IL1B and Alzheimer disease: Cui et al. [197] reported that Exos released from hypoxia-preconditioned MSCs (MSC-Exos) downregulated TNF-α and IL-1β, hindered NF-κB and STAT3 (signal transducer and activator of transcription 3) activation, and decreased Aβ peptides levels and senile Aβ plaques, while upregulating anti-inflammatory IL-4 and IL-10, and exo-miR-21, which improved memory and learning in APP/PS1 AD-model mice.