Identification of immune cells infiltrating in hippocampus and key genes associated with Alzheimer’s disease

Abstract

Alzheimer’s disease (AD) is the most prevalent cause of dementia and is primarily associated with memory impairment and cognitive decline, but the etiology of AD has not been elucidated. In recent years, evidence has shown that immune cells play critical roles in AD pathology. In the current study, we collected the transcriptomic data of the hippocampus from gene expression omnibus database, and investigated the effect of immune cell infiltration in the hippocampus on AD, and analyzed the key genes that influence the pathogenesis of AD patients. The results revealed that the relative abundance of immune cells in the hippocampus of AD patients was altered. Of all given 28 kinds of immune cells, monocytes were the important immune cell associated with AD. We identified 4 key genes associated with both AD and monocytes, including KDELR1, SPTAN1, CDC16 and RBBP6, and they differentially expressed in 5XFAD mice and WT mice. The logistic regression and random forest models based on the 4 key genes could effectively distinguish AD from healthy samples. Our research provided a new perspective on immunotherapy for AD patients.

A review and analysis of key biomarkers in Alzheimer’s disease

“… Guo et al (2023) identified 10 hub genes and found neuroinflammation and T-cell antigen receptor (TCR)-associated genes (LCK, ZAP70, and CD44) were the top three hub genes and validated using machine learning. Liu C. et al (2023) collected transcriptomic data from the hippocampus to investigate the impact of immune cell infiltration on AD. It was found that monocytes are important immune cells associated with AD, and four genes related to AD and monocytes were identified: KDELR1, SPTAN1, CDC16, and RBBP6.…”

Unraveling neurovascular mysteries: the role of endothelial glycocalyx dysfunction in Alzheimer’s disease pathogenesis

“…There is substantial evidence of increased levels of shed GCX components like HS and syndecan in the plasma of stroke victims ( Rehm et al, 2007 ; DellaValle et al, 2019 ). The deteriorated extracellular GCX structure allows for direct interaction between immune cells and the endothelium, eventually exacerbating neurological impairment ( Mockl, 2020 ; Bettcher et al, 2021a ; Bettcher et al, 2021b ; Liu et al, 2023 ). Another acute event that occurs upstream of neurodegenerative diseases, traumatic brain injury, is also known to induce a GCX-related neuropathological cascade ( Gonzalez Rodriguez et al, 2018 ; Zou et al, 2021 ; Anand et al, 2023 ).…”