Cobbers on the Brain – Page 6 – Student Commentary on the Neurological Sciences

Glio-not a blast-toma

Posted on April 30, 2025 by rhurley1 / 0 Comment

The article we have covered in a previous week, “Understanding and exploiting cell signaling convergence nodes and pathway cross-talk in malignant brain cancer” by Nok Him Funga, Corrina A. Grimaa, Samuel S. Widodoa, Andrew H. Kaye, Clarissa A. Whitehead, Stanley S. Stylli, and Theo Mantamadiotisa was an article about recently uncovered mysteries on cancer. Basically, we know already that cancer continues to evolve over time. However, due to this feature, we know that is why Glioblastoma is a very aggressive and invasive cancer.

The article informs us of what cancer specifically is in a intense detail. Though, the article specifically focuses mainly on the aspect of Glioblastoma. As a result of this article, we learnt much on this invasive condition.

Figure one, pictured above, from the article mentioned above is especially excellent at explaining this where it was needed (excellently timed, or in other words placed well). That piece is a diagram expressing the MAPK and the MI3K pathways to elaborate on the condition.^1 The myriad, but consistent colors complements the black words. Although, one slight problem could be that it could feel a large bunch overwhelming if you’re not too familiar with the applied terms and acronyms of figure one in the Neuroscience field. This was an excellent piece to me for it is maximized simplicity because, for clear reasons, that kind of thing strongly helps. The figure may also benefit people uninvolved in Neuroscience as well because figure one uses so much brief, yet descriptive, labeling, and I find that effective myself in general because it’s easy on the eyes to track or logicate.

Now, at this point, one, such as yourself, may wonder why people really should care about all the above information. Well, let’s answer with essential basics to answer ourselves by quickly asking ourselves something simpler first; what really is a cancer? Well, the answer is absolutely nothing short of deeply important, and very, very scary. According to the National Cancer Institute, a cancer is known as a scenario where a cells develops mutated in a harmful, bypasses various immune responses meant to kill this exact kind of thing, and then divides into clusters of mass.^2 Considering what we know about cancer long by now, it’s no shock to pretty much anyone that such a scenario can turn serious fast. Let us put this into perspective with similar topic.

In my class, I personally examined the various ways that something called a Xenograft benefits humanity. Surprisingly, I learned from Caroline Mitchellthat Xenografts are not some kind of scientific instrument like i originally suspected when I first heard it, but rather its actually the concept of using biological cells, tissues, and even organs beyond human origins.^3 Using pigs as an example, we can accept their hearts in our bodies to serve as our own, use their skin to temporarily treat burn victims, use their kidneys as our own when we lose to kidney failure and need new kidneys, and much more (including cancer treatments of course) all because we share a lot of biology with pigs. It is little short of incredible how essential Xenografts could very much be to resolve issues like the infamous organ donor hospitals dread worldwide. In the end, however, we must continue to strive toward scientific excellence to uncover the best possible solutions. As I conclude this blog post, I actually conclude my final blog on all, so I wish to shout out my teacher for being incredible to me.

References:
1) “Understanding and exploiting cell signaling convergence nodes and pathway cross-talk in malignant brain cancer” by Nok Him Funga, Corrina A. Grimaa, Samuel S. Widodoa, Andrew H. Kaye, Clarissa A. Whitehead, Stanley S. Stylli, and Theo Mantamadiotisa
2) https://www.cancer.gov/about-cancer/understanding/what-is-cancer
3) https://www.taconic.com/resources/what-is-xenograft (Caroline Michell)

Community/Disease/Health/Hot topics

Signaling Pathways in Glioblastoma: A Convergence of Pathways and a Convergence of Hope

Posted on April 30, 2025 by Meg / 0 Comment

Glioblastoma (GBM) is one of the most aggressive and treatment-resistant cancers, with a median survival of just 14 months despite advances in therapy[1]. The review article “Understanding and Exploiting Cell Signaling Convergence Nodes and Pathway Crosstalk in Malignant Brain Cancer” [2] dives into the complex molecular mechanisms driving GBM progression and treatment resistance, focusing on three key signaling pathways: PI3K, MAPK, and cAMP.

The Complexity of Glioblastoma: Resistant and Persistent

GBM is characterized by intertumoral heterogeneity, meaning that different regions of the tumor may exhibit distinct genetic and molecular profiles. This heterogeneity complicates treatment, as therapies targeting one pathway may fail due to compensatory activation of another. The Cancer Genome Atlas has classified GBM into four molecular subtypes:

Classical – Driven by EGFR amplification.
Mesenchymal – Associated with NF1 and PTEN mutations.
Proneural – Linked to PDGFRA amplification and IDH1 mutations.
Neural – Lacks clear driver mutations but expresses neuronal markers[2].

