Catechins in insomnia-Alzheimer’s disease comorbidity: A network pharmacology and molecular docking study

Feb 24, 2026Medicine

How Catechins May Affect Both Insomnia and Alzheimer's Disease: A Network and Molecular Study

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Abstract

The identified pivotal targets include , HMOX1, and IGF1, which may play critical roles in the interplay between circadian rhythm disruption and immune dysfunction.

Insomnia and Alzheimer's disease are associated with disruptions in circadian rhythms and immune system function.
, a type of polyphenol, may modulate both circadian and immune processes, although their exact mechanisms are not yet clear.
Machine learning algorithms were utilized to pinpoint key genes involved in the connection between insomnia and Alzheimer's disease.
PDE4D is notably involved in the complement pathway, which is crucial for immune response.
Significant enrichment of the complement pathway and the phosphatidylinositol 3-kinase/Akt signaling pathway was observed.
These pathways may influence microglia-mediated synaptic pruning, linking sleep regulation and neurodegeneration.

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The comorbidity of insomnia and Alzheimer's disease (AD) is strongly driven by the interplay between circadian rhythm disruption and immune dysfunction. are multi-target polyphenols capable of modulating both processes, yet their precise mechanism of action remains elusive. Insomnia and AD related differentialy expressed target genes were specifically sourced from circadian rhythm and immune phenotypes. Two machine learning algorithms were then applied to refine and identify the pivotal targets from this phenotype-driven target pool. Functional enrichment analyses, including kyoto encyclopedia of genes and genomes and gene set enrichment analysis, were performed to elucidate the involved signaling pathways. The compound-comorbidity differentialy expressed target genes related to circadian and immunity network identified catechin (C) and epicatechin as core components. PED4D, HMOX1, and IGF1 were robustly identified as the pivotal targets. was found to be centrally involved in the complement pathway. The complement pathway and the phosphatidylinositol 3-kinase/Akt signaling pathway were significantly enriched. This dual pathway regulation converges to govern microglia-mediated synaptic pruning, a process integral to both sleep and neurodegeneration. This study unveils a mechanistic link from core catechins to the regulation of synaptic pruning via circadian-immune crosstalk, offering a novel therapeutic perspective for the insomnia-AD comorbidity.

Key numbers

Key Target Interaction Degree (C)

Degree of interaction for catechin (C) with identified targets.

Key Target Interaction Degree (EC)

Degree of interaction for epicatechin (EC) with identified targets.

Upregulated Genes in Insomnia and AD

Key candidate genes identified: , HMOX1, IGF1.

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Catechins in insomnia-Alzheimer’s disease comorbidity: A network pharmacology and molecular docking study

Abstract

Key numbers

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