Have you ever heard the claim, "You only use 10% of your brain"?  It's complete bullshit.  It's based on an underlying historical theory of how the brain functions called The Neuron Doctrine, a theory put forth in the late 1800s that neurons are the functional cells of the brain and responsible for all of the heavy lifting.  This led to 150 years of limiting brain research studying primarily neurons and neglecting the 'other 90% of the brain,' collectively referred to as 'glial' cells, Latin for 'glue.'  The incomplete Neuron Doctrine was propagated by a Spanish researcher, Santiago Ramon y Cajal, who was on a quest of perceived scientific superiority against his Italian scientific rival, Camillo Golgi.  Cajal believed the brain was a contiguous (touching or adjacent to) network of connected parts, and when he was able to show this continuity of the neuronal road map with a new staining method, he declared victory... to the detriment of the entire field of neurology.  Golgi, in comparison, believed the brain functioned more like a syncytium, or net, with continuity (uninterrupted and ceaseless).  Later recognition of the synapse, or space between two communicating neurons, became evident, and the idea that neurons were the primary powerhouse cells of the brain promulgated.

Research for the next 100-150 years was primarily focused on these neurons, and the rest of the brain cells were collectively termed 'glia,' despite a wide array of diverse functions.  Upon re-examination of Golgi and Cajal's theories, much of their disagreements appear to be semantic differences.  If you look at a textbook picture of a synapse, there are always two neurons budded up against each other, with a bevy of neurotransmitter and cellular activity occurring between them.  However, later research found the existence of multiple glial cells also surrounding the synapse, helping to clean up the milieu of chemicals and neurotransmitters, in conjunction with the neurons.  There is a continuous nature to this cellular picture as well, as all of these are floating around in a cellular goop, a fluid-filled space called the synaptic cleft.  Even the extensive astro-glial matrix (astrocytes are one type of 'glial cell' and have been shown to be interconnected with diverse cellular functions). Would you call a body of water continuous or contiguous?

Long story short, it really doesn't matter.  Cajal got so caught up in disproving Golgi and being scientifically superior that he extrapolated his work to most brain functions and neglected the impact and importance of glial cells.  The point here is that neurons took the front lines in terms of research for a long time, stunting our overall understanding of brain function.  Cajal could have corresponded with Golgi (who actually developed the original stain allowing him to prove his research) to develop a more full picture of brain development.  The scientific hubris and desire for certainty and academic recognition and accolades really set the field back, for nearly a century.  From the late 1800s until the mid-to-late 1900s, we didn't make huge strides in our understanding of neurodevelopmental and neurodegenerative conditions like autism, schizophrenia, bipolar disorder, epilepsy, Alzheimer's disease, Parkinson's, ALS, and more.

It took extensive research into the roles of glial cells, as well as differentiation of specific cell types, to expand our understanding of what's going on in the brain.  Now we've been able to bust several myths.  We know all 100% of our brain cells are important for good brain function.  We know neurons are not molded into their final form in childhood and some do regenerate and change significantly throughout life.  We know glia have much more diverse functions than just 'support,' 'nutrition,' and insulation, that they have major roles in changing how neurons function.  We now know neurons and glia signal to each other constantly, that glia are able to dictate what neurons do and how they function, that glia independently facilitate widespread macro-messages amongst their own network, and affect overall brain function.  If you're a city developer commissioning a network of roads and highways around your city, it's almost as if the construction workers are neurons, and their work is dictated by supervisors, or glia, with a more bird's eye view of the entire project and a bigger vision.

We now know a lot about glial cell capabilities.  On a very basic level, the ratio of glia:neurons is higher and higher amongst more intelligent and developed species, from 9:1 in humans, to 4:1 in chimpanzees, 3:2 in rodents, and 1:30 in basic leeches.  Also, most brain tumors are gliomas, showing that some glial cells actually function as stem cells and are able to regenerate neurons and other brain cell types.  Others contain their own electrical potential and are capable of intercellular communication via calcium wave propagation (thanks for sticking that tiny electrode into a rat brain Ann Cornell Bell and later research showing astrocyte stimulation led to an increase in calcium in the neuron next door neighbor).  Their calcium influence is necessary in order for neurons to release neurotransmitters... or maybe we should call them gliotransmitters.  It appears as if astrocytes process the incoming sensory information and instigate outgoing motor actions using neurons as tools, telling them what to do.  The real convincing work came in 2006, when Wegner et al isolated neurons in a petri dish and showed zero activity between them... however, when he sprinkled in some cortical astrocytes, life and communication between neurons was made possible.

