BACE1-/- mice exhibit seizure activity that does not correlate with sodium channel level or axonal localization.

ABSTRACT:

Background

BACE1 is a key enzyme in the generation of the Abeta peptide that plays a central role in the pathogenesis of Alzheimer's disease. While BACE1 is an attractive therapeutic target, its normal physiological function remains largely unknown. Examination of BACE1-/- mice can provide insight into this function and also help anticipate consequences of BACE1 inhibition. Here we report a seizure-susceptibility phenotype that we have identified and characterized in BACE1-/- mice.

Results

We find that electroencephalographic recordings reveal epileptiform abnormalities in some BACE1-/- mice, occasionally including generalized tonic-clonic and absence seizures. In addition, we find that kainic acid injection induces seizures of greater severity in BACE1-/- mice relative to B

SUBMITTER: Hitt BD 

PROVIDER: S-EPMC2933677 | biostudies-literature | 2010 Aug

REPOSITORIES: biostudies-literature