| First Author | Kuwabara Y | Year | 2014 |
| Journal | J Neurochem | Volume | 130 |
| Issue | 3 | Pages | 432-43 |
| PubMed ID | 24684630 | Mgi Jnum | J:214689 |
| Mgi Id | MGI:5603698 | Doi | 10.1111/jnc.12728 |
| Citation | Kuwabara Y, et al. (2014) Impairments of long-term depression induction and motor coordination precede Abeta accumulation in the cerebellum of APPswe/PS1dE9 double transgenic mice. J Neurochem 130(3):432-43 |
| abstractText | Alzheimer's disease (AD) is a neurodegenerative disorder that represents the most common type of dementia among elderly people. Amyloid beta (Abeta) peptides in extracellular Abeta plaques, produced from the amyloid precursor protein (APP) via sequential processing by beta- and gamma-secretases, impair hippocampal synaptic plasticity, and cause cognitive dysfunction in AD patients. Here, we report that Abeta peptides also impair another form of synaptic plasticity; cerebellar long-term depression (LTD). In the cerebellum of commonly used AD mouse model, APPswe/PS1dE9 mice, Abeta plaques were detected from 8 months and profound accumulation of Abeta plaques was observed at 18 onths of age. Biochemical analysis revealed relatively high levels of APP protein and Abeta in the cerebellum of APPswe/PS1dE9 mice. At pre-Abeta accumulation stage, LTD induction, and motor coordination are disturbed. These results indicate that soluble Abeta oligomers disturb LTD induction and cerebellar function in AD mouse model. |
