Health

The Brain’s Breaking Point: What Really Happens After a Concussion

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Imagine an athlete taking a hard hit during a game. They seem fine—no visible injury on a brain scan—but beneath the surface, a silent storm is unfolding. The impact triggers a neurometabolic cascade, a chain reaction that disrupts the brain’s delicate balance. Ions flood in and out of neurons, and a surge of glutamate—a key neurotransmitter—fires indiscriminately, setting off a wave of cellular chaos. To restore order, the brain scrambles to pump ions back into place, demanding enormous amounts of energy. But here’s the problem: blood flow remains restricted, creating a metabolic crisis where the brain is starving for fuel just when it needs it most.

In the following hours and days, this energy imbalance lingers, leaving the brain in a fragile state. The axons—the brain’s communication highways—are stretched and damaged, slowing down thought and reaction time. Neurotransmitters misfire, affecting mood, memory, and cognitive function. Meanwhile, inflammation and oxidative stress take their toll, making the brain more vulnerable to further injury. If a second concussion happens before the brain fully recovers, the damage can be exponentially worse, with a higher risk of long-term impairment. [1]

 

The Role of Age in Concussion Recovery

Recovery from a concussion isn’t the same for everyone. Age plays a significant role in how the brain responds to injury. There’s ongoing debate about whether younger or older individuals are more vulnerable. Children’s brains are still developing, which may make them more susceptible to injury—but also more resilient in terms of recovery. Some studies suggest that children aged 10-14 have the highest rates of emergency visits for sports-related concussions (SRCs), yet their long-term outcomes may not necessarily be worse than adults. However, repeated concussions during this critical developmental stage can lead to longer recovery times and exacerbate symptoms. [2]

On the other hand, older adults face unique challenges in concussion recovery. Research suggests that multiple concussions can accelerate cognitive decline and increase the risk of mild cognitive impairment (MCI) and Alzheimer’s disease. Former athletes who have suffered repeated concussions often show subtle deficits in attention and motor control—effects that may not be immediately noticeable but can surface later in life. A study comparing high school and college athletes found no major difference in concussion severity, although younger athletes took slightly longer to return to baseline. [2]

[3]

The Search for Biomarkers

With concussions being difficult to diagnose through traditional imaging, researchers are turning to biomarkers—biological indicators that can help detect and track brain injury. Several key biomarkers have been identified:

Astroglial Injury: Elevated levels of S100β and glial fibrillary acidic protein (GFAP) indicate astrocyte activation due to brain trauma. [4]

Neuronal Injury: Neuron-specific enolase (NSE) and ubiquitin carboxyl-terminal hydrolase L1 (UCH-L1) are released when neurons are damaged, with UCH-L1 levels being linked to intracranial lesions seen on CT scans.

Axonal Injury: Structural proteins like Alpha-II-spectrin, tau, and neurofilament light protein (NFL) provide insight into axonal damage, with tau deposits being particularly concerning due to their association with Alzheimer’s disease. [4]

 

[5]

 

The Long-Term Impact

For many, the symptoms of concussion—headaches, dizziness, and light sensitivity—feel eerily similar to migraines. This overlap isn’t a coincidence; research suggests that the same metabolic dysfunction seen in concussion may also underlie migraines. [6] More concerning is the potential for repeated concussions to contribute to chronic neurodegeneration, with evidence linking multiple head injuries to conditions like chronic traumatic encephalopathy (CTE).

 

Scientists are now using advanced imaging and biomarkers to track these changes in real-time, searching for ways to better diagnose, treat, and prevent long-term damage. As we learn more, one thing is clear: the effects of a concussion don’t end when the symptoms fade—what happens in those critical early days may set the stage for brain health years down the line.

Learn more about the science behind concussions at The New Neurometabolic Cascade of Concussion

[1]

C. Giza and D. A. Hovda, “The New Neurometabolic Cascade of Concussion,” Neurosurgery, vol. 75, no. Supplement 4, pp. S24–S33, Oct. 2014, doi: 10.1227/NEU.0000000000000505.

[2]

A. Hoge, J. Vanderploeg, M. Paris, J. M. Lang, and C. Olezeski, “Emergency Department Use by Children and Youth with Mental Health Conditions: A Health Equity Agenda,” Community Ment Health J, vol. 58, no. 7, pp. 1225–1239, Oct. 2022, doi: 10.1007/s10597-022-00937-7.

[3]

Concussion Infographics & Fact Sheets. [Online]. Available: https://biausa.org/public-affairs/media/concussion-awareness-infographics

[4]

Papa, “Potential Blood-based Biomarkers for Concussion,” Sports Medicine and Arthroscopy Review, vol. 24, no. 3, pp. 108–115, Sep. 2016, doi: 10.1097/JSA.0000000000000117.

[5]

S. Ghaith et al., “A Literature Review of Traumatic Brain Injury Biomarkers,” Mol Neurobiol, vol. 59, no. 7, pp. 4141–4158, Jul. 2022, doi: 10.1007/s12035-022-02822-6.

[6]

Sachdev and M. J. Marmura, “Metabolic Syndrome and Migraine,” Front. Neur., vol. 3, 2012, doi: 10.3389/fneur.2012.00161.

Health

Rethinking Concussion Protocols: Are We Doing Enough to Protect Athletes?

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Concussion protocols in sports are designed to protect athletes and prevent long-term brain damage. However, many athletes are still returning to play before they are fully recovered. Current protocols rely heavily on self-reported symptoms and subjective assessments, which can lead to players downplaying their injuries in order to compete​.1 As research determines the long-term risks of concussions, it’s time to reevaluate how we assess and manage these injuries.

