Abstract
Amyloid-β protein precursor (AβPP) is overexpressed in Alzheimer's disease (AD), Down syndrome (DS), autism, and fragile X syndrome. Seizures are a common phenotype in all of these neurological disorders, yet the underlying molecular mechanism(s) of seizure induction and propagation remain largely unknown. We demonstrate that AD (Tg2576) and DS (Ts65Dn) mice exhibit audiogenic seizures, which can be attenuated with antagonists to metabotropic glutamate receptor 5 (mGluR5) or by passive immunization with anti-amyloid-β antibody. Our data strongly implicates AβPP or a catabolite in seizure susceptibility and suggests that mGluR5 mediates this response.
| Original language | English (US) |
|---|---|
| Pages (from-to) | 1009-1013 |
| Number of pages | 5 |
| Journal | Journal of Alzheimer's Disease |
| Volume | 20 |
| Issue number | 4 |
| DOIs | |
| State | Published - 2010 |
Keywords
- Alzheimer's disease
- Down syndrome
- amyloid-β
- amyloid-β protein precursor
- audiogenic seizure
- metabotropic glutamate receptor 5
ASJC Scopus subject areas
- Neuroscience(all)
- Clinical Psychology
- Geriatrics and Gerontology
- Psychiatry and Mental health
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Westmark, C. J., Westmark, P. R., & Malter, J. S. (2010). Alzheimer's disease and down syndrome rodent models exhibit audiogenic seizures. Journal of Alzheimer's Disease, 20(4), 1009-1013. https://doi.org/10.3233/JAD-2010-100087