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Updated: Jun 24, 2026
09:07
Electroconvulsive Seizures in Rats and Fractionation of Their Hippocampi to Examine Seizure-induced Changes in Postsynaptic Density Proteins
Published on: August 15, 2017
Amyloid beta-induced neuronal hyperexcitability triggers progressive epilepsy
Rimante Minkeviciene1, Sylvain Rheims, Marton B Dobszay
1A. I. Virtanen Institute, University of Kuopio, FIN-70211 Kuopio, Finland.
Summary
Alzheimer's disease causes seizures by altering neuronal function. Fibrillar amyloid-beta disrupts pyramidal cell excitability, leading to epileptiform activity in the brain.
Area of Science:
- Neuroscience
- Pathology
- Genetics
Background:
- Alzheimer's disease (AD) is linked to a higher risk of unprovoked seizures.
- The mechanisms driving seizure induction in AD remain unclear.
Purpose of the Study:
- To investigate the prevalence and underlying mechanisms of unprovoked seizures in a mouse model of Alzheimer's disease.
Main Methods:
- Video-electroencephalography (EEG) recordings in APdE9 mice and wild-type littermates.
- Patch-clamp electrophysiology to assess neuronal excitability.
- In vitro application of amyloid-beta (Abeta) species to brain slices.
Main Results:
- 65% of APdE9 mice exhibited unprovoked seizures, with 46% experiencing multiple seizures.
- Seizures correlated with altered neuronal membrane potentials and network hyperexcitability.
- Fibrillar amyloid-beta (proto-fibrils) induced neuronal depolarization and increased excitatory activity.
Conclusions:
- Fibrillar amyloid-beta is a key factor in AD-associated epileptiform activity.
- Altered neuronal membrane properties and hyperexcitability contribute to seizures in AD.
- This study elucidates a mechanism linking amyloid pathology to seizures in Alzheimer's disease.
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