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Back To Blog > Our Brain – More Than Just Neurons

This post is by guest blogger Matthew Savage 

When we think about the nervous system, we often just think about neurons. However, we have just as many non-neuronal cells as neuronal cells in the brain. And in some regions, neurons are outnumbered by glial cells, once thought to be just the “glue” of the brain. For example, the cerebral cortex has approximately 16 billion neurons but 61 billion non-neuronal cells. Studies have found that this higher brain functioning region, as well as many areas of the brain, are heavily influenced by glial cells which aid in the regulation of normal brain function. The extent of glial involvement in brain structure and function has been heavily researched over the last few years, and a strong body of literature notes that glial cells are vitally important to our brains. Dysfunction in these cells can be as disastrous as neuronal death, leading to a whole host of brain disorders and degenerative conditions.

What are “glial cells”

Our brain is full of neurons, cells which fire off communication signals and which dictate how we think and behave. Glial cells, which include Astrocytes, Oligodendrocytes, Ependymal and Microglia in the brain, are involved in a variety of important functions, including supporting, protecting and nourishing the brain. When glial cell functions are disrupted, this contributes to a number of neurodegenerative conditions and brain disorders such as Parkinson’s disease (PD) as well as contributing to the pathophysiology of depression.


Astrocytes are the most populous glial subtype (Booth, 2017) and play vital roles in maintaining the blood brain barrier (covering 95% of the BBB), providing structural support, regulating iron, nutrient and dissolved gas concentrations, as well as absorbing and recycling neurotransmitters by actively clearing the synapses. They are vital for maintaining neuronal health by providing metabolic and structural support and blocking the spread of toxic signals to surrounding tissue when an immune response is initiated by microglia (Wang et al., 2015). Astrocyte disfunction is a major contributor to neuroinflammation in conditions such as Parkinson’s disease and this contributes to neurodegeneration. This has been shown in multiple clinical and preclinical studies, with disruption to astrocyte immune responses leading to disease states. For example, Iliff et al. (2014) amongst numerous others have found that an astrocytic inflammatory state in mice resulted in mis-localisation of AQP4, a membrane bound protein found in the feet of astrocytes, potentially offering a common mechanism between injury, inflammation and glymphatic failure. Similar disruption has also been found to be a major contributor to major depressive disorder and potentially bipolar disorder.


Microglia are the primary immune cells of the brain, reacting to pathogens, injury or damage. They alert cells such as astrocytes to take action and protect the brain following injury. When this function runs smoothly, microglia contribute to an effective protection strategy for the brain, working together to clear the brain of anything unwanted. However, overactive microglia over extended periods of time can lead to accumulations in the brain, levels of inflammation that are higher than required and this can kill brain cells. This is a negative consequence of glial cell dysfunction, and this increase in inflammation is a contributing factor to neurodegeneration. In addition to this, many gene alterations that are associated with a number of psychiatric disorders including schizophrenia, autism spectrum disorder and Alzheimer’s are highly expressed in microglia.


The final glial cell to be examined are the Oligodendrocytes. These are supportive cells found in the central nervous system (CNS) and generate lipids which are utilised by the brain to myelinate axons, aiding in rapid signal transmission in white matter. They also provide metabolic support to neurons in grey matter. An understanding of Oligodendrocyte functions in myelination has led to further understanding of conditions such as mood disorders and neurodegenerative conditions as disturbed myelination can cause a whole heap of problems.

Why is it important we understand glial cells?

Now that we understand that glial cells are more than just “glue”, more treatments targeting these cells can be developed. At this moment, new technologies need to understand the principles of treating brain disorders, such as how specific cells contribute to these disorders and new modalities can be generated from increased understanding of the computations of the brain. Research may focus on finding cures for conditions whereby defective cells and neuronal circuits could be corrected and reconfigured. For example, research suggests that a lack of dopamine is a major contributor to Parkinson’s disease. Glial cells are overactivated by dopaminergic neurons that are in trouble, calling to glial cells for support. This overactivation leads to inflammation and degradation of these neurons and eventually, cell death. Parkinson’s disease therapy currently focuses on the alleviation of symptoms but, it is hoped with the use of Optogenetics and fMRI (functional magnetic resonance imaging), it may be possible to reactivate defective dopamine producing cells or to stop glial inflammation and thus provide a potential cure for the condition. Further understanding of gene expression in these cells and how they interact is also vitally important to the future of research in psychiatric disorders, opening up more opportunities for treating conditions such as schizophrenia and major depressive disorder.

About Matt Savage

Matthew Savage has an MSc in Psychology, is a qualified personal trainer, and has worked within the field of cognitive rehabilitation for 5 years. He is an FA qualified football coach, with a keen interest in moral behaviour and wellbeing within team sports. Matthew is also one of our Mental Health Triage Practitioners. 


Booth, H., Hirst, W. D., & Wade-Martins, R. (2017). The Role of Astrocyte Dysfunction in Parkinson's Disease Pathogenesis. Trends in neurosciences. 40(6), pp. 358–370. DOI: 10.1016/j.tins.2017.04.001

Gerhard, A., Pavese, N., Hotton, G., Turkheimer, F., Es, M., Hammers, A., Eggert, K., Oertel, W., Banati, R.B., Brooks, D.J. (2006). In vivo imaging of microglial activation with [11C](R)-PK11195 PET in idiopathic Parkinson's disease. Neurobiology of Disease. 21(2). Pp. 404-412. DOI: 10.1016/j.nbd.2005.08.002

Iliff JJ, Chen MJ, Plog BA, Zeppenfeld DM, Soltero M, Yang L, Singh I, Deane R, Nedergaard M. Impairment of glymphatic pathway function promotes tau pathology after traumatic brain injury. J Neurosci. 2014 Dec 3;34(49):16180-93. doi: 10.1523/JNEUROSCI.3020-14.2014. PMID: 25471560; PMCID: PMC4252540.

Hu, X., Li, P., Guo, Y., Wang, H., Leak, R. K., Chen, S., Gao, Y., & Chen, J. (2012). Microglia/macrophage polarization dynamics reveal novel mechanism of injury expansion after focal cerebral ischemia. Stroke. 43(11). pp. 3063–3070. DOI: 10.1161/STROKEAHA.112.65965

Wang, Q., Liu, Y., & Zhou, J. (2015). Neuroinflammation in Parkinson's disease and its potential as therapeutic target. Translational neurodegeneration, 4(19). DOI: 10.1186/s40035-015-0042-0



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