A study by the UPV/EHU’s Department of Neurosciences establishes that astrocytes, which are the most abundant cells in the brain, are a critical element to take into consideration in Parkinson’s patients when the disease spreads and degree of neuronal degeneration intensifies:
We are all bound to have heard people talking about neurons at some point and about how important it is that they should function correctly to prevent the onset of some of the most common neurodegenerative diseases, such as Alzheimer’s or Parkinson’s. However, neurons are not the only ones in the brain and many of their functions are supported by other cells, the so-called glial cells. Among these great unknowns are the astrocytes, the most abundant cells in the brain and whose functions range from providing the neurons with nutrients and energy even supporting them.
Parkinson’s disease is related to the deterioration of dopaminergic-type neurons and the build-up of alpha-synuclein protein.
“Since neurons are the cells most affected by the disease, the vast majority of studies have, so far, focussed on understanding the events that lead to these cells dying off. So, given that very little is known about the role played by astrocytes in this disease, we decided to gear our research towards understanding whether these cells, which are crucially important in neuronal survival, contribute towards the development of Parkinson’s,” said Paula Ramos-González, a researcher in the UPV/EHU’s Department of Neurosciences.
Two lines of research were conducted in this work. Firstly, “we worked on rat cells, on neurons as well as on astrocytes, and we were able to establish that astrocytes are capable of contributing towards the transmission of the toxic alpha-synuclein protein —the protein that builds up in the brain of Parkinson’s patients— and encouraging neuronal death, suggesting a significant role is played by these cells in the spread of the disease”, explained the researcher.
Secondly, “in order to get closer to the reality, we opted for a second study using human cells. To do this, we generated astrocytes using the skin cells of Parkinson’s patients. Once these astrocytes had been generated, we compared various significant parameters between the astrocytes coming from healthy donors and the astrocytes with the mutation. To our surprise, we found that the astrocytes with the mutation were not only eight times smaller than the healthy astrocytes, they also generated high levels of oxidised proteins which may be toxic for the cells”, added Ramos-González.
Finally, “we thought it would be important to co-cultivate these astrocytes directly with neurons, and to analyse the effects that the cells with the mutation might have on neuronal survival. Using a technique that allows us to monitor the neurons individually, we saw that when they coexisted with the astrocytes with the mutation, the risk of neuronal death significantly increased, contrary to what happened when cultivating them along with healthy astrocytes”, she remarked.
The researcher stressed that “all these results suggest that dysfunctional astrocytes contribute towards the onset and spread of Parkinson’s by encouraging the neurodegenerative process that is typical of the disease. Although it is necessary to explore the subject further and study it in depth with new experiments, this study is proposing a new, possible therapeutic target designed to maintain the functionality of the astrocytes and open up a range of possibilities in terms of potential treatments in the future”.