The Limitations of Current Concussion Protocols

Concussion protocols vary across sports and organizations, often including sideline assessments, symptom checklists, cognitive testing, and gradual return-to-play (RTP) guidelines.1 However, key problems remain:

  • Self-reported symptoms are unreliable – Studies show that symptoms alone do not accurately identify all concussed athletes or determine full recovery.1 Athletes may underreport symptoms to avoid being sidelined​.
  • Subjective assessments create inconsistencies – Tests like the Sport Concussion Assessment Tool (SCAT) rely on athlete-reported symptoms, which can be influenced by external pressures and personal motivation to compete​.

Because of these limitations, athletes may unknowingly return before their brain has fully healed, increasing the risk of repeat concussions and long-term consequences​.

The Effects of a Concussion

Concussions can trigger a wide range of effects within the brain. Figure 1 illustrates the complex cascade of events that follow this type of injury.2 The process begins with an influx of cations, such as sodium and calcium. This forces neurons to increase energy production in the form of ATP. This increased activity quickly reduces the neuron’s resources, leading to an energy crisis.

As the cell works to restore this cation balance, more issues occur. The excessive production of ATP generates oxidative stress, which compromises the integrity of the cell membrane.3 The influx of calcium activates proteases enzymes that break down proteins which can result in protein loss within the cell. These disruptions can lead to axonal injury and cell death.2

Figure 1. Neurometabolic cascade of events that can occur after a concussion.2

This cascade of events within the neuron can lead to a variety of symptoms. Table 1 provides a detailed overview of these symptoms and their connection to the affected pathophysiological processes.

Table 1. Symptoms related to their affected pathophysiological process.2

A more detailed explanation of the cascade of effects caused by concussions can be found in this article.

The Science of Recovery and the Impact of Repeat Injuries

While it may seem that the symptoms are gone, the brain remains vulnerable​. Returning too soon can lead to:

  • Second-impact syndrome – A condition where a second concussion occurs before the first has healed.
  • Chronic traumatic encephalopathy (CTE) – A degenerative brain disease linked to repeated head trauma.
  • Long-term cognitive impairment – Problems such as memory and behavioral issues.

Research confirms that even after successful completion of a graduated RTP protocol, athletes may still be at a higher risk of neurological and musculoskeletal injuries​.1 More measures are needed to track recovery.

Improving Concussion Protocols

Advancements in brain imaging and neurocognitive research can offer promising ways to enhance concussion management. Key improvements for concussion protocols could include:

  • Objective diagnostic tools – Tests like biomarker analysis, diffusion tensor imaging (DTI), and functional MRI (fMRI) can provide more accurate assessments of brain recovery​.2
  • Stronger return-to-play goals – Rather than relying solely on self-reports, RTP should incorporate standardized neurocognitive assessments that detect lingering impairments​.
  • Education – Athletes, coaches, and medical professionals should prioritize brain health over competition. RTP decisions should be made with long-term well-being in mind.

Beyond Sports: Why Better Concussion Protocols Matter for Everyone

Concussion management isn’t just a concern for professional athletes. It affects youth sports, military personnel, and everyday individuals. Improved protocols could:

  • Protect young athletes from long-term cognitive issues.
  • Help military veterans reduce the risk of neurodegenerative diseases.
  • Improve workplace and recreational injury management to prevent lasting damage.

If we continue relying on outdated or lenient concussion protocols, are we prioritizing competition over health? With advancements in science and technology, we have an opportunity to develop more accurate, evidence based concussion management strategies. It’s time to rethink our approach and ensure we are truly protecting those at risk.

Footnotes:

(1)      Wellm, D.; Zentgraf, K. Diagnostic Tools for Return-to-Play Decisions in Sports-Related Concussion. J Concussion 2023, 7. https://doi.org/10.1177/20597002231183234.

(2)      Giza, C. C.; Hovda, D. A. The New Neurometabolic Cascade of Concussion. Neurosurgery 2014, 75, S24–S33. https://doi.org/10.1227/NEU.0000000000000505.

(3)      Hong, Y.; Boiti, A.; Vallone, D.; Foulkes, N. S. Reactive Oxygen Species Signaling and Oxidative Stress: Transcriptional Regulation and Evolution. Antioxidants. Multidisciplinary Digital Publishing Institute (MDPI) March 1, 2024. https://doi.org/10.3390/antiox13030312.

 

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AI: The Game Changer in Concussion Diagnosis

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The Hidden Danger of Concussions in the NFL – The Cherokee Scout

Concussions are one of the most common yet misunderstood brain injuries. And they don’t just affect professional athletes—students, military personnel, and everyday people suffer concussions from falls, car accidents, and sports injuries. And while many assume concussions are easy to diagnose, their symptoms can be subtle, delayed, or mistaken for other conditions.

But here’s the problem: traditional concussion diagnosis relies heavily on subjective symptom reporting and outdated tests, leading to misdiagnoses and long-term health risks. Many people go undiagnosed, putting them at risk for chronic traumatic encephalopathy (CTE), memory loss, and cognitive decline. [1]

Therefore, AI is stepping in as a game-changer, offering faster, more accurate concussion detection that could revolutionize brain health. But, in what ways? Let’s read more!

