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Title Bullet News - Progress for gene therapy in epilepsy
 
21 September 2010

In science, genes can be isolated from the DNA of one species (species I) and can be made to function in a completely different species (species II). Once the required gene has been sourced, it is 'added' to the nucleus of a weakened virus, which then multiplies, producing many copies of the gene. The virus particles are then injected into a specific group of cells in species II, taking the gene with them. The gene becomes incorporated into the DNA of the cells in species II and functions normally. A virus commonly used in gene therapy is the adeno-associated virus (AAV), because it is small and can infect a wide range of cells, but is not known to cause disease.

Neuropeptide Y (NPY) is a protein-like substance secreted by the hypothalamus (an important structure found deep within the brain that regulates several mechanisms including body temperature, hunger, thirst and fatigue). It (NPY) can act on a number of different types of receptor and is involved in a range of physiological processes, including the regulation of energy balance, memory and learning. NPY has also been shown to play a role in seizure suppression, by acting on a receptor known as Y2. Larger amounts of NPY and increased numbers of Y2 receptors are found in the brain in response to seizure activity.

    

Researchers at Lund University in Sweden, and elsewhere, have previously shown that it is possible to inject AVV particles carrying a gene designed to over-produce NPY into the hippocampus of animals with epilepsy; causing over-production of NPY in the hippocampus and a large degree of seizure suppression.

    

In their latest study, the team at Lund University wanted to compare the effects of Y2 receptor over-production with those of both Y2 and NPY over-production, by the hippocampus. They used the same method, but this time they used two groups of animals with temporal lobe epilepsy. Group one received a gene designed to over-produce Y2, whilst group two received genes that would cause over-production of both NPY and its Y2 receptor.

The team found that over-production of Y2 receptors by the hippocampus had marked seizure-suppressing effects, but that when both NPY and the Y2 receptor were over-produced, these effects were a lot greater.

These results are exciting, because if they are replicated in humans, gene therapy to increase Y2 receptor production by the hippocampus, alone or in combination with NPY, could be an alternative treatment for epilepsy in the future; particularly for people who are unresponsive to anti-epileptic drugs and are not suitable candidates for surgery.

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