Explores executive control deficits linked to daily activities in Alzheimer’s patients, suggesting diagnostic potential.
Background Early clinical manifestations of Alzheimer’s disease (AD) include an apparent decline in memory and executive function. Executive function is closely related to activities of daily living (ADL) and is important for maintaining an independent, high-quality lifestyle. Objective This study aimed to explore the executive control ability and neuromechanisms of AD patients through stop-signal task (SST) elicited event-related potentials (ERPs) and their relationship with ADL. Methods Thirty-six patients with AD and 36 sex and age matched healthy controls (HCs) were recruited. Electroencephalography (EEG) data recorded during the SST was compared between groups, and SST-related indicators were determined to assess executive control ability in AD patients. The relationship between ADL and SST-related indicators was explored. We performed Receiver Operating Characteristic (ROC) analysis on SST- and EEG-related indices. Results Differences in the following indices were found between the two groups: Go accuracy ( P < 0.001), Go omissions ( P < 0.001), Go errors ( P < 0.001), Go error reaction time (RT) ( P < 0.001), failed stop RT ( P = 0.021), all accuracies ( P = 0.005), mean amplitude of N300 ( P = 0.043), peak amplitude of N300 ( P = 0.043), and peak latency of N300 ( P < 0.001). And Go accuracy ( r = −0.603, P = 0.005) and all accuracy ( r = −0.624, P = 0.003) in the AD group were negatively partially correlated with ADL. These SST- and EEG-related indicators had an Area Under the Curve of 0.771 and 0.831, both of which could be used to jointly diagnose AD (both P < 0.001). Conclusion This study suggests that the worse the executive function of AD patients, the more serious the ADL impairment. AD patients have electrical abnormalities associated with executive control. Different SST- and EEG-related indicators can be used to diagnose AD. This provides a new avenue for further elucidation of the pathological mechanisms of AD.
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Gao et al. (2026) studied this question.
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