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- W2022703432 abstract "Individuals with Down’s syndrome (DS) develop neuropathological features similar to Alzheimer’s disease (AD) early in life, including dementia, accumulation of β-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 β-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." @default.
- W2022703432 created "2016-06-24" @default.
- W2022703432 creator A5006414984 @default.
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- W2022703432 date "2004-08-01" @default.
- W2022703432 modified "2023-09-27" @default.
- W2022703432 title "Behavioral and neurobiological markers of Alzheimer’s disease in Ts65Dn mice: effects of estrogen" @default.
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- W2022703432 doi "https://doi.org/10.1016/j.neurobiolaging.2003.10.010" @default.
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