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Volume 09
Journal of Alzheimers Disease & Parkinsonism
ISSN: 2161-0460
Epilepsy 2019
Parkinsons Congress 2019
August 29-31, 2019
JOINT EVENT
conferenceseries
.com
August 29-31, 2019 Vienna, Austria
&
5
th
International Conference on
Epilepsy & Treatment
5
th
World Congress on
Parkinsons & Huntington Disease
The effects of CLCN2 knockout on epileptic absence seizures
Navin Naik
University of Virginia, USA
E
pilepsy is a neurological disorder affecting about 1 percent of Americans. Epileptic seizures are caused by nerve
cell activity in the brain and can vary from being nearly undetectable to long periods of shaking. Idiopathic
generalized epilepsy includes a group of epileptic disorders that are believed to have a strong genetic basis. The
seizures of interest here are petit mal seizures, or absence seizures. Absence epilepsy is one of the most common
forms of childhood epilepsy. It is characterized by brief, frequent seizures and affects children from the ages of 4 to
early adolescence. Absence seizures are also characterized by generalized spike-and-slow wave electrical discharges
(SWD), which can be detected using electroencephalography (EEG). Due to the prevalence and comorbidities
associated with absence epilepsy, it is important to study it further. Based on research published in a 2003 paper
by Haug et al, we decided to examine the effects of a chloride channel gene CLCN2 in a mouse model. Data was
collected via EEG recordings of mice over a 5-day period. Two mouse models were used: wild-type mice and CLCN2
knockout mice. EEG recordings were scored for spike-and-wave discharges to determine seizure occurrence. Due
to time constraints, only limited data was obtained. This data confirmed the hypothesis that CLCN2 KO mice
would have increased seizures. However, the insufficient data prevented us from creating a significant conclusion.
Nevertheless, important procedural information was found to aid in future experiments.
J Alzheimers Dis Parkinsonism 2019, Volume 09