If the evaluation and forwarding of information is interrupted, the result can be the simultaneous firing of impulses. This overstimulation of the brain through electric impulses then leads to convulsive seizures, the typical symptom of epilepsy.

An NGFN project headed by Dr. Albert Becker focuses on epilepsies in the temporal lobe. This part of the brain is responsible e.g. for the processing of language or for the remembrance of items and faces.

Dr. Becker and his team have found 18 genes that are overactive in temporal lobe epilepsy – both in patients as well as in animal models. In the language of the scientists, overactive means that the information contained on this gene is read off more frequently than is normally the case. The result usually is that the respective protein, whose blueprint is enciphered in the gene, would be produced too great a quantity.

For example, the gene for the ion channel KCNK 1, located in the temporal lobe, is read off about three times as often in the brain of epilepsy patients as in healthy brains. The channel KCNK1 forms tiny pores in the cell membrane. Through these pores, potassium particles are channeled into the cell or discharged.

Synapsin II, another overactive gene, plays an important part in packaging biochemical messengers into vesicles, which could be described as shipping containers within cells.

Page 2: Overactive genes disarrange the information transfer in the nervous system.