This research aims to evaluate the peripheral nervous system's pathology in Alzheimer's disease, focusing on neuromuscular junction (NMJ) function.
Utilization of a functional human NMJ microphysiological system
Analysis of fAD mutations' impact on NMJ functionality
Assessment of motor and cognitive deficits independently
Confirmation that fAD mutations cause NMJ deficiencies
Induction of motor deficits independent of cognitive declines
Demonstration of distinct paths of impairment in neurodegeneration
Abstract
These findings confirmed that fAD mutations lead to NMJ deficiencies, supporting that motor deficits can be induced independently from cognitive deficits.
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Evaluating the peripheral nervous system pathology of Alzheimer's disease utilizing a functional human NMJ microphysiological system | Synapse