The Role of Mesenchymal Stem Cell Exosomes in the Onset and Progression of Alzheimer's Disease

Abstract

Alzheimer's disease (AD) is a neurodegenerative disease with progressive loss of memory and cognitive function. Because its pathogenesis has not been fully elucidated, there is still a lack of understanding of its pathogenesis and effective treatment. Many studies have shown that Mesenchymal stem cells Exosomes (MSCs-Exo) can promote anti-inflammatory, regulate immune function, enhance amyloid (Aβ) degradation, and promote axon growth of nerve cells. Exosomes can effectively cross the blood-brain barrier, and have better biocompatibility and biosafety than nanomaterials, and more diverse ways to carry drugs. Adipose stem cell exosomes can not only treat AD by their own characteristics, but also regulate AD and other neurological diseases as A drug carrier that can efficiently and freely cross the blood-brain barrier: they can effectively reduce Aβ42 plaques and improve the neuronal microenvironment through microglia. In AD model mice, excessive activation of microglia demonstrated the formation of an inflammatory microenvironment in the brain. The inflammatory microenvironment erodes healthy neurons to a certain extent, forcing them to overactivate inflammatory signaling pathways so that they can't function normally, Adipose stem cell exosomes can effectively clear the expression of inflammatory factors in hypoxia-induced AD neuronal model and promote synaptic repair through microRNA/ phosphatase and tensin homolog (miR-223/PTEN) and phosphatidylinositol kinase (PI3K/Akt) pathways. It can promote the polarization of microglia towards anti-inflammatory phenotype and promote neuronal repair. Adipose stem cell exosomes can also be used to improve memory and cognitive dysfunction by alleviating Tau phosphating or delaying hippocampus volume decay, targeting the core pathological mechanism of AD to achieve therapeutic effects. This article mainly introduces the role of MSC exosomes in the pathogenesis and development of AD.