| First Author | Hunter CL | Year | 2004 |
| Journal | Neurobiol Aging | Volume | 25 |
| Issue | 7 | Pages | 873-84 |
| PubMed ID | 15212841 | Mgi Jnum | J:95707 |
| Mgi Id | MGI:3526830 | Doi | 10.1016/j.neurobiolaging.2003.10.010 |
| Citation | Hunter CL, et al. (2004) Behavioral and neurobiological markers of Alzheimer's disease in Ts65Dn mice: effects of estrogen. Neurobiol Aging 25(7):873-84 |
| abstractText | Individuals with Down's syndrome (DS) develop neuropathological features similar to Alzheimer's disease (AD) early in life, including dementia, accumulation of beta-amyloid, and irregular phosphorylation of tau proteins. Ts65Dn mice, an animal model of DS, provide a unique method to investigate the mechanisms related to AD-like symptoms in DS and possible therapeutic interventions. Ts65Dn mice undergo a decline in cholinergic phenotype and cognitive deterioration beginning at 6-8 months of age. In middle-aged female Ts65Dn mice, estrogen supplementation alleviated these cholinergic and cognitive impairments. The current study investigated AD-like markers and the effects of estrogen in male Ts65Dn mice. Estrogen treatment prior to behavioral testing did not improve cognitive deficits in 6-month-old male Ts65Dn mice, but decreased total and phosphorylated (pS199) tau in the entorhinal cortex compared to normosomic animals. Hippocampal beta-amyloid(1-42) levels were increased in Ts65Dn animals, regardless of estrogen treatment. These findings further support Ts65Dn mice as a model for specific AD-like symptoms, and demonstrate that estrogen treatment of this type does not improve the cognitive ability of male Ts65Dn mice. |
