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 |
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Keywords
- Alzheimer's disease
- amyloid-β
- amyloid-β protein precursor
- audiogenic seizure
- Down syndrome
- metabotropic glutamate receptor 5
ASJC Scopus subject areas
- Psychiatry and Mental health
- Geriatrics and Gerontology
- Clinical Psychology
- Medicine(all)
Cite this
Alzheimer's disease and down syndrome rodent models exhibit audiogenic seizures. / Westmark, Cara J.; Westmark, Pamela R.; Malter, James S.
In: Journal of Alzheimer's Disease, Vol. 20, No. 4, 2010, p. 1009-1013.Research output: Contribution to journal › Article
}
TY - JOUR
T1 - Alzheimer's disease and down syndrome rodent models exhibit audiogenic seizures
AU - Westmark, Cara J.
AU - Westmark, Pamela R.
AU - Malter, James S.
PY - 2010
Y1 - 2010
N2 - 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.
AB - 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.
KW - Alzheimer's disease
KW - amyloid-β
KW - amyloid-β protein precursor
KW - audiogenic seizure
KW - Down syndrome
KW - metabotropic glutamate receptor 5
UR - http://www.scopus.com/inward/record.url?scp=77954546643&partnerID=8YFLogxK
UR - http://www.scopus.com/inward/citedby.url?scp=77954546643&partnerID=8YFLogxK
U2 - 10.3233/JAD-2010-100087
DO - 10.3233/JAD-2010-100087
M3 - Article
C2 - 20413855
AN - SCOPUS:77954546643
VL - 20
SP - 1009
EP - 1013
JO - Journal of Alzheimer's Disease
JF - Journal of Alzheimer's Disease
SN - 1387-2877
IS - 4
ER -