Astrocytes – cells that until only recently have been dismissed as merely brain “glue” – are becoming increasingly important and flexible tools in confronting a range of neurological disorders. New research shows that the right kind of astrocyte can restore order and rescue cells in brains ravaged by Parkinson’s disease.
The hallmark of Parkinson’s is the loss of brain cells responsible for producing dopamine, a chemical that plays an important role in the transmission of signals between nerve cells and the control of muscle movement. As these cells progressively die off during the disease the brain’s supply of dopamine steadily decreases, contributing to the motor control symptoms of Parkinson’s.
While many existing Parkinson’s therapies and much of the ongoing research strive to increase the brain’s supply of dopamine or preserve and/or replace dopaminergic neurons, it is becoming clear that there are significant limitations to this approach. Parkinson’s is a complex disease that impacts many aspects of brain function and contributes to the loss of cell populations beyond dopamine producing neurons, all of which contribute to the symptoms of the disease.
Using human brain tissue, biomedical geneticist Chris Proschel, Ph.D. and a team of URMC researchers were able to isolate glial precursors, cells that give birth to the brain’s astrocytes. Through careful manipulation of culture conditions and molecular signaling, the researchers were able to produce a class of astrocyte that behaves in a manner similar to the cells found in the developing brain. These cells turn out to be ideal for nurturing the growth and repair of nerve cells and creating a healthy environment in the brain.
When implanted into the brains of rats with Parkinson’s disease, the researchers observed that not only did populations of dopaminergic neurons recover, but so too did interneurons, cells that play an important role in information processing and movement control. The rats consequently regained normal motor control, erasing the symptoms of the disease.
You can read more about that study, which was published in the European journal EMBO Molecular Medicine, here.
Mark Michaud |
| 2 comments