1. Faster And More Accurate Diagnosis

Unlike traditional methods that rely on a doctor’s judgment, AI can analyze large amounts of brain data quickly, improving accuracy. AI models can scan MRI and CT images, detecting patterns that even trained professionals might miss! This means fewer misdiagnoses and faster treatment.

Figure 1. This scan demonstrates the use of fMRI and AI to decode language signals in the brain [2]

2. Tracking Recovery in Real-Time

Concussions don’t just disappear overnight—they require careful monitoring. AI-powered apps and wearables can track symptoms over time, alerting doctors when a patient isn’t healing properly. This is especially useful for athletes and soldiers, helping them avoid returning to activity too soon. [3]

3. Reducing Long-Term Brain Damage

Early detection is crucial. AI can identify subtle signs of brain trauma long before they become serious, helping doctors intervene early and prevent lasting damage. This could mean fewer cases of CTE and a better quality of life for concussion patients.

The Bigger Picture: AI and The Future of Brain Health

Future in Mental Health: How AI is Personalizing Treatment Plans
Figure 2. This diagram demonstrates the different advancements AI can be expanded towards. [4]

AI’s impact goes beyond concussions. The same technology used to diagnose brain injuries could be applied to mental health, neurodegenerative diseases, and stroke detection. Cool, right?  But with these advancements come ethical concerns—how do we ensure AI diagnoses are reliable? Who is responsible if AI makes a mistake?

As AI continues to shape the future of medicine, it’s important to ask: How can we use this technology responsibly while maximizing its benefits?

AI is changing the way we detect and treat concussions, making diagnosis faster, monitoring more precise, and recovery safer. And as technology evolves, it has the potential to protect millions from long-term brain damage. But responsibility and accountability is absolutely critical—we need to ensure AI is accurate, accessible, and ethically used.

Therefore, the future of concussion care isn’t just about better technology—it’s about how we use it to improve lives. Will AI redefine brain health as we know it? Will AI be the next  ultimate game changer in the future of medicine? The answer is closer in time than we think!

Resources

[1] Mayo Clinic. (2023, November 18). Chronic traumatic encephalopathy – Symptoms and causes. Mayo Clinic. https://www.mayoclinic.org/diseases-conditions/chronic-traumatic-encephalopathy/symptoms-causes/syc-20370921

[2] Hamilton, J. (2023, May). A decoder that uses brain scans to know what you mean — mostly. NPR. https://www.npr.org/sections/health-shots/2023/05/01/1173045261/a-decoder-that-uses-brain-scans-to-know-what-you-mean-mostly

[3] Haffeman, D. (2015). New ResearchKit App to Track Concussions in NYU Langone Study. NYU Langone News. https://nyulangone.org/news/new-researchkit-app-track-concussions-nyu-langone-study

[4] Singh, G. (2024, December 9). Future in Mental Health: How AI is Personalizing Treatment Plans. Resources. https://www.knowledge-sourcing.com/resources/thought-articles/future-in-mental-health-how-ai-is-personalizing-treatment-plans/

 

 

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Photophobia: The Fear of Light After TBI’s

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PHOTOPHOBIA

Although photophobia literally means to have a ‘fear of light’, it actually refers to pain or discomfort caused by light exposure.

This is a neuro-ophthalmological disorder, which means the optic nerves are affected along with the brain. So, even though eye disorders commonly involve light sensitivity, photophobia can be caused by a variety of things.

Photophobia is one of the most common ocular conditions that occur with tension headaches, migraines, or TBI’s (Traumatic brain injury’s).

TBI’s (Traumatic Brain Injury)

Photophobia is one of the most common symptoms of concussions and TBI’s. TBI produces cognitive symptoms such as dizziness, vertigo, nausea, irritability, cognitive delays, and vision related symptoms to light-sensitivity. About 40% of individuals with brain injuries experience sensitivity to light. But, Light sensitivity can show up post-concussion or 6 months to even years after the concussion occurred.

Cranial Nerve 5- trigeminal CN V

The star of the show in pain processing within the head and eyes is cranial nerve five (the trigeminal nerve), the largest cranial nerve. The trigeminal nuclei and nerves play a crucial role in moderating pain, particularly in the eyes and head.

The trigeminal ganglion houses the ophthalmic branch (V1), which is primarily responsible for transmitting pain signals from the cornea, conjunctiva, sclera, and uvea–these structures are extremely sensitive to pain.The trigeminal nerve is an essential player in processing sensory information from the face and head.

When pain is experienced, it is often linked to the release of (CGRP) Calcitonin gene-related peptide. This peptide is released in response to stimulation from the trigeminal nerve and plays a critical role in the pain signal transmission to the brain. CGRP is located in the trigeminals ganglion, which is triggered by stress, brain vessels, and or inflammation.

Figure 2, The CGRP pathway in response to migraines within CN V

What Causes Photophobia in TBI’s?

With TBIs, photophobia (light sensitivity is usually caused by injury to the thalamus, preventing it from getting oxygen. This disruption impairs its function, leading to heightened sensitivity to light. But, in a TBI light sensitivity could mean dysregulation in one or multiple areas of the brain. The problem isn’t always isolated.

This creates a symptom cascade, where an issue in one area can trigger problems in others area. Dysfunction in the visual process could possibly affect focus, balance, or overall symptoms which creates a harder recovery process.

Thalamus

The thalamus is in charge of relaying sensory information to the brain. It is crucial for directing sensory signals, when a TBI occurs the process is disrupted.

The dysregulated mechanism that occurs is neurovascular coupling, which happens in the brain and retina. When communication pathways are faulty, neurons and blood vessels start malfunctioning and there isn’t always enough oxygen to be used.

