the brain. The gene used leads to the production of an enzyme which helps to manage PD symptoms or protects the brain from further damage. One of the gene therapy based approach involves gene delivery of neurturin and glial cell line-derived neurotrophic factor (GDNF) to the putamen in patients with advanced Parkinson's disease. GDNF protects dopamine neurons in vitro and animal models of parkinsonism; neurturin is a structural and functional analogue of GDNF that protected dopamine neuron in animal model of the disease. Despite open-label trials showing benefits of continuous infusion of GDNF, the results were not confirmed in double-blind studies. This may be due to the distribution factor; the trophic factor was not distributed sufficiently throughout the target place. Another gene therapy of PD involved insertion of the glutamic acid decarboxylase (GAD) into the subthalamic nucleus. GAD enzyme controls GABA productions. In Parkinson's disease, the activity of both GABA efferents to the subthalamic nucleus and its target within the basal ganglia circuitry are affected. This strategy used adeno-associated viral vector (AAV2) to deliver GAD to the subthalamic nucleus. The trial was done to compare the effect of bilateral delivery of AAV2-GAD into the subthalamic nucleus with bilateral sham surgery in patients with advanced Parkinson's disease. The study showed the first success of randomised, double-blind gene therapy trial for a neurodegenerative disease and justified the continued development of AAV2-GAD for treatment of PD. Neuroprotective treatments Investigations on neuroprotection are at the forefront of PD research. Currently, no proven neuroprotective agents or treatments are available for PD. While still theoretical, neuroprotective therapy is based on the idea that certain neurons that produce dopamine and are susceptible to premature degeneration and cell death can be protected by the introduction of neuroprotective pharmaceuticals. This protection can occur before any symptoms manifest based on genetic risk, and also during early- or late-stage PD when other treatments have ceased their impact due to the progression of the disease. Accordingly, neuroprotective therapy seeks to delay the introduction of levodopa. Several molecules have been proposed as potential treatments. However, none of them has been conclusively demonstrated to reduce degeneration. Agents currently under investigation include antiapoptotics (omigapil, CEP-1347), antiglutamatergics, monoamine oxidase inhibitors (selegiline, rasagiline), promitochondrials (coenzyme Q10, creatine), calcium channel blockers (isradipine) and growth factors (GDNF). Preclinical research also targets alpha-synuclein. Selegiline Selegiline is in a group of medications called monoamine oxidase type B (MAO-B) inhibitors. Selegiline is