What's the clinical fallout?  Well, one example is Alzheimer's disease research and the beta-amyloid hypothesis (which I actually found out after recording this that some of the research supporting that hypothesis was based on photoshopped images).  We've developed drugs that remove beta-amyloid from the brain... and they have next to no clinical impact (with significant risks) and appear to be just another pharmaceutical rollout with profit-focused goals.  It makes me think the deposition of the beta-amyloid protein is just the final end-product of a process that has an entirely different root cause.  Is it more likely that dysfunctional astrocytes, whose roles include removal of toxic by-products, fail to remove beta-amyloid, but once its deposited, it has done it's harm in disrupting the astroglial matrix of the brain?  That the decreasing ratio of regenerating glial cells to degenerating glial cells better explains the insidious onset and progression of so many dementias... that local or regional areas of the brain help to explain what we call Alzheimer's dementia (starting in hippocampus or memory center of the brain) vs Parkinson's (motor centers of the brain), and give insight into the overlap in symptoms and progression of the different dementias?  That, in ALS, glutamate washing over the neurons kills them... but whose responsibility, brain cell-wise, is it for taking in extra glutamate from the astroglial goop of the brain.  Not to mention that glial cells give a much better explanation for our ability to imagine things and come up with innovative thoughts and ideas (this series was significantly influenced by Andrew Koob's book, The Root of Thought).

Some of these conditions and questions are really complex and detailed.  The point of this series is to illuminate that we CANNOT anchor on our scientific theories.  We have to remain open to the likely reality that our theories about anything are incomplete.  It doesn't mean we're wrong, it doesn't mean we're right.  We just ARE.  We pursue science for the purpose of advancing our understanding of what's happening around us and within us, not for the primary goal of being recognized and getting accolades (though, of course, it does feel good to be recognized).  These ideas need to be at the forefront of every researcher's mission statement.  No matter what happens with any given bit of research, we all need to remain open to unimagined possibilities and influences, so we don't miss out on a hundred years-worth of potentially revealing data and information in the future. 

Hell, who am I kidding... I probably don't understand a fraction of a percent of how the brain actually functions and we'll all be laughed at by futuristic humans hundreds of years down the road... who will then be laughed at by futuristic humans thousands of years down the road (if we make it that far, of course).  And, all that is okay; our job is to embrace uncertainty, continue in our quest for scientific truth and understanding, and do what we can to discuss ideas with others in an open and considerate and engaged fashion, so maybe we develop pharmaceuticals or other tools that are ACTUALLY USEFUL to use humans.


“The Root of Thought” book, Andrew Koob


  1. https://www.frontiersin.org/articles/10.3389/fnhum.2018.00541/full

Mindfulness improves emotion regulation and executive control on bereaved individuals fmri study

            -fMRI shows slight decline in fronto-parietal network



Mindfulness and emotion regulation fMRI study

            -Increased activation in brain regions associated with emotion regulation, along with reduced activation in brain regions involved in processing of emotional valence and arousal. Specifically, Mindfulness group showed increased activation in DMPFC and other prefrontal regions as compared with basic group with reduced activity in regions involved in emotion processing during the perception of negative simuli in the R amygdala, parahippocampal, and insular regions



Functional brain changes during MBCT associated with Tinnitus Severity

            -FMRI shows decreases in functional connectivity among the DMN, cingulo-opercular network, and amygdala



The impact of mindfulness-based interventions on brain activity: a systematic review of fmri studies

            -Mindfulness a/w increased neural activation in the insula



Neuronal survival depends on EGFR signaling in cortical but not midbrain astrocytes, Wagner 2006



Deciphering the Astrocyte Reaction in Alzheimer’s Disease

Perez-Nievas 2018, Frontiers Aging Neuroscience