As a result, patients experience light sensitivity in order to minimize their sensory overload and are recommended to stay in dark rooms. This reduces the amount of visual input letting the brain rest and recover

Autonomic Nervous System

The autonomic nervous system (ANS) is in charge of involuntary system, which involves functions like heart rate, breathing, and digestion Within light sensitivity, pupils dilate more than needed in a post concussion scenario causing exposure to light causing sensitivity. The dysregulation in the ANS causes abnormal pupil responses.

Vestibular System

The vestibular system involves the inner ear, sight, and touch. Dysfunction in this area causes the body to become off balance, leading to dizziness and vertigo. When the Vestibular system and visual system disagree, this increases optic sensitivity–which in turn creates an overload of sensory information.

Superior Colliculus

The superior colliculus is in charge of visual mapping and coordination, aiding in detecting and locating visual and audio stimuli. This contributes motor functions to orient the head and eyes toward or away from a stimulus. This is described as a looming stimulus which can be perceived as a threat from an object moving towards you and initiates a response from fear. For example a snake would be processed in the superior colliculi and  initiate a motor response which would orient an individual away from the snake, as the brain perceives it as dangerous. This can occur without eye movements as an instinct response.

Photophobia in TBI’s

Therefore, Photophobia in TBI’s is involved in several structures including thalamus, ANS, vestibular system, and superior colliculus. Light sensitivity is commonly found as a system of ocular disorders, in TBI’s it is a neurological dysfunction. This dysfunction occurs by dysregulation in sensory processing, such as lack of oxygen supplied to the brain or the miscommunication between sensory and visual pathways which increase light sensitivity.

CN V, The trigeminal nerve is responsible for transmitting these pain signals after TBI occurs. With the involvement of the CGRP pathway, the trigeminal nerve is responsible for a cascade of symptoms depending on the brain structure that is affected. Understanding photophobia in TBI’s in important for deciding treatment, limiting sensory input, and understanding multi-system dysfunction.

 

Footnotes:

Abusamak, Mohammad, and Hamzeh Mohammad Alrawashdeh. “Post-Concussion Syndrome Light Sensitivity: A Case Report and Review of the Literature.” Neuro-Ophthalmology 46, no. 2 (n.d.): 85–90. https://doi.org/10.1080/01658107.2021.1983612.

Grossman, Elan J., and Matilde Inglese. “The Role of Thalamic Damage in Mild Traumatic Brain Injury.” Journal of Neurotrauma 33, no. 2 (January 15, 2016): 163–67. https://doi.org/10.1089/neu.2015.3965.
Grossman, Ela

n J., and Matilde Inglese. “The Role of Thalamic Damage in Mild Traumatic Brain Injury.” Journal of Neurotrauma 33, no. 2 (January 15, 2016): 163–67. https://doi.org/10.1089/neu.2015.3965.

russ. “Light Sensitivity After a Brain Injury.” Optometrists.Org (blog). Accessed February 8, 2025. https://www.optometrists.org/vision-therapy/neuro-optometry/vision-and-brain-injuries/traumatic-brain-injury-and-neuro-optometry/light-sensitivity-after-a-brain-injury/.
Staff, By. “Neuroimaging Shines Light on Chronic Ocular Surface Pain, Photophobia.” Accessed February 10, 2025. https://www.reviewofoptometry.com/article/neuroimaging-shines-light-on-chronic-ocular-surface-pain-photophobia.
Health

Why Your Axons Matter After a Concussion & How It Could Impact Post-Concussion Healthcare Plans

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Have you ever had a concussion? Whether it be due to a sports injury or fall, concussions are one of the most common mild traumatic brain injuries (mTBIs), and the way your body handles them can differ based off your age, genetics, and the frequency in which you suffer TBIs. (Giza & Hovda, 2014).

This can make determining when you’ve recovered from a concussion difficult, but luckily, a lot is already known regarding how neurons are impacted and work to recover from concussions. As seen in Figure 1 below, mTBIs cause an influx of cations into neurons, inducing an energy crisis where ATP-requiring pumps shift into overdrive, eventually causing the sequestration of calcium within cellular mitochondria. This causes the mitochondria to become dysfunctional, thereby preventing the energy powerhouse of the cell from doing its job. Thus, restoration of ATP amounts is needed to recovery from a concussion (Giza & Hovda, 2014). For a deeper dive into the effects of mTBI on a neuron illustrated in Figure 1, click here.

Figure 1 – What occurs in a neuron after a mild traumatic brain injury (mTBI), such as a concussion (Giza & Hovda, 2014).

Axonal Regeneration

Aside from the need to restore the amount of ATP within a neuron to what is needed to fuel neuronal machinery, the regeneration of a neuron’s axon is vital to neuronal regeneration. Membrane lipids, specifically phospholipids, glycolipids, and cholesterol, make up a large part of axons. As seen in Figure 2, normal axon growth involves these newly synthesized lipids being transported from a neuron’s cell body to an axon’s growth cone, where lipids fuse with the acceptor membrane and expand the membrane (Roy & Tedeschi, 2021).

Figure 2 – this is an illustration of the growth cone that forms and lengthens an axon during neuron development/membrane expansion. (Roy & Tedeschi, 2021).

