Although Aβ levels were not altered, the NSC-derived EVs rescued cognitive deficits in APP/PS1 mice, enhanced mitochondrial function, SIRT1 activation and synaptic activity, decreased inflammatory response, and rescued cognitive deficits in mouse models of AD [184], suggesting the capacity of exosomes to influence AD pathological environment through both Aβ-dependent and -independent mechanisms. Here, APP is linked to Alzheimer disease.