Electroencephalogram microstates in Alzheimer’s dementia and mild cognitive impairment: A systematic review and meta-analysis

• Meta-analysis summarizes EEG microstate alterations across the MCI–AD continuum. • Prolonged microstate A and B durations are most consistent in AD, whereas MCI effects are smaller and more heterogeneous. • Findings highlight need for standardized methods and longitudinal studies. Electroencephalography (EEG) microstate analysis has emerged as a tool for investigating the spatial organization and temporal dynamics of large-scale cortical networks. Its potential role in identifying risk and progression of Alzheimer’s dementia (AD) remains unclear. We conducted a systematic review and meta-analysis of EEG microstate parameters in AD and mild cognitive impairment (MCI). PubMed, PsychINFO, EMBASE, and MEDLINE were searched, identifying 30 eligible studies (16 included in meta-analysis). Random-effects models were used to pool effect sizes and 95% confidence intervals comparing microstate parameters between AD, MCI, and healthy controls. Sixteen studies were included in the meta-analysis. In AD vs controls, microstate A duration (g = 0.41, 95% CI [0.10, 0.72]) and microstate B duration (g = 0.48, 95% CI [0.23, 0.73]) were significantly increased. In MCI vs controls, microstate D duration was significantly decreased (g = −0.26, 95% CI [−0.48, −0.04]) and microstate A occurrence rate was increased (g = 0.40, 95% CI [0.07, 0.74]), while microstate A and B duration were not significantly different. Heterogeneity was substantial for several outcomes. Pooled evidence suggests prolonged microstate A/B duration as the most reproducible alteration in AD, with reduced microstate D duration emerging as a modest finding in MCI. However, substantial heterogeneity and possible small-study effects indicate that current evidence is best interpreted as hypothesis-generating pending standardized, longitudinal, and multimodal studies. EEG microstate analysis may provide complementary information about large-scale network dysfunction in MCI and AD, but methodological limitations currently constrain clinical biomarker interpretation.