| First Author | Baek H | Year | 2018 |
| Journal | Sci Rep | Volume | 8 |
| Issue | 1 | Pages | 17369 |
| PubMed ID | 30478329 | Mgi Jnum | J:269715 |
| Mgi Id | MGI:6271511 | Doi | 10.1038/s41598-018-35030-1 |
| Citation | Baek H, et al. (2018) Bee venom phospholipase A2 ameliorates Alzheimer's disease pathology in Abeta vaccination treatment without inducing neuro-inflammation in a 3xTg-AD mouse model. Sci Rep 8(1):17369 |
| abstractText | Alzheimer's disease (AD) is the most common form of dementia and is characterized by an imbalance between the production and clearance of amyloid-beta (Abeta) and tau proteins. Although vaccination against Abeta peptide results in a dramatic reduction in Abeta pathology in experimental mouse models, the initial clinical trial for an active Abeta vaccine was halted early due to the development of acute meningoencephalitis in 6% of the immunized patients, which likely involved a T-cell mediated pro-inflammatory response. In this study, we aimed to determine whether bee venom phospholipase A2 (bvPLA2) treatment would induce Tregs and ameliorate AD pathology without unwanted T cell-mediated inflammation. First, we investigated the effects of bvPLA2 on the inflammatory infiltration caused by Abeta vaccination. Inflammatory aggregates of CD3(+) T lymphocytes and macrophages were found in the brains and spinal cords of mice treated with Abeta. However, administration of bvPLA2 dramatically eliminated central nervous system inflammation following Abeta immunization. In AD model mice (3xTg-AD mice), bvPLA2 administration significantly ameliorated cognitive deficits and reduced Abeta burdens in the brains of Abeta-vaccinated 3xTg-AD mice. Additionally, we examined brain glucose metabolism using positron emission tomography with (18)F-2 fluoro-2-deoxy-D-glucose. Cerebral glucose uptake was considerably higher in the brains of Abeta-vaccinated 3xTg-AD mice that received bvPLA2 than those that did not. The present study suggests that the modulation of Treg populations via bvPLA2 treatment may be a new therapeutic approach to attenuate the progression of AD in conjunction with Abeta vaccination therapy without an adverse inflammatory response. |
