Washington, Feb 10 (ANI): Scientists have discovered a molecular link between Parkinson's disease and defects in the ability of nerve cells to communicate.
The study, from The Montreal Neurological Institute and Hospital he Neuro - at McGill University, offers new insight into the mechanisms underlying Parkinson's disease, and could lead to innovative new therapeutic strategies.
Parkinson's is a neurodegenerative disease that causes muscle stiffness and tremor and prevents people from controlling their movements in a normal manner.
The disease is characterized by the degeneration and death of dopamine neurons in specific regions of the brain, causing neurological impairment. It is not known exactly what causes the death of these neurons.
Mutations in the parkin gene are responsible for a common inherited form of Parkinson's disease. To understand how a mutated parkin protein causes Parkinson's, researchers looked at where mutations are found on the gene and focused on understanding the function of region that is commonly mutated and searched for proteins that bind to this particular domain of the protein.
They identified that parkin binds to a protein called endophilin-A, which is central to the process of synaptic transmission, specifically synaptic vesicle trafficking.
Synaptic transmission is the process whereby one nerve cell communicates with another. It involves the release of neurotransmitters from a synaptic vesicle at the surface of the cell.
The neurotransmitter travels across the gap or synapse and is brought into (or endocytosed) the communicating neuron. Synaptic vesicles are spheres that transport and release neurotransmitters, the 'signal' required for the propagation of nerve cell signals across the synapse.
The binding protein, endophilin-A plays an important role in regulating synaptic vesicle endocytosis, which is the formation, as well as recycling of synaptic vesicles.
"One of the most consistent and intriguing findings associated with both dominant and recessive forms of Parkinson's, including those due to parkin mutations, have been defects in synaptic transmission, possibly related to altered synaptic vesicle endocytosis, recycling or release," Dr. Dr. Edward Fon said.
"Yet, until now, the molecular mechanisms involved have remained completely unknown. Thus, by linking parkin to endophilin-A, a protein at the heart of synaptic vesicle endocytosis and ecycling, our findings provide a molecular link between recessive Parkinson's genes and defects in synaptic transmission. This now gives us a whole new set of potential treatment targets," Dr. Fon added.
The study has been published in the prestigious journal Molecular Cell. (ANI)