Alzheimer’s disease (AD) is a leading cause of cognitive decline, with no curative therapy currently available. Emerging research highlights epileptic activity as a modifiable risk factor contributing to disease progression. Animal models and human studies indicate an increased prevalence of epileptic seizures and subclinical epileptiform activity (SEA) in AD, which may exacerbate cognitive impairment. However, significant variability exists in reported SEA prevalence, ranging from 3% to 54%, potentially due to differing definitions, diagnostic methodologies, and biological heterogeneity of AD subtypes. Recent evidence suggests SEA may be more common in individuals with hippocampus-sparing AD, a rapidly progressing variant characterized by distinct neuroimaging and clinical features. Advanced neuroimaging techniques, including MRI and PET, have identified structural and functional brain alterations associated with SEA in AD, providing potential biomarkers for disease phenotyping. Given the role of neuronal hyperexcitability in AD, targeting SEA represents a promising therapeutic strategy. Early clinical trials suggest that levetiracetam may mitigate hyperexcitability and improve cognitive function in SEA-positive individuals. Future research should focus on refining SEA detection methods, integrating neuroimaging biomarkers, and developing personalized treatment approaches to modify AD progression effectively.