| First Author | Kong Y | Year | 2021 |
| Journal | Front Cell Dev Biol | Volume | 9 |
| Pages | 609908 | PubMed ID | 34277597 |
| Mgi Jnum | J:329964 | Mgi Id | MGI:6730928 |
| Doi | 10.3389/fcell.2021.609908 | Citation | Kong Y, et al. (2021) The Synaptic Vesicle Protein 2A Interacts With Key Pathogenic Factors in Alzheimer's Disease: Implications for Treatment. Front Cell Dev Biol 9:609908 |
| abstractText | Alzheimer's disease (AD), a serious neurodegenerative disease, is pathologically characterized by synaptic loss and dysfunction. Synaptic vesicle protein 2A (SV2A) is an indispensable vesicular protein specifically expressed in synapses and can be used as a biomarker for synaptic density. We found that the expression of SV2A was down-regulated in the hippocampus of AD patients, yet the relation of SV2A to other hallmarks of AD pathology such as amyloid precursor protein (APP), beta-amyloid (Abeta), and Tau protein is not thoroughly clear. In addition, SV2A colocalized with APP and was down-regulated at Abeta deposition. Moreover, we found that SV2A deficiency leads to a simultaneous increase in Abeta and Tau hyperphosphorylation, while SV2A overexpression was associated with downregulation of beta-site APP cleaving enzyme 1 and apolipoprotein E genes. In addition, evidence gained in the study points to the phosphatidylinositol 3-kinase signaling pathway as a possible mediator in SV2A regulation influencing the incidence and development of AD. With limited effective diagnostic methods for AD, a close interplay between SV2A and AD-related proteins demonstrated in our study may provide novel and innovative diagnostic and therapeutic opportunities. |
