Apraxic imitation deficits in Alzheimer’s disease are associated with altered dynamic connectivity

Abstract

Apraxia is a common symptom in individuals with Alzheimer's disease (AD). However, the neural mechanisms underlying apraxic deficits in AD remain elusive. Therefore, the current study focuses on the association between altered functional connectivity and apraxia in individuals with AD examining the hypothesis that apraxic deficits in AD result from dysfunction in praxis-related networks. To this aim, we examined the association between changes in static and dynamic functional connectivity (FC) of resting-state networks and apraxia in AD. Resting-state functional MRI data was acquired in 13 patients with tau- and amyloid-positive AD, who underwent an extensive neuropsychological, motor and apraxia assessment, and 13 matched healthy control participants. The static and dynamic functional connectivity of resting state networks revealed by independent component analysis (ICA) were assessed and connectivity measures were correlated with apraxia scores. Across all participants, we identified two distinct dynamic FC states using a sliding window approach. Patients with AD exhibited prolonged dwell times in the first state characterized by weaker connectivity and spent overall more time in this state, i.e., showed an increased fraction time in the first state. Apraxic deficits, especially deficits in imitating gestures, correlated significantly with the fraction time of both states as well as with the dwell time of the weakly connected dynamic state. Data suggest that apraxic imitation deficits in AD are associated with dysfunction of praxis networks characterized by altered dynamic FC.