Each subtype responds differently to treatment, creating an increased need for personalized therapeutic strategies.

Key Signaling Pathways in GBM

The MAPK Pathway: Cell Proliferation and Survival

The mitogen-activated protein kinase (MAPK) pathway is a critical regulator of cell proliferation, survival, and metastasis. In GBM, this pathway is frequently hyperactivated due to:

EGFR amplification (seen in ~40% of cases).
Loss of NF1, a negative regulator that inactivates Ras by converting GTP to GDP.

Upon growth factor binding (e.g., EGF), receptor tyrosine kinases (RTKs) dimerize and phosphorylate downstream adaptor proteins, leading to Ras → Raf → MEK → ERK activation. ERK then translocates to the nucleus, promoting transcription of oncogenes like c-Myc and CREB.

MAPK-based therapeutic implications:

Vemurafenib, a BRAF inhibitor, has shown promise in GBM patients with BRAF V600Emutations[2].
However, resistance often arises due to pathway redundancy, where tumors activate alternate survival mechanisms.

The PI3K Pathway: Regulating Cell Growth

The phosphoinositide 3-kinase (PI3K) pathway is another major player in GBM, regulating cell growth, metabolism, and survival. Key alterations include:

PTEN loss, leading to unchecked PIP3 accumulation and AKT/mTOR activation.
PI3K mutations, driving oncogenic signaling.

PI3K signaling promotes invadopodium formation, enhancing tumor invasiveness by upregulating matrix metalloproteinases (MMPs).

PI3K-based therapeutic implications:

BKM120 is a PI3K inhibitor, which could be used as a potential therapy.
Combining PI3K inhibitors with MAPK inhibitors may prevent resistance by blocking compensatory signaling[2].

The cAMP Pathway: Tumor Suppression

Unlike MAPK and PI3K, the cAMP pathway is generally suppressed in GBM, correlating with higher tumor malignancy. cAMP, produced by adenylate cyclase, activates protein kinase A (PKA), which can:

Inhibit Raf, suppressing MAPK signaling.
Induce apoptosis via Bim upregulation.

Therapeutic implications:

PDE inhibitors (e.g., IBMX) increase cAMP levels, promoting apoptosis in some GBM cell lines.
Combining cAMP activators with MAPK inhibitors may overcome resistance in tumors with high ERK activity[2].

Pathway Convergence: CREB as a Critical Molecule

A major theme in the review is pathway convergence on transcription factors like CREB (cAMP response element-binding protein) [2]. CREB integrates signals from MAPK (via ERK phosphorylation of Ser133), PI3K (via RSK and MSK kinases), and cAMP (via PKA).

CREB regulates genes involved in cell survival, proliferation, and stemness, making it an attractive therapeutic target. Small-molecule CREB inhibitors are being explored in leukemia and lung cancer, suggesting potential applicability in GBM[2].

Overcoming Drug Resistance: The Need for Combinatorial Therapy

A major challenge in GBM treatment is adaptive resistance, where tumors rewire signaling networks to bypass targeted inhibition. Strategies to overcome this include:

Dual PI3K/MAPK inhibition – Prevents compensatory pathway activation.
Targeting downstream molecules – Blocks multiple oncogenic signals simultaneously by targeting factors like CREB.
Combining pathway inhibitors with immunotherapy – Enhances anti-tumor immune responses[2].

Toward Precision Medicine in GBM

Understanding signaling crosstalk can inform better therapies for GBM. Future research should focus on identifying biomarkers to predict drug response and developing inhibitors targeting signaling hubs like CREB. For now, this review emphasizes the importance of understanding the convergence of pathways in tackling one of the most formidable challenges in neuro-oncology.

This article provides a fascinating glimpse into the molecular battlefield of GBM and the innovative strategies being developed to fight it. It’s a powerful reminder that cancer is not just a genetic disease, but a signaling disease—and defeating it will require disrupting its communication networks at multiple levels.

Glioblastoma is one of the most aggressive and treatment-resistant cancers AND is driven by hyperactive PI3K and MAPK signaling pathways that promote tumor growth and invasion. BUT these pathways exhibit crosstalk and redundancy, leading to drug resistance. THEREFORE, targeting downstream convergence points like CREB or using combination therapies may overcome resistance and improve treatment outcomes.

References

[1] “About Glioblastoma,” National Brain Tumor Society. Accessed: Apr. 29, 2025. [Online]. Available: https://braintumor.org/events/glioblastoma-awareness-day/about-glioblastoma/

[2] N. H. Fung et al., “Understanding and exploiting cell signalling convergence nodes and pathway cross-talk in malignant brain cancer,” Cell. Signal., vol. 57, pp. 2–9, May 2019, doi: 10.1016/j.cellsig.2019.01.011.

Disease/Health/Uncategorized

Inside the Tumor: The Complex Biology of Glioblastoma

Posted on April 30, 2025 by jcopiske / 0 Comment

Biophysical interaction temozolomide ...

INSIDE THE TUMOR: THE COMPLEX BIOLOGY OF GLIOBLASTOMA

Glioblastoma (GBM) is a highly aggressive brain cancer that stems from glial cells, these cells known for their supportive role in the brain. This cancer is notorious for its high mortality rate and poor prognosis, and it is often regarded as the deadliest type of cancer. GBM is one of the most challenging cancers to treat, largely due to its resistance to current therapies.

Cell signaling regulates cell behavior; therefore, cell behavior influences tumor development. GBM rewires neuronal networks and intervenes with three common signaling pathways: PI3K, MAPK, and cAMP. The hyper-activation of these pathways drives tumor malignancy. This raises the question: Why is GBM so aggressive compared to other types of cancer?

WHAT IS GLIOBLASTOMA?

In a healthy brain, glial cells regulate their gene expression very precisely to support neurons and maintain homeostasis. However, in glioblastoma, these cells undergo malignant transformation, which is frequently accompanied by the over-expression of certain genes and proteins, such as EGFR (Epidermal Growth Factor Receptor). EGFR is involved in cell signaling pathways that control cell division and survival. When mutations occur, an excess of EGFR appears on cancer cells, causing them to divide more rapidly.

Figure 1. early stage of glioblastoma versus tumor cells in the advanced stage.

The over-expression of EGFR drives the over-activation of signaling pathways such as PI3K/AKT and MAPK as shown in Figure 1. The tumor environment also has an increasing number of peripheral cells that accumulate within the tumor tissue, further promoting tumor progression. This progression can impair the blood-brain barrier (BBB), as shown in Figure 2. which is the semi-permeable membrane that regulates movement between the blood and the brain. Such impairment can manifest as inflammation.[1]

Glioblastoma - an overview | ScienceDirect Topics — Figure 2. GBM presence in the BBB

FOUR SUBTYPES OF GLIOBLASTOMA

Classical GBM:

Amplified EGFR signaling but minimal TP53 mutations.
Responds well to aggressive treatment.

Mesenchymal GBM:

Frequent NF1 and PTEN mutations, along with altered MAPK and PI3K pathways.
Aggressive therapy improves survival.
longer average survival time

Pro-neural GBM:

Common in younger patients, with mutations like IDH1 and TP53 and amplified PDGFRA.
Longer survival but poor response to aggressive treatments.

Neural GBM:

Characterized by neuronal gene expression, with no obvious mutations.
Offers the worst survival prognosis.
symptoms only slightly improve with treatment

The Multifaceted Metabolism of Glioblastoma | SpringerLink — Figure 3. subtypes of Glioblastoma

HOW GLIOBLASTOMA DISRUPTS NEURONAL SIGNALING

Glioblastoma invades the brain, rewiring neuronal networks and disrupting signaling:

PI3K and MAPK Pathways

These pathways use cellular signaling to regulate cell proliferation and survival. In GBM, PI3K and MAPK are cross-regulated, which poses a challenge for research because it becomes difficult to target a singular pathway.

cAMP

cAMP is distinct from the PI3K and MAPK pathways because it generally exerts tumor-suppressive effects rather than driving cell proliferation. cAMP, which stands for cyclic Adenosine Monophosphate, is produced by adenylyl cyclase in response to various extracellular signals. Elevated levels of cAMP activate protein kinase A (PKA), which then phosphorylates downstream targets that promote cell cycle arrest, differentiation, and apoptosis. In contrast, the PI3K and MAPK pathways typically generate proliferative signals that support tumor growth.

WHAT IS CROSSTALK

Crosstalk is a term that indicates the interaction between different signaling pathways. In GBM, a tumor will disrupt the communication between the pathways. dysregulated pathways—such as PI3K/AKT, MAPK, and cAMP—don’t operate in isolation. Instead, they interfere with and amplify each other’s signals, leading to a network of communication that is difficult to shut down with targeted therapies. [2]

TREATMENT CHALLENGES

Despite decades of intense research, GBM remains one of the most challenging cancers to treat. Drug resistence is driven by mulitple factors in GBM, making it difficult to achieve lasting therapeutic responses. As targeting GBM is a major focus of research, two main strategies have been pursued:

EGFR

Researchers have investigated EGFR inhibitors to counter the over-expression of EGFR, which promotes rapid cell division and survival. However, clinical results with EGFR inhibitors have often shown limited benefits, partly because the drugs are unable to fully inhibit downstream signaling and overcome intrinsic resistance mechanisms.

PI3K/AKT/mTOR

Regulatory PI3k/Akt/ mTOR as shown in Figure 4. This pathