The development of new drugs for improving treatment of Alzheimers and Parkinsons disease is a step closer after recent research into how stem cells migrate and form circuits in the brain.
The results from a study by researchers at The University of Aucklands Centre for Brain Research may hold important clues into why there is less plasticity in brains affected by Parkinsons and Alzheimers disease, and links to insulin resistance and diabetes.
The major five-year project to understand how stem cells start and stop migrating in the brain has also helped to unlock the secrets of how stem cells migrate during development and in adulthood.
The study revealed new information on how connectivity between brain cells is improved or worsened, says senior study author, Dr Maurice Curtis who conceived and directed the research. The experiments were carried out at the Centre for Brain Research laboratories by Dr Hector Monzo. Collaborators included a director of the CBR, Distinguished Professor Richard Faull, Dr Thomas Park, Dr Birger Dieriks, Deidre Jansson and Professor Mike Dragunow.
We have begun testing new novel drug compounds that target how polysialic acid is removed from the cell in the hope of improving neuron connectivity, says Dr Curtis.
He explains that stem cells in the brain are immature brain cells that must migrate from their birthplace to a position in the brain where they will connect with other brain cells, turn into adult brain cells (neurons) and become part of the brains circuitry.
Even once the neuron has found its location, the neurons tentacles (or dendrites) need to forage to find other neurons to connect with to form circuits. This would be easy except that in the adult brain the cells are surrounded by a fairly rigid matrix (extracellular matrix) and so migration or foraging becomes almost impossible in this high friction environment.
The way the cell overcomes this friction is by placing large amounts of a special slippery molecule called polysialic acid-neural cell adhesion molecule onto the cell surface, says Dr Curtis. This allows the cell to migrate or forage with only a fraction of the friction it once had and this also reduces the energy requirements of the cell.
Once the cell has migrated to its destination, the slippery coating is removed and the cell becomes locked in place ready to connect with other cells. In the case of the dendritic foraging, the polysialic acid must be removed in order for the dendrite to connect with another cell (synapse formation).
We have known for at least 20 years that this process occurs but despite extensive studies by a number of groups internationally we have been in the dark about what controls this process, he says. Studies in my laboratory have demonstrated what happens to the slippery molecules once the cell no longer needs them.
Read more from the original source:
Stem cell research reveals clues to brain disease