Research progress of the CXCR4 mechanism in Alzheimer's disease

Wang, Qiu‐Lin; Fang, Chang‐Le; Huang, Xueyan; Xue, Lu‐Lu

doi:10.1002/ibra.12026

Cited by 14 publications

(7 citation statements)

References 68 publications

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“…Increased plasma level of GFAP is also suggested as a potential prognostic marker in COVID-19, associated with mortality risk [81]. CXCR4 is another up-regulated hub gene in AD and COVID-19 patients [82,83]. CXCR4 is a G protein coupled receptor that binds to CXCL12 and triggers downstream signaling pathways associated with inflammatory pathways [82].…”

Section: Discussionmentioning

confidence: 99%

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Common molecular signatures between coronavirus infection and Alzheimer’s disease reveal targets for drug development

Abyadeh

Yadav

Kaya

2023

Preprint

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Cognitive decline has been reported as a common consequence of COVID-19, and studies have suggested a link between COVID-19 infection and Alzheimer's disease (AD). However, the molecular mechanisms underlying this association remain unclear. To shed light on this link, we conducted an integrated genomic analysis using a novel Robust Rank Aggregation method to identify common transcriptional signatures of the frontal cortex, a critical area for cognitive function, between individuals with AD and COVID-19. We then performed various analyses, including the KEGG pathway, GO ontology, protein-protein interaction, hub gene, gene-miRNA, and gene-transcription factor interaction analyses to identify molecular components of biological pathways that are associated with AD in the brain also show similar changes in severe COVID-19. Our findings revealed the molecular mechanisms underpinning the association between COVID-19 infection and AD development and identified several genes, miRNAs, and TFs that may be targeted for therapeutic purposes. However, further research is needed to investigate the diagnostic and therapeutic applications of these findings.

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Section: Discussionmentioning

confidence: 99%

“…CXCR4 is another up-regulated hub gene in AD and COVID-19 patients [82,83]. CXCR4 is a G protein coupled receptor that binds to CXCL12 and triggers downstream signaling pathways associated with inflammatory pathways [82]. CXCR4 is involved in neuronal guidance and apoptosis via astroglial signaling and microglial activation [84].…”

Section: Discussionmentioning

confidence: 99%

Common molecular signatures between coronavirus infection and Alzheimer’s disease reveal targets for drug development

Abyadeh

Yadav

Kaya

2023

Preprint

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“…These clues support the synapse, a key site where the functional connection between neurons occurs ( Faria-Pereira and Morais, 2022 ), whose information transmission was in chaos post infection. Alterations in synaptic signaling, in the release of neurotransmitters from presynaptic neurons, changes in binding to postsynaptic receptors, and synaptic degeneration are evident in the course of many neurodegenerative diseases ( Parmar et al., 2022 ; Peng et al., 2022 ; Wang et al., 2022a ). Indeed, we found that several differentially expressed proteins were involved in the pathways of KEGG associated with neurodegenerative diseases, autophagy, and other signaling.…”

Section: Discussionmentioning

confidence: 99%

Understanding global changes of the mouse brain proteome after vaginal infection with HSV-2 using a label-free shotgun approach

Cheng

Wang

et al. 2022

Front. Cell. Infect. Microbiol.

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Herpes simplex virus type 2 (HSV-2) is a common human pathogen that establishes lifelong latency in neurons of the nervous system. The number of severe central nervous system infections caused by the virus has increased recently. However, the pathogenesis of HSV-2 infection in the nervous system is not fully understood. Here, we demonstrated global proteomic changes in the brain tissue in BALB/c mice vaginally infected with HSV-2. Data are available via ProteomeXchange with identifier PXD034186. A total of 249 differentially expressed proteins were identified in infected brain tissue. The GO and KEGG enrichment analysis of these proteins indicated that they were mainly involved in the regulation of synapse formation and synaptic excitability. In addition, genes affecting autophagy, the development of other neurodegenerative diseases, and signaling pathways relevant to other neurologic diseases were identified. Additional experiments, comparing the brain tissue of asymptomatic and symptomatic mice showed a differential expression of proteins involved in synapse formation and synaptic transmission. Others were involved in autophagy, addiction, and signaling pathways of other neurologic diseases. These results suggest that changes in synaptic structure and function, as well as autophagy, may be related to the development of neurologic abnormalities that follow HSV-2 infection. We also identified a protein GluN2A encoded by Grin2a was continuously expressed at high levels after infection. We propose that GluN2A may be a key molecule in the pathogenesis of HSV-2-induced neurologic diseases.

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“…AD is a CNS degenerative disease characterized by pathological changes of cortical and hippocampal neuron loss, amyloid β‐protein (Aβ) aggregation‐formed plaques, and tau protein hyperphosphorylation‐induced neurofibrillary tangles, which is clinically manifested by progressive cognitive impairment, especially memory (Spence et al, 2017; Wang et al, 2022). Therefore, reducing the accumulation of Aβ in the brain and protecting neurons may become an effective way in the prevention and treatment of AD.…”

Section: The Regulatory Potentials Of P75ntr In Neurological Diseasesmentioning

confidence: 99%

P75 neurotrophin receptor as a therapeutic target for drug development to treat neurological diseases

Xiong

Chen

Deng

et al. 2022

Eur J of Neuroscience

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The interaction of neurotrophins with their receptors is involved in the pathogenesis and progression of various neurological diseases, including Alzheimer's disease, Parkinson's disease, amyotrophic lateral sclerosis, spinal cord injury and acute and chronic cerebral damage. The p75 neurotrophin receptor (p75NTR) plays a pivotal role in the development of neurological dysfunctions as a result of its high expression, abnormal processing and signalling. Therefore, p75NTR represents as a vital therapeutic target for the treatment of neurodegeneration, neuropsychiatric disorders and cerebrovascular insufficiency. This review summarizes the current research progress on the p75NTR signalling in neurological deficits. We also summarize the present therapeutic approaches by genetically and pharmacologically targeting p75NTR for the attenuation of pathological changes. Based on the evolving knowledge, the role of p75NTR in the regulation of tau hyperphosphorylation, Aβ metabolism, the degeneration of motor neurons and dopaminergic neurons has been discussed. Its position as a biomarker to evaluate the severity of diseases and as a druggable target for drug development has also been elucidated. Several prototype small molecule compounds were introduced to be crucial in neuronal survival and functional recovery via targeting p75NTR. These small molecule compounds represent desirable agents in attenuating neurodegeneration and cell death as they abolish activation‐induced neurotoxicity of neurotrophins via modulating p75NTR signalling. More comprehensive and in‐depth investigations on p75NTR‐based drug development are required to shed light on effective treatment of numerous neurological disorders.

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Research progress of the CXCR4 mechanism in Alzheimer's disease

Cited by 14 publications

References 68 publications

Common molecular signatures between coronavirus infection and Alzheimer’s disease reveal targets for drug development

Common molecular signatures between coronavirus infection and Alzheimer’s disease reveal targets for drug development

Understanding global changes of the mouse brain proteome after vaginal infection with HSV-2 using a label-free shotgun approach

P75 neurotrophin receptor as a therapeutic target for drug development to treat neurological diseases

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