After severing of an axon, rapid sealing of disrupted membrane is necessary to restore the integrity of the axonal compartment. As seen in Figure 3, this involves phospholipids inserting themselves to create a new membrane in the area where the axon is severed, creating a new growth cone by restoring the axonal lipid bilayer. Not explicitly seen in Figure 3 but needed are glycolipids, which allow specific signal transduction and contribute membrane stability to axons, and cholesterol, which makes up a large component of the myelin sheath around axons that speeds of signal transmission (Roy & Tedeschi, 2021). Since membrane lipids are needed in axonal, and therefore neuronal, regeneration post-concussion, research into neuronal lipid homeostasis re-establishment has potential to progress society’s approach to treating concussions. More specifically, the ingestion of dietary lipids is a field of study being investigated as a route to treat concussions (Giza & Hovda, 2014).

Figure 3 – the top illustration shows how phospholipids made up the lipid bilayer of the neuronal membrane and what occurs if that membrane is disrupted, like during mTBIs. The bottom illustration displays what the myelin sheath and axonal membrane look like immediately after a TBI and then during axonal regeneration (Roy & Tedeschi, 2021).

Barriers to Understanding

But despite our knowledge of how phospholipids, glycolipids, and cholesterol contribute to axonal regeneration, current research has shown that administration of cholesterol-lowering drugs has conflicting impacts on axonal membrane and myelin sheath regeneration (Roy & Tedeschi, 2021). This challenge is significant in the field of TBI recovery because both the axonal membrane and myelin sheath, which contain cholesterol, are integral parts of a neuron in propagating an electrochemical signal and allowing efficient neuronal communication. Also, it begs the question: do other membrane lipid-altering drugs have conflicting impacts on neuronal regeneration?

Future Research & Its Potential Impact in Medicine

Therefore, current research into if and how administration/ingestion of dietary fatty acids can promote axon regeneration is being done, but it must be advanced. Two findings that address this challenge include:

  1. A study showed that increased expression of lipin 1, an enzyme that increases storage of lipids as triglycerides, contributed to failure to regenerate axons because it did not produce the phospholipids necessary for membrane expansion. Furthermore, depletion of lipin 1 promoted axonal regeneration (Roy & Tedeschi, 2021). This presents a new pathway for research, where a lipin 1 protease (degradation enzyme) or fatty acid that increases phospholipid levels may be investigated as helpful in promoting axonal recovery.
  2. It was found that lowering cholesterol promoted CNS axonal regeneration but negatively impacted myelin formation and repair (Roy & Tedeschi, 2021). Therefore, a research pathway that can be investigated is determining if cholesterol or cholesterol-containing fatty acids can be delivered with a spatial and temporal precision that promotes both axon and myelin regeneration.

For a description of the studies that concluded the findings upon which these research proposals are based, click here.

Answering these questions would broaden our understanding of the role of lipids in axonal regeneration, which would help us determine whether decisions such as the food we eat when recovering from a concussion can promote quicker and more effective neuronal regeneration. This can help ensure that our brains keep as many neurons as possible from dying, which would prevent the cognitive deficits seen after some TBI cases. If research supporting the ingestion of specific foods whilst recovering from concussion or other injuries came out, how would this impact what insurance policies cover, cost of healthcare regarding TBI recovery, and what physicians can prescribe as treatments?

Overall, research has shown that the most effective interventions and treatments for TBI are yet to be determined, but diet is a research area that has shown potential promise to yield recovery advice that does not need to be medically prescribed. Whether or not insurance would cover the cost of foods containing recovery-promoting lipids/other molecules is unknown, but the cost of that food is likely to be less than any prescription medications that could be prescribed, so advancement in our knowledge has potential to allow more accessible recovery from concussions. To learn more about the role of lipids in axon growth and regeneration after central nervous system injury, visit: https://pubmed.ncbi.nlm.nih.gov/34062747/

Footnotes:

1Giza, C., Hovda, D. “The New Neurometabolic Cascade of Concussion.” Congress of Neurological Surgeons, vol. 75, no. 4, 2014, pp. 524-533.

2Roy, D., Tedeschi, A. “The Role of Lipids, Lipid Metabolism and Ectopic Lipid Accumulation in Axon Growth, Regeneration and Repair after CNS Injury and Disease.” Cells, vol 10, no. 5, 2021, doi: 10.3390/cells10051078.

Health/Uncategorized

Watch your head! The Detrimental Effects of Traumatic Brain Injuries

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According to the CDC [1], every day 586 people are hospitalized for Traumatic Brain Injury (TBI), and this does not include urgent care or emergency room visits for TBI. 

This injury can happen from blunt force to the head or your brain getting jostled around. Car accidents, sports, and falls are common culprits of brain jostling.[2] Unfortunately, the brain may be unable to just “walk it off.” Two scientists, Giza and Hovda, investigated the neurometabolic cascade of concussion (2014). 

Concussion vector illustration. Labeled educational post head trauma scheme
Figure 1: concussion symptoms from Adobe Stock
Short-Term and Immediate Effects of TBI

When we get blasted in the head with force, many processes go wrong. Our cells in the brain called neurons have sodium, potassium, and calcium inside and around them. When force hits our brain, these molecules start spilling out of our neurons, while calcium enters in at high rates. Neurons don’t like things moving out of control, so they use a lot of energy to try and get all our important molecules back where they need to be. 

Figure 2: Neuron

However, at the same time, the structural integrity of our neurons is harmed by the blunt force, so the neuron needs more energy to fix this as well! The neuron is now in an energy crisis. Consider when you’ve been pulled in fifty different directions and all you want to do is nap, that is how the neurons are feeling.

Neurons cannot communicate with each other as effectively, and inflammation occurs after TBI. All of these dysfunctions present themselves as brain fog, headaches or migraines, slow reaction speeds, impaired learning, and overall discomfort.                                        

Long-Term Effects of TBI

After severe TBI or patients with multiple TBI injuries, proteins that are seen in neurodegeneration are present. Specifically, tau protein accumulates, which creates tangles in our neurons that disrupt important cell functions and can lead to cell death. Even when cell death doesn’t happen, the tangles can harm cognitive functioning. Cell death can lead to neurodegenerative diseases, but more research is needed to determine the risk of neurodegeneration from TBI.

Neurons are more vulnerable because of the structural damage done after the head trauma. Many neurons have white matter, a protective sheath, but TBI can damage this beyond repair for some neurons. Similar white matter damage is seen in some patients with PTSD and depression. 

Protective Measures

The energy crisis and structural neuronal instability can typically recover within 10 days after injury, but repeated injuries too close together may create long-term damage. This raises the important topic of rest after TBI. 

Rest after TBI can help the neurons get back to normal functioning levels. More research is needed to understand the exact length of time needed to recover, but it’s highly important to prevent a further head injury. 

The more scientists understand the mechanisms behind concussions and TBI, the closer they can get to preventing long-term damage. Until then, watch your head! 

 

Resources

 [1] Centers for Disease Control and Prevention. (2024). TBI data. Centers for Disease Control and Prevention. https://www.cdc.gov/traumatic-brain-injury/data-research/index.html

[2] Mayo Foundation for Medical Education and Research. (2021, February). Traumatic brain injury. Mayo Clinic. https://www.mayoclinic.org/diseases-conditions/traumatic-brain-injury/symptoms-causes/syc-20378557

[3] Giza, C. C., & Hovda, D. A. (2014). The new neurometabolic cascade of concussion. Neurosurgery, 75(Supplement 4). https://doi.org/10.1227/neu.0000000000000505

 

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Your Body’s Natural High…..

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The endocannabinoid system (ECS) is mainly found in the central nervous system (CNS) and plays important roles to modulate plasticity and homeostasis in the brain. When we talk ECS, the major receptors for binding are CB1 and CB2 receptors and the two main endocannabinoids are 2-AG  and anandimide   [1]

The CB1 receptor is known to be the most abundant GPCRs in the CNS and does the function of inhibiting the release of both excitatory and inhibitory neurotransmitters. The CB1 receptor also binds the many ligands, including the notable THC, AEA, and 2-AG. THC is an active ingredient in marijuana and can elicit feelings of calm, just like endocannabinoids. However, endocannabinoids are naturally produced by the body.

While CB1 receptors are abundant in areas like the hippocampus and neocortex, CB2 receptors are found in areas such as cells and tissues of the immune system. CB2 receptors are also localized to the microglia, which relates to neuroinflammation in the CNS. Neuroinflammation also relates to diseases such as Alzheimer’s disease (AD), which is a huge area of research today. [2]

Now endocannabinoids. These are natural chemicals that are produced by the body. They interact with the cannabinoid receptors in the CNS, and affect process relating mood, memory, appetite, and pain sensation. These molecules are similar to the compounds found in the cannabis plant, which is they are called “endocannabinoids” meaning cannabinoids produced inside our bodies.

Societal stereotypes have taught us to associate cannabis with words like addiction, failure, druggie, crazy, and many other negative words. It is agreeable that the feelings of calmness induced by cannabis may lead to high risks of addiction, but did you know that cannabis may also hold some potential in increasing the quality of health when used appropriately? Currently, only the University of Mississippi is allowed to conduct research with cannabis. This confirms the existing research gaps in this area.

Relating this to AD, preclinical studies in animal studies have shown that modulating the endocannabinoid system can have neuroprotective effects, reducing inflammation and oxidative stress which are implicated in AD. Researchers also believe that the endocannabinoid system may serve as a  therapeutic target to provide pharmacological benefits for AD. The neuroprotective effects of endocannabinoids may be due to interference with several cellular and molecular mechanisms, including apoptosis and inflammation. The progression of AD is related to the changes in the endocannabinoid system. Both cannabinoid receptor agonists and endocannabinoids, such as AEA, can reduce the neurotoxicity caused by Aβ-peptide in a mitogen-activated protein kinase (MAPK) pathway. [3]

Figure 1. Diagram showing the binding action for the two main endocannabinoids in the body, 2-AG and AEA. [4]

Figure 2. Diagram explaining the binding action for CB1 and CB2 receptors. [5]

Figure 3. Artstract by student depicting how stereotypes and uncertainties around cannabis hold back research on how cannabis might improve human health.

References.

[1] Zou, S., & Kumar, U. (2018, March 13). Cannabinoid receptors and the endocannabinoid system: Signaling and function in the central nervous system. International journal of molecular sciences. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5877694/#:~:text=As%20the%20two%20major%20endocannabinoids,D%20(NAPE%2DPLD).

[2] Kendall, D. A., & Yudowski, G. A. (2017, January 4). Cannabinoid receptors in the central nervous system: Their signaling and roles in disease. Frontiers in cellular neuroscience. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5209363/

[3] Li, S., Huang, Y., Yu, L., Ji, X., & Wu, J. (2023). Impact of the cannabinoid system in alzheimer’s disease. Current neuropharmacology. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10207907/#:~:text=In%20addition%2C%20another%20study%20reported,role%20in%20the%20brain%2Dblood

[5] Levin, M. (2022, December 5). 7 natural ways to activate your endocannabinoid system. CBD.market. https://cbd.market/cbdblog/7-natural-ways-to-activate-your-endocannabinoid-system

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My past or my future?

Posted on by smacgeor / 0 Comment

This blog post will focus on the interesting intersection between anxiety and memories. I personally found this fascinating because before discussing this in class, I never considered how memories of past events register in our brains, and how these events translate into trauma. I mostly investigated this topic from a psychology perspective but what does neuroscience have to say about this topic?

The brain’s ability to remember things is very important for our daily lives. Memories help us navigate the world, both physically and socially. They also help us adapt to changes and prepare for similar situations in the future. Sometimes, really stressful events can leave a lasting impact on our memory, especially if they’re traumatic.

Figure 1. Diagram showing past events that could potentially lead to cases of anxiety disorders such as Post Traumatic Stress Disorder (PTSD) [2]

Research using animal models suggest that stress affects learning and memory processes in the brain, particularly the hippocampus. Stress-induced hormones enhance memory formation, which can be observed in various behavioral tests like the forced swim test. This test involves placing rodents in water where they show an immobility response, which is considered a learned behavior. Drugs that increase neurotransmitter levels can affect this behavior, making it an important tool for antidepressant drug screening. Glucocorticoid hormones play a crucial role in memory consolidation, particularly through the action of the glucocorticoid receptor in the hippocampus. This receptor is essential for the acquisition and consolidation of memories associated with stressful experiences. [2]

Looking into more of the neuroscience, the roles of glucocorticoid hormones as well as histone modifications are crucial in the brain’s response to stress. Studies found that stress-induced changes in specific histone marks in neurons of the hippocampus, a brain region involved in memory and stress response, were associated with increased transcription of certain genes. These changes were observed after exposure to psychological stressors like forced swimming and novelty but not physical stressors like cold exposure.

Another interesting knowledge on this topic is the role of the HPA axis  in responding to stress. The release of cortisol regulated by the HPA axis (hypothalamic-pituitary-adrenal axis) and begins with the release of CRH from the hypothalamus. Cortisol is a glucocorticoid. Cortisol acts on glucose metabolism to maintain normal glucose levels especially during times of stress. [3]. Fluctuations in cortisol secretion often accompany psychiatric disorders, and normalization of its levels correlates with improvement in a patient’s health. This also means that cortisol may be useful as a biological marker that can help determine the likelihood of a mental illness, its onset, and the severity of symptoms. [4]

Figure 2. Schematic representing the brain’s response to stress [5]

References.

[1] Matthew Tull, P. (2021, April 21). How traumatic events cause PTSD. Verywell Mind. https://www.verywellmind.com/ptsd-causes-and-risk-factors-2797397

[2] Reul J. M. (2014). Making memories of stressful events: a journey along epigenetic, gene transcription, and signaling pathways. Frontiers in psychiatry, 5, 5. https://doi.org/10.3389/fpsyt.2014.00005

[3] Chourpiliadis, C. (2023, July 17). Physiology, glucocorticoids. StatPearls [Internet]. https://www.ncbi.nlm.nih.gov/books/NBK560897/

[4] Dziurkowska, E., & Wesolowski, M. (2021). Cortisol as a Biomarker of Mental Disorder Severity. Journal of clinical medicine, 10(21), 5204. https://doi.org/10.3390/jcm10215204

[5] Abercrombie, H. C., Abrari, K., Arbel, I., Barrett, D., Beato, M., Beckwith, B. E., Bisaz, R., Bohus, B., Brewin, C. R., Brown, E. S., Buchanan, T. W., Buss, C., Campeau, S., Cleare, A. J., … Bierer, L. M. (2009, March 31). Glucocorticoids and the regulation of memory in health and disease. Frontiers in Neuroendocrinology. https://www.sciencedirect.com/science/article/abs/pii/S009130220900003X#preview-section-abstract

 

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Battling the Brain Beast: Glioblastomas

Posted on by smacgeor / 0 Comment

When we talk about tumors, they can grow and exist differently. There are canceorus (malignant) tumors and non-cancerous (benign) tumors. A tumor is a solid mass of tissue that forms when abnormal cells group together. They can affect different parts of the body including the bone, skin, tissue, and organs. Factors that increase the risk of developing a tumor include gene mutations, smoking, family history of certain types of cancer and smoking. [1]

Glioblastomas (GBM) are brain tumors that affect the normal intracellular and intercellular signaling for the advantage of the tumor cells but to the disadvantage of the whole organism. Some of the subtypes of glioblastomas include classical GBM, mesenchymal GBM, proneural GBM, and neural GBM.

GBM can also occur as a primary tumor or a secondary tumor developing from pre-existing lower grade tumor glioma tumors. Primary GBM develop very quickly, without evidence of preexisting symptoms while secondary GBM develop from a lower grade tumor. Some of the common symptoms of glioblastomas include perisistent headaches, double or blurred vision, vomiting, new onset of seizures, changes in mood and personality. [2]

To delve more into the neuroscience of cellular processes involved in GBM, the Mitogen- activated protein kinase (MAPK) signaling and pathways are interrupted in GBM. This can affect functions such as cell survival. The MAPK pathway contains three activated protein kinases that are key components of a series of vital signal transduction pathways and regulte regulate proceses such as cell proliferation, cell differentiation, and cell death. Below is a diagram showing the MAPK pathways. [3]

 

Figure 1. Diagram showing the major MAPK pathways (cascades) in mammalian cells [4]

Think of the MAPK pathway like a chain reaction in your body’s cells that gets started when certain growth factors, like epidermal growth factor (EGF), bind to their special receptors on the cell surface. These receptors are like switches that turn on the pathway. When the growth factor binds to the receptor, it causes the receptor to team up with other proteins inside the cell, like GRB2 and SOS. These proteins then pass signals along to another protein called Ras, which acts like a messenger. Ras gets activated and starts a series of events that ultimately lead to the activation of MAPK, a protein that helps control cell growth and division.

In cancer, this pathway can go haywire. Sometimes, certain genes like the one for the epidermal growth factor receptor (EGFR) get too active, causing the MAPK pathway to go into overdrive. This can make cells grow and divide uncontrollably, leading to tumor growth and making the cancer more aggressive.

Figure 2. Cartoon schematizing the crostalk between glioblastoma cancer stem cells (GSCs) and major cellular components of glioblastoma tumor environment.

 

References.

[1] Professional, C. C. medical. (n.d.-a). Tumor: What is it, types, symptoms, treatment & prevention. Cleveland Clinic. https://my.clevelandclinic.org/health/diseases/21881-tumor

[2] Jigisha, T., Pier, P., & Vikram, P. (n.d.). Glioblastoma multiforme. AANS. https://www.aans.org/en/Patients/Neurosurgical-Conditions-and-Treatments/Glioblastoma-Multiforme

[3] Morrison, D. K. (2012, November 1). MAP kinase pathways. Cold Spring Harbor perspectives in biology. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3536342/#:~:text=Mitogen%2Dactivated%20protein%20kinase%20
[4] ZHANG, W., LIU, H. MAPK signal pathways in the regulation of cell proliferation in mammalian cells. Cell Res 12, 9–18 (2002). https://doi.org/10.1038/sj.cr.7290105
[5] Ryskalin, Larisa & Biagioni, Francesca & Lenzi, Paola & Frati, Alessandro. (2020). mTOR Modulates Intercellular Signals for Enlargement and Infiltration in Glioblastoma Multiforme. Cancers. 12. 10.3390/cancers12092486.
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Putting the “fun” in dysfuntion!

Posted on by smacgeor / 0 Comment

Did you know that even your psychiatrist might be suffering from a mental illness? Increased awareness on mental illness today shows how far humans have come in trying to understand each other. While some places around the world are still trying to figure it out, many countries have embraced the need for empathy when dealing with people suffering from a mental illness.

Now, some neuroscience behind it. Relating this to mental illness, Wnt signaling may play a role in mental illness specifically schizophrenia  . This mental illness is characterized by disruptions in thinking, emotions, and behavior, just like the figure below depicts. The wnt signaling pathway  is like a set of instructions inside our cells that tells them what to do. It involves a protein called β-catenin. Normally, β-catenin is tagged for disposal by a group of proteins when there’s no Wnt signal around. But when a Wnt signal comes along and connects with its receptor, it’s like a green light for the pathway. This stops the disposal process, allowing β-catenin to build up inside the cell. Then, it moves into the nucleus, where it helps turn on specific genes that control cell behavior.

Figure 1. Cartoon depicting the common symptoms of schizophrenia

Research suggests that the irregular signaling in the Wnt signaling pathways may contribute to the development of schizophrenia by affecting brain development, neurotransmitter function, and synaptic plasticity. But specifically, the  dysregulation of Wnt signaling pathways may disrupt the formation and function of synapses, which are the connections between neurons in the brain. This disruption could lead to impaired communication between brain cells, contributing to the symptoms of schizophrenia. However, the exact relationship between Wnt signaling and schizophrenia is complex and requires further investigation.

Figure 2. Diagram showing wnt signaling pathway [1]

To break it down further, without Wnt ligand binding, an intracellular complex including GSK3β, Axin, APC, and CK1α keeps β-catenin phosphorylated and marked for degradation. However, Wnt ligands binding to their receptors cause a cascade leading to the dissociation of the destruction complex. This stabilizes β-catenin, allowing it to accumulate in the cytoplasm and move into the nucleus.

Looking at treatments, Lithium is  widely used as a treatment for bipolar disorder and sometimes schizophrenia, due to its potential impact on Wnt signaling pathways. Lithium is known to increase the levels of β-catenin and therefore subsequent activation of canonical Wnt signaling, which may play a role in mediating the mood-balancing effects of lithium. [2]

A note on empathy. Seeing how complex the science behind mental illness is, it makes us wonder when scientists might be able to figure it all out. These gaps in knowledge reveals how complex it might be for those actually experiencing an illness no one entirely understands. Therefore, it is important to always show empathy to individuals living with the symptoms of mental illness. Because even though they may not have received a diagnosis yet, they may be tangled in navigating through their own experiences. Someone suffering from a mental illness could be your neighbor or even best friend. Who knows?

 

Figure 3. Artstract created by student showing a word cloud to raise awareness on mental health

References.

[1] Inestrosa, N.C., Montecinos-Oliva, C. & Fuenzalida, M. Wnt Signaling: Role in Alzheimer Disease and Schizophrenia. J Neuroimmune Pharmacol 7, 788–807 (2012). https://doi.org/10.1007/s11481-012-9417-5

[2] Singh KK. An emerging role for Wnt and GSK3 signaling pathways in schizophrenia. Clin Genet. 2013 Jun;83(6):511-7. doi: 10.1111/cge.12111. Epub 2013 Apr 1. PMID: 23379509.

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