Concussions or traumatic brain injuries (TBI) occur when the head experiences an impact that causes structural damage to brain tissue. Depending on the severity of the injury, this damage may or may not be visible in images of the brain. Despite this, microstructural damage to neural tissue can have significant metabolic and neurochemical effects. This damage can induce chronic cell death and neurodegeneration. Alterations in cellular function can impair neurotransmission, induce metabolic changes, and trigger ionic shifts [1]. Even though these effects can be serious, there is not a universally accepted treatment protocol that modulates these altered pathways.

What Happens After TBI?

Immediately following a brain injury which results in damage to neural cell membranes, an ionic flux and hyperacute glutamate release can be observed. When the trauma alters the outer membrane of neurons, potassium ions rush out of the cell and sodium and calcium ions rush into the cell, due to the natural ionic gradient between the intracellular and extracellular regions. This initiates a depolarization within the cell, which induces a state of spreading depression which can be a major contributor to acute post-concussive symptoms such as headaches, migraines, and seizures [1].

Similarly, injury to axons of neural cells can promote extreme glutamate releases. Since glutamate is a major excitatory neurotransmitter, this can cause significant alterations to neurotransmission. Increased glutamate levels following TBI are associated with changes in the NMDA glutamate receptor which can affect memory, neuroplasticity, and electrophysiology of the brain. Glutamate release may also be related to increased cytokine and inflammatory gene responses following TBI which is associated with oxidative stress and cellular injury [1].

Alterations in GABA, the major inhibitory neurotransmitter, and its receptors have also been observed in TBI models. This could be correlated to the increased susceptibility to anxiety and PTSD following a TBI. GABA transmission is known to produce anti-anxiolytic effects. For this reason, decreased levels of GABA and GAD67 (the enzyme that turns glutamate into GABA) in the amygdala following TBI may specifically contribute to the long-term increases in anxiety observed after brain injury [1].

Likely related to the ionic alterations following structural damage is the metabolic shift that is observed immediately and sustained for 7-10 days following TBI. Immediately following structural damage which induces ionic flux, the cells enter a period of hyperglycolysis in their attempt to return ionic gradients to resting levels. Following this initial increase in glucose metabolism that lasts less than 24 hours, the brain enters a period of impaired glucose metabolism. During this time, it is suggested increased fatty acid consumption could decrease some of the axonal damage that occurs after a concussion [1].

Ketones and Concussions

Fatty acid supplementation could be beneficial following TBI because ketones from the metabolism of fats can be used for fuel instead of glucose in the hypometabolic state. For this reason, it appears that direct ketone supplementation or a ketogenic diet may have more advantageous effects than fatty acid supplementation because ketone body levels are raised more effectively [6].

The ketogenic diet (KD) is a high fat, low carbohydrate diet originally used to treat epilepsy. This diet initiates a metabolic state of ketosis where ketone bodies are used for fuel instead of glucose. In a study investigating the potential benefits of a KD following TBI it was shown that compared to a standard diet, a KD produced more ketone bodies, reduced loss of neurons, reduced inflammation, and increased SIRT1 protein following SIRT1 loss due to injury. SIRT1 is a neuroprotective protein that is active in the hippocampus where it activates Akt and inhibits GSK [7].

 

Given the significant neurochemical and metabolic changes observed following TBI, as well as the vast and serious symptoms this can cause, it is concerning that there are not any highly effective medications or treatments to help heal the structural and metabolic damage that has occurred. The structural damage leads to ionic fluxes which alters brain metabolism, leading to a wide range of behavioral and physiological symptoms. In light of the current understanding of the neural ionic flux and its alterations to neurometabolism, ketone supplementation or a ketogenic diet may be a viable treatment option following a concussion.

References:

What is Glioblastoma?

Glioblastoma (GBM) is a type of cancer that forms in the brain or spinal cord. GBM forms from astrocytes that support nerve cells. [1]

Classical GBM

Characterized by amplification or mutation of the EGFR gene. This type typically responds better to aggressive treatment compared to other types. 

Mesenchymal GBM

Characterized by mutations of NF1 and PTEN, and mutations of P53 are also common. This type is also responsive to aggressive treatment. 

Proneural GBM

Characterized by amplification of chromosome 4q12 and high levels of the PDGFRA gene. IDH1 and TP53 mutations are also typically present in this type. People with this type tend to live longer compared to other types, but it does not respond well to aggressive treatment. 

Neural GBM

This type does not have any obvious patterns of mutations or amplifications and typically has the worst prognosis of all types. [2]

Signal Transduction Pathways in Relation to GBM

MAPK 

High levels of MAPK signaling are connected to GBM. What could contribute to this is that in the mesenchymal type, NF1 is mutated which typically negatively regulates MAPK signaling by inactivating Ras. Another factor could be that in the classical type, the EGFR gene is amplified which hyperactives MAPK. 

PI3K 

The PI3K signaling pathway is hyperactive in GBM cases. What could cause this is the mutation of PTEN in the mesenchymal type which typically suppresses PI3K signaling by dephosphorylating PIP3. The EGFR gene amplification typical in the classical type also hyper-activates PI3K signaling. 

cAMP 

It has been found that cAMP signaling is hypoactive in GBM cases as there are low levels of cAMP and adenylyl cyclase in GBM tumor samples. CREB is a transcription factor that is activated through the cAMP signaling pathway, so if cAMP signaling is suppressed, CREB is inhibited which is connected to tumor growth.

Convergence of pathways

MAPK and PI3K cross regulate each other in many ways. For one, they are both activated by the same receptors and both activated by Ras proteins. ERK, a MAPK pathway, can downregulate PI3K by phosphorylating GAB1 which then reduces the activation of PI3K. ERK can also inhibit PI3K by activating mTOR. PI3K can also downregulate the MAPK signaling pathway by inhibiting Raf through the action of AKT and its phosphorylation of Raf. All three pathways involved, MAPK, PI3K, and cAMP seem to have some link to CREB and its inability to perform correctly which results in the modulation of tumor growth. [2]

Current Treatments for Glioblastoma

Surgery

Surgery can remove some of the tumor but it often spreads to healthy tissue, so typically surgery is not fully effective. After surgery, patients tend to have other treatments done to get whatever is left. 

Radiation

Radiation therapy uses energy beams from X-rays or protons to kill cancer cells. Radiation is typically used in combination with chemotherapy. 

Chemotherapy

Chemotherapy uses drugs to kill cancer cells and can be taken as a pill or through a vein. 

Tumor treating fields (TTF) therapy

TTF uses an electrical field to keep cancer cells from multiplying. [1]

References

[1] Mayo Clinic. (March 7, 2024). Glioblastoma. https://www.mayoclinic.org/diseases-conditions/glioblastoma/cdc-20350148#:~:text=It%20can%20form%20in%20the,can%20happen%20at%20any%20age

[2] Fung, N. H., Grima, C. A., Widodo, S. S., Kaye, A. H., Whitehead, C. A., Stylli, S. S., & Mantamadiotis, T. (2019). Understanding and exploiting cell signalling convergence nodes and pathway cross-talk in malignant brain cancer. Cellular Signaling, 57, 2-9. https://doi.org/10.1016/j.cellsig.2019.01.011

[3] Kwatra, G. (2021, August 30). Glioblastoma: What Every Patient Needs to Know. Glioblastoma Foundation. https://glioblastomafoundation.org/news/glioblastoma-multiforme

[4] Li, X., Oziel, M., & Rubinsky, B. (2022). Evaluating the therapeutic effect of tumor treating fields (TTFields) by monitoring the impedance across TTFields electrode arrays. PeerJ, 10. https://doi.org/10.7717/peerj.12877 

Autism Characteristics

Autism Spectrum Disorder (ASD) is a common neurodevelopmental disorder that is diagnosed based on behavioral symptoms. Given the wide-ranging manifestations of the symptoms of ASD, it would be helpful to be able to find more precise diagnostic criteria to provide more specific diagnoses which could allow for more precise treatments. The symptoms of ASD are broadly described as deficits in social communication and interaction as well as restrictive, repetitive behaviors [1]. Since these symptoms are very broad, it is no wonder that there is not thought to be a single cause of ASD. Alternatively, many assorted mechanisms and genetic variations are thought to be associated with behavioral expressions that can be characterized as ASD [2].

The high heritability of ASD is strong evidence for the genetic influence on the variety of manifestations of the condition. This is also supported by the discovery of many de novo single nucleotide variants as well as transmitted and de novo copy number variants. Because of the wide range of possible contributions and outcomes related to ASD, it is suggested that ASD diagnoses should be subcategorized based on mechanistic commonalities found within different expressions of ASD. One mechanism that could be used to subcategorize ASD is that of dopamine signaling dysfunction [2].

Dopamine Dysfunction in ASD

A strong piece of evidence for this theory is found in MRI studies of the caudate nucleus. The caudate nucleus is a major target of dopamine signaling. Multiple studies have found enlargement of the caudate nucleus (Image 1) in individuals with ASD. This suggests that ASD is associated with alterations in dopamine related structures and the function of these structures. Similarly, increases in connectivity of the fronto-striatal networks has been positively associated with the severity of repetitive behaviors in ASD. This also links ASD symptoms with abnormal dopaminergic connectivity to cortical structures [2].

There have been many ASD-associated variants within the dopamine signaling pathway reported from various models (Figure 1). Although the direct application of these variants and the degrees of their effects cannot be completely deduced at this time, the significance in this information is that there appears to be many sites of action within the dopamine pathway that are altered in ASD models. Both upregulation and downregulation at specific points within the pathway emphasize the role of dopamine dysfunction in the behavioral manifestations of ASD [2].

Given the vast projection patterns of dopamine in the brain (Figure 2), the many variants in dopamine signaling with ASD (Figure 1), as well as the studies linking ASD with changes in dopamine signals and structures, it is difficult to deny the evidence supporting a connection between dysfunction of the dopamine system and ASD behaviors. Dopamine has extensive effects on human behavior including social drive, reward-associated behaviors, allocation of physical energy, attention, and working memory, just to name a few. This broad scope of dopamine related activity could have many implications on the broad scope of ASD manifestations [2].

Resources:

When I chose to come to Concordia for college, I didn’t know the impact it would have on my life.  I don’t want to be a clique… but what everyone says is true, “these 4 years have really flown by.” When thinking about life after college, I have been thinking a lot recently about how my experiences at Concordia have helped prepare me for the future.

Concordia has a goal for its liberal arts education called BREW – Becoming Responsibly Engaged in the World. My liberal arts education has prepared me to not only be a curious thinker and the importance of mentor and classmate relationships, but Concordia specifically emphasizes experimental learning that allows students to connect the concepts they are learning outside the classroom as well. This has helped me to build critical thinking skills and to realize the importance of community outreach and gaining multiple perspectives.

When I read about Concordia’s 5 goals for liberal learning, I thought of research. Research is committing to learn for the rest of your life. It’s a love for learning and a drive to follow whatever research questions interest you. Research is continuing to build on your foundation of knowledge and research techniques (i.e. research process, scientific writing, safe laboratory practices, etc.). Research is being able to communicate your findings so that anyone can understand. Wanting to go into a future career in research, I’ll be taking what I have learned at Concordia and applying it to all aspects of my life.

This neurochemistry course has been one of my favorites at Concordia because of its unique structure (it also helps that this is basically the theory behind what I want to do for the rest of my life). During this class, I have learned how to take real-world issues, read current literature, and discuss the complex problems in their mechanisms, treatment, and public perceptions with my classmates. Each week when we read about a new disease, my favorite part is getting to the point where I have learned enough to consider and pose future directions for research on the disrupted signaling pathways and treatments that target them.

If I were to highlight skills or competencies that I improved upon this semester in my resume or an interview, I would be sure to include reading and comprehending complex diseases from recent literature, collaborating with peers, writing blog posts to present findings to the public, and applying critical thinking to understand complex issues involved in diseases. In my future career, I will take what I have learned from this neurochemistry course and use it to understand complex neurological disorders and work to communicate scientific topics effectively with diverse audiences.

I’ve experienced how the lives of children who have ASD as well as their families can be impacted. To research autism from translational approaches in my future career, I am going to need to learn and draw from multiple disciplinary perspectives: Genetics to study the common mutations found and their possible implications in the different pathologies (E/I imbalances, abnormal synapse formations, etc.);  Biochemistry to understand the underlying signaling pathways that are disrupted; Psychology to understand the impact on behavior; and Neuroscience to bridge all these disciplines in a translational approach to understanding, diagnosing, and treating ASD.

I know my experiences at Concordia have prepared me for my future, the kernel was planted, and I can’t wait to see how it grows!

CB1 Receptors

CB1 receptors are G-protein coupled receptors (GPCRs) that are mostly found in the central nervous system (CNS) but can also be found in peripheral tissues and the peripheral nervous system (PNS). They are found on presynaptic neurons. These receptors play an essential role in learning and memory and synaptic plasticity. When these receptors are coupled with Gi/o proteins, they inhibit adenylyl cyclase, and when they are coupled with Gs proteins, they stimulate adenylyl cyclase. [1]

CB2 Receptors

CB2 receptors can be found in cells and tissues of the immune system and are typically only expressed when there is active inflammation in the body. They are typically localized to microglia which have anti-inflammatory effects. [2]

Endocannabinoid System 

Endocannabinoids are natural agonists for the CB1 and CB2 receptors. They are triggered by the release of calcium at the postsynaptic neuron. The endocannabinoid system controls mood, pain perception, and learning and memory. It can also provide protection against traumatic brain injury (TBI) and can repair neurodegeneration. Learning and memory comes into play with the endocannabinoid system as it plays a key role in modulating synaptic plasticity—the ability of the brain to change connections between neurons. [4]

THC vs CBD

CBD and THC are both derived from cannabis plants and have very similar molecular structures. The primary difference between the two is that THC is psychoactive and CBD is non-psychoactive. CBD products are federally legal whereas THC is not and is only legal in some states. CBD is also not considered addictive whereas THC can lead to addiction (about 30% of marijuana users become addicted). [6]

Cannabis as Treatment for Neurodegenerative Diseases 

Multiple Sclerosis

Cannabis, particularly THC, can have positive effects on spasticity and pain in multiple sclerosis (MS). Sativex, a spray that is ingested through the mouth or nose and is composed of both CBD and THC, has been used to treat MS. This treatment acts on both CB1 and CB2 receptors to reduce both pain and inflammation. 

Huntington’s Disease

In Huntington’s disease, CB1 receptor expression is reduced which decreases motor performance. To treat Huntington’s disease, CB1 can be activated to reduce symptoms. 

Alzheimer’s Disease

Alzheimer’s disease (AD) is partially characterized by dementia and synthetic endocannabinoids may better dementia symptoms in AD. AD is believed to be caused by amyloid-beta plaques and tau protein phosphorylation. Activation of both CB1 and CB2 receptors can provide protection against amyloid-beta toxicity, and CBD can reduce tau protein phosphorylation. [4]

Ethical Concerns in Research 

Since cannabis is not federally legal and only legal in some states, research participants could be at legal risk if their identity is disclosed. Another issue is impairment of participants and making sure that researchers are getting informed consent. Ensuring that consent is received prior to any ingestion of the drug is imperative for ethics of the study. Individuals’ ability to understand and make sound decisions could be impaired under the influence of cannabis. [8]

References

[1] Howlett, A. C., Blume, L. C., & Dalton, G. D. (2010). CB(1) cannabinoid receptors and their associated proteins. Current medicinal chemistry, 17(14), 1382–1393. https://doi.org/10.2174/092986710790980023 

[2] Bie, B., Wu, J., Foss, J. F., & Naguib, M. (2018). An overview of the cannabinoid type 2 receptor system and its therapeutic potential. Current opinion in anaesthesiology, 31(4), 407–414. https://doi.org/10.1097/ACO.0000000000000616 

[3] What is the Endocannabinoid System? | Sona Pharmacy + Clinic. (2020, April 1). https://sonapharmacy.com/what-is-the-endocannabinoid-system/

[4] Kendall, D. A. & Yudowski, G. A. (2017). Cannabinoid Receptors in the Central Nervous System: Their Signaling and Roles in Disease. Frontiers in Cellular Neuroscience, 10(294). doi: 10.3389/fncel.2016.00294 

[5] ​​Goldberg, Ian. (March 2, 2023). Cannabis use and its effects on mood disorders | Talkiatry. Retrieved April 29, 2024, from https://www.talkiatry.com/blog/cannabis-use-and-its-effects-on-mood-disorders

[6] Center, L. H. T. (2023, November 15). CBD vs THC: Learn the Differences. La Hacienda. https://www.lahacienda.com/blog/cbd-vs-thc-learn-the-differences 

[7] ​​CDC. (2023, March 1). What We Know about Marijuana. Centers for Disease Control and Prevention. https://www.cdc.gov/marijuana/featured-topics/what-we-know-about-marijuana.html

[8] Fitzgerald, Kelly. (n.d.) Research and Cannabis: Ethical Research in a Changing Regulatory Landscape. Retrieved April 29, 2024, from https://www.wcgclinical.com/insights/research-and-cannabis-ethical-research-in-a-changing-regulatory-landscape/ 

[9] Corder, Katie-Leigh. (August 23, 2018). How UNC Researchers are Studying Cannabis. https://www.unco.edu/news/articles/unc-cannabis-research-projects.aspx 

Melanocortin System

The melanocortin system is located in the hypothalamus. The primary role of the melanocortin system is to maintain glucose homeostasis as well as insulin secretion and glucose production and utilization [1]. The melanocortin system contains neural populations that have high levels of receptors that respond to metabolic cues to control food intake and energy expenditure. One type of neuron in the melanocortin system is POMC neurons which are inhibitory, anorexigenic neurons which inhibit appetite, and the other primary type of neuron is AgRP neurons which are excitatory, orexigenic neurons which stimulate appetite. When the brain is working “normally,” AgRP neuron expression is increased during fasting to induce feeding and suppress energy expenditure. In obesity or metabolic disease, AgRP neurons are activated more than they should be and positively regulates feeding behavior. [2]

 

High-Fat Diet

A high-fat diet (HFD) is a diet in which at least 35% of the calories consumed come from either saturated or unsaturated fats [3]. Long-term consumption of a HFD many times results in obesity. Consuming a HFD for a long period of time has various acute effects. Obesity causes activation of cytokines and inflammatory pathways in the hypothalamus. A HFD has been found to reduce insulin sensitivity in the hypothalamus in rats. [2]

Saturated Fatty Acids 

Saturated fatty acids (SFAs) are more problematic than unsaturated fatty acids because they tend to stay solid at room temperature, and therefore are more likely to clog the arteries compared to unsaturated fats which are liquid at room temperature. SFAs can negatively modulate energy homeostasis by inducing hypothalamic inflammation and promote positive energy balance by passing the blood-brain barrier (BBB). SFAs can also trigger the activation of the inflammatory signaling cascade TLR4. [2] 

Inflammatory Pathway

SFAs have a big impact on the PI3K pathway (insulin pathway) by inhibiting PI3K, so the FOXO protein does not translocate to the nucleus and does not allow transcription to occur. TNFɑ, an inflammatory cytokine, is activated which then activates JNK which inhibits the insulin pathway by inhibiting PI3K. The Jak/Stat pathway (leptin pathway) is also inhibited in this case as NFB activates SOCS which inhibits the pathway. TLR4 also has an effect on NFB as IKK dissociates from ​​NFB and activating it. This all results in an increase in cytokines and AgRP neurons while simultaneously decreasing POMC neurons. [2]

Treatment Options

Dietary Changes

One of the best ways to overcome obesity is cutting calories and making healthier eating choices. There is no specific “magical” diet that works for everyone, but generally the best habits for eating changes include: cutting calories, eating foods that have less calories, eating more plant-based foods, and restricting high-carb and high-fat foods. 

Exercise and Activity 

It is recommended that individuals with obesity get at least 2 and a half hours of exercise every week at a moderate intensity. This will increase as time goes on and fitness improves. Any extra opportunities to move your body are also recommended like taking the stairs rather than the elevator or parking further away from entrances so you have to walk farther. 

Behavior Modification

It can be helpful to speak to a counselor to discuss emotional and behavioral issues that are related to eating. This can also help with understanding overeating and recognizing triggers for eating and food cravings. 

Medications

There are some medications that are FDA approved to treat obesity, but they are not meant to be a replacement for adopting a healthy lifestyle. These medications are meant to be taken alongside regular exercise and diet changes. [6]

References

[1] Hill, J. W., & Faulkner, L. D. (2017). The Role of the Melanocortin System in Metabolic Disease: New Developments and Advances. Neuroendocrinology, 104(4), 330–346. https://doi.org/10.1159/000450649 

[2] Jais, A., & Brüning, J. C. (2017). Hypothalamic inflammation in obesity and metabolic disease. The Journal of Clinical Investigation, 127(1), 24–32. https://doi.org/10.1172/JCI88878

[3] Krisanits, B., Randise, J. F., Burton, C. E., Findlay, V. J., & Turner, D. P. (2020). Chapter Three—Pubertal mammary development as a “susceptibility window” for breast cancer disparity. In M. E. Ford, N. F. Esnaola, & J. D. Salley (Eds.), Cancer Health Equity Research (Vol. 146, pp. 57–82). Academic Press. https://doi.org/10.1016/bs.acr.2020.01.004

[4] Zimmerman, B.; Kundu, P.; Rooney, W.D.; Raber, J. The Effect of High Fat Diet on Cerebrovascular Health and Pathology: A Species Comparative Review. Molecules 2021, 26, 3406. https://doi.org/10.3390/molecules26113406

[5] Explain saturated fatty acids. + Example. (n.d.). Socratic.Org. Retrieved April 28, 2024, from https://socratic.org/questions/explain-saturated-fatty-acids

[6] Obesity—Diagnosis and treatment—Mayo Clinic. (n.d.). Retrieved April 28, 2024, from https://www.mayoclinic.org/diseases-conditions/obesity/diagnosis-treatment/drc-20375749 

[7] Learn About How Obesity Is Treated and Managed. (n.d.). Verywell Health. Retrieved April 28, 2024, from https://www.verywellhealth.com/treatment-for-obesity-7971239 

What is PTSD?

Post traumatic stress disorder (PTSD) is a psychological disorder that develops in some people after they have experienced some sort of trauma or been through a traumatic event. Some common traumas include war, natural disasters, sexual assault, terrorist attacks, domestic violence, and others. Symptoms include repeated intrusive thoughts and memories and flashbacks from the event, avoiding reminders of the traumatic event, distorted thoughts and negative thoughts and feelings, and being irritable and having angry outbursts. [1]

 

Glucocorticoid Receptor

The glucocorticoid receptor is an intracellular receptor that is located in the cytoplasm and moves to the nucleus when glucocorticoid hormones bind to the receptor. This receptor modulates transcription. Glucocorticoid hormones are steroid hormones that are released from the adrenal glands and are important for maintaining stress-related homeostasis. [2]

ERK/MAPK Pathway

Extracellular signal-regulated kinase 1/2 (ERK) is part of the mitogen-activated protein kinase (MAPK) family which is important for transmitting extracellular signals to intracellular components. MAPK cascades regulate various cell processes including proliferation, apoptosis, and stress responses. The MAPK cascade transmits signals through sequential activation of protein kinase layers: MAPKKK, MAPKK, and MAPK. The ERK pathway includes specific kinases of Ras, Raf, MEK, and ERK. [4]

How Do You Develop PTSD?

Glucocorticoid receptors are essential in the development of PTSD as stress induces the release of glucocorticoid hormones which are ligands for glucocorticoid receptors. Following a stressful event or trauma, a dual histone mark H3s10p-K14A appears in granule cells in the dentate gyrus which is part of the hippocampus. This histone mark is important for opening up DNA strands to express immediate-early genes (IEGs), in this case, c-Fos and EGR1. After the appearance of this dual histone mark, PTSD symptoms develop. The ERK/MAPK pathway is essential for creation of emotional memories and the behavioral response associated with them. Glucocorticoid hormones act as a scaffold for phosphorylation in the ERK pathway. Without this, the dual histone mark does not appear, and histone marks are important for the consolidation of memory formation. When this chain of events happens too often, PTSD occurs. [5]

How Can PTSD be Treated?

Cognitive Behavioral Therapy (CBT)

Therapy that focuses on problematic and/or dysfunctional patterns of thinking and how they affect behavior patterns. Key of therapy is to change current ways of thinking and make them more functional so that, in turn, behaviors change to be more productive. In relation to PTSD, the therapist works with the client to see if what the client is describing about their trauma and about themselves is accurate. 

Exposure Therapy

Type of CBT that teaches the client to gradually expose themselves to situations that are related to their trauma. This could also be gradually approaching trauma-related memories and feelings. These previously avoided memories, feelings, and situations are faced which conditions the client to understand that these are not dangerous and do not need to be avoided. 

Eye Movement Desensitization and Reprocessing (EMDR)

This therapy encourages the client to think about a traumatic memory while also experiencing bilateral stimulation through eye movements. This has been found to reduce vividness and emotion associated with those traumatic memories. [7]

References

[1] What is Posttraumatic Stress Disorder (PTSD)? (n.d.). Retrieved April 27, 2024, from https://www.psychiatry.org:443/patients-families/ptsd/what-is-ptsd

[2] Nicolaides NC, Chrousos G, Kino T. Glucocorticoid Receptor. [Updated 2020 Nov 21]. In: Feingold KR, Anawalt B, Blackman MR, et al., editors. Endotext [Internet]. South Dartmouth (MA): MDText.com, Inc.; 2000-. Available from: https://www.ncbi.nlm.nih.gov/books/NBK279171/

[3] Heitzer, Marjet & Wolf, Irene & Sanchez, Edwin & Witchel, Selma & DeFranco, Donald. (2008). Glucocorticoid receptor physiology. Reviews in endocrine & metabolic disorders. 8. 321-30. 10.1007/s11154-007-9059-8. 

[4] Guo, Y. J., Pan, W. W., Liu, S. B., Shen, Z. F., Xu, Y., & Hu, L. L. (2020). ERK/MAPK signalling pathway and tumorigenesis. Experimental and therapeutic medicine, 19(3), 1997–2007. https://doi.org/10.3892/etm.2020.8454

[5] Reul, J. M.H.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. 

[6] Encyclopedia on Early Childhood Development. (Dec 5, 2008). Centre of Excellence for Early Childhood Development. https://www.child-encyclopedia.com/sites/default/files/docs/glossaire/Glossary_Brain_DG.pdf 

[7] Treatments for PTSD. (n.d.). Https://Www.Apa.Org. Retrieved April 28, 2024, from https://www.apa.org/ptsd-guideline/treatments 

[8] Carretta-Stein, D. What are the benefits of EMDR Therapy? (n.d.) https://www.danacarretta.com/post/what-are-the-benefits-of-emdr-therapy