Bee Venom as a Neuroprotective Agent in Parkinson's Disease
Rapid Response Innovation Awards, 2008
Based on a serendipitous obsrevation in one patient with Parkinsonís disease (PD), resaerchers wish to verify, in a pre-clinical model of the disease, whether bee venom and one of its components, apamine, are able to stop or slow the loss of dopaminergic neurons.
Models will be injected with two substances that induce the slow loss of dopaminergic neurons. In parallel, these models will be treated with bee venom or one of its components called apamine. Investigators believe the latter to be largely responsible for the beneficial effects on the survival of dopaminergic neurons. The behavior and the function of the neuronal system underlying the motor features of PD in the models will be analyzed.
Relevance to Diagnosis/Treatment of Parkinsonís Disease:†
Bee venom injections are used for desesentization treatments against allergies to bee venom. Usually, patients are injected once/monthly into the muscle. This treatment is safe, easy and cheap. If used in PD patients, it could represent either an adjunct to existing symptomatic therapies or even be used as a single therapy in the early disease course.
These researchers wish to know whether bee venom and/or its constituent, apamine, are able to slow or halt the disease process in Parkinsonís. They believe that these substances sustain the function of dopaminergic neurons, the neuronal cell type most severely affected in PD. This study would pave the way for a first clinical trial, which would be fairly easy to organize since bee venom injections are considered to be safe and simple.
Researchers verified, in a pre-clinical model of the disease, that bee venom and one of its components, apamine, are able to stop or slow the loss of dopaminergic neurons, the neuronal cell type most severely affected in PD. They showed that regular bee venom injections are indeed able to slow the degeneration of dopaminergic neurons in the PD model used, and that this effect is partially due to apamine. However, the complete list of compounds responsible for this effect and the mechanism(s) of action remain to be characterized.
Principal Investigator and neurologist at INSERM U 679, Pitiť-SalpÍtriŤre Hospital
Location: Paris, France