Research Progress of Exosomes in Alzheimer's Disease
Alzheimer's disease (AD) is characterized by A deposition and tau hyperphosphorylation, which has become an important health challenge in the global aging society. Exosomes (EXOs), as nanoscale vesicle for intercellular information transmission, has been found to be involved in the pathological spread of AD by transporting pathological molecules such as A and tau protein. Current studies have shown that EXO can not only accelerate the transmission of A and tau proteins between neurons to worsen the disease process, but also alleviate the pathological burden through the lysosomal degradation pathway mediated by microglia. Furthermore, EXO derived from mesenchymal stem cells has demonstrated therapeutic potential in animal models to reduce A deposition and improve cognitive function. However, the dual mechanism of EXO in AD and its dynamic regulatory network have not been fully clarified. This article systematically analyzed the multi-dimensional role of EXO in the pathological occurrence and treatment strategies of AD, and found that it aggravates nerve injury by mediating the transcellular transmission of A and tau proteins. Meanwhile, exogenous EXO has neuroprotective effects. Confirming potential that EXO possessesas a diagnostic and cure target for AD provides a theoretical basis for the development of early biomarkers and targeted therapy technologies. In the future, it is necessary to further explore the molecular mechanism of EXO function regulation, optimize its delivery efficiency and specificity, and solve the contradiction of its dynamic role during various stages of the illness, so as to promote application break through EXO in precision medicine for AD.
Authors
- Shuo Zhang (ORCID: https://orcid.org/0009-0001-5671-6273)
Institutions
- Shenyang University (CN)
Publication Details
- Journal
- Theoretical and Natural Science
- Published
- 2025-07-20
- DOI
- https://doi.org/10.54254/2753-8818/2025.au25165
- Primary Topic
- Extracellular vesicles in disease
- Type
- article
- Field-Weighted Citation Impact
- 0.00