD using Mendelian randomization analysis (MR). The expression of the target gene NBR2 and the downstream mRNA GJA1 and GJA1-related genes, pathway enrichment, and association with immune cells were further explored. Using the gene cluster-drug target interaction network, we obtained potential therapeutic drugs. Our study provides evidence for a causal link between AD and LTL, suggesting medicines that may treat and alleviate AD symptoms.

摘要

阿尔茨海默病(AD)是一种神经退行性疾病,在中老年人中较为普遍。随着疾病的发展,患者逐渐丧失自理能力,给家庭带来沉重负担。白细胞端粒长度(LTL)与认知能力之间存在关联。为了寻找可能的发病机制和潜在的治疗药物,我们使用孟德尔随机分析(MR)证明了 LTL 与 AD 之间存在因果关系。进一步探索了靶基因 NBR2 的表达以及下游 mRNA GJA1 和 GJA1 相关基因、通路富集和与免疫细胞的关联。利用基因簇-药物靶标相互作用网络,我们获得了潜在的治疗药物。我们的研究为 AD 与 LTL 之间的因果关系提供了证据,表明可能有治疗和缓解 AD 症状的药物。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b0be/11466486/e50981434fb1/aging-16-206107-g006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b0be/11466486/bb68e666d043/aging-16-206107-g001.jpg
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https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b0be/11466486/cb0a8b555676/aging-16-206107-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b0be/11466486/dab845b34278/aging-16-206107-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b0be/11466486/c21a60e78c6d/aging-16-206107-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b0be/11466486/e50981434fb1/aging-16-206107-g006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b0be/11466486/bb68e666d043/aging-16-206107-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b0be/11466486/1e165528a9dd/aging-16-206107-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b0be/11466486/cb0a8b555676/aging-16-206107-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b0be/11466486/dab845b34278/aging-16-206107-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b0be/11466486/c21a60e78c6d/aging-16-206107-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b0be/11466486/e50981434fb1/aging-16-206107-g006.jpg

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本文引用的文献

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