Extracellular vesicles derived from astrocyte-treated with haFGF_14-154 attenuate Alzheimer phenotype in AD mice

Abstract

Background: aFGF content in serum and cerebrospinal fluid is increased in Alzheimer's disease (AD) patients and attenuates the activation of astrocytes. Extracellular vesicles (EVs) are a major mediator in astrocyte-neuron communications. Since excessive or persistent reactive astrocytes lead to chronic inflammation and neuronal dysfunction, and the activation of astrocytes can be inhibited by aFGF, we proposed that the cargoes of astrocyte-derived EVs (AEVs) might be modified by aFGF stimulation, playing an important role in AD progression. However, the mechanisms underlying the role of aFGF remain unclear.