Alzheimer’s disease (AD) is a chronic, progressive, and irreversible neurodegenerative disorder that typically manifests with subtle onset and slow progression. It is pathologically characterized by two major features: the extracellular accumulation of β-amyloid protein (Aβ), forming senile plaques, and the intracellular hyperphosphorylation of Tau protein, resulting in neurofibrillary tangles(NFTs). These pathological changes are accompanied by substantial neuronal and synaptic loss, especially in critical brain regions such as the cerebral cortex and hippocampus. Clinically, AD presents as a gradual decline in memory, language abilities, and spatial orientation, which severely impairs the quality of life of affected individuals. As the aging population continues to expand in China, the incidence of AD is rising steadily, making it a major public health concern that demands urgent attention. The increasing societal and economic burden of AD highlights the pressing need to identify effective diagnostic biomarkers and develop novel therapeutic strategies. Among the various molecular signaling pathways involved in neurological disorders, the Notch signaling pathway is particularly notable due to its evolutionary conservation and regulatory roles in cell proliferation, differentiation, development, and apoptosis. In the central nervous system, it is essential for neurodevelopment and synaptic plasticity and has been implicated in several neurodegenerative processes. Although some studies suggest that Notch signaling may influence AD-related pathology, its precise role in AD remains poorly defined. In particular, the interaction between Notch signaling and non-coding RNAs (ncRNAs)—key regulators of gene expression—has received limited attention. NcRNAs, including long non-coding RNAs (lncRNAs) and microRNAs (miRNAs), are known to exert extensive regulatory functions in gene expression at transcriptional and post-transcriptional levels. Above dysregulation has been widely associated with various diseases, including cancers, cardiovascular conditions, and neurodegenerative disorders. Notably, the interaction between ncRNAs and major signaling pathways such as Notch can produce widespread biological effects. Although such interactions have been increasingly reported in several disease models, comprehensive studies investigating the regulatory relationship between Notch signaling and ncRNAs in the context of AD are still limited. Given the ability of ncRNAs to modulate signaling cascades and form complex regulatory networks, a deeper understanding of their crosstalk with Notch signaling could reveal novel insights into AD pathogenesis and uncover potential targets for diagnosis and treatment. In this study, we investigated the regulatory landscape involving the Notch signaling pathway and associated ncRNAs in AD using bioinformatics methods. By integrating data from multiple public databases, we systematically screened for significantly dysregulated Notch pathway-related genes and their interacting ncRNAs in AD. Based on this analysis, we constructed a lncRNA–miRNA–mRNA regulatory network to elucidate the potential mechanisms linking Notch signaling with ncRNA-mediated gene regulation in AD pathogenesis. Furthermore, we explored the internal relationships and molecular mechanisms involved in this network and assessed the feasibility and clinical application value of these molecules as early diagnostic biomarkers and potential therapeutic targets for AD. This study aims to provide new insights into the underlying molecular basis of AD and offers novel strategies for its diagnosis and treatment.