| First Author | Rothman SM | Year | 2012 |
| Journal | Neurobiol Aging | Volume | 33 |
| Issue | 4 | Pages | 830.e1-12 |
| PubMed ID | 21855175 | Mgi Jnum | J:188192 |
| Mgi Id | MGI:5439679 | Doi | 10.1016/j.neurobiolaging.2011.07.005 |
| Citation | Rothman SM, et al. (2012) 3xTgAD mice exhibit altered behavior and elevated Abeta after chronic mild social stress. Neurobiol Aging 33(4):830.e1-12 |
| abstractText | Chronic stress may be a risk factor for developing Alzheimer's disease (AD), but most studies of the effects of stress in models of AD utilize acute adverse stressors of questionable clinical relevance. The goal of this work was to determine how chronic psychosocial stress affects behavioral and pathological outcomes in an animal model of AD, and to elucidate underlying mechanisms. A triple-transgenic mouse model of AD (3xTgAD mice) and nontransgenic control mice were used to test for an affect of chronic mild social stress on blood glucose, plasma glucocorticoids, plasma insulin, anxiety, and hippocampal amyloid beta-particle (Abeta), phosphorylated tau (ptau), and brain-derived neurotrophic factor (BDNF) levels. Despite the fact that both control and 3xTgAD mice experienced rises in corticosterone during episodes of mild social stress, at the end of the 6-week stress period 3xTgAD mice displayed increased anxiety, elevated levels of Abeta oligomers and intraneuronal Abeta, and decreased brain-derived neurotrophic factor levels, whereas control mice did not. Findings suggest 3xTgAD mice are more vulnerable than control mice to chronic psychosocial stress, and that such chronic stress exacerbates Abeta accumulation and impairs neurotrophic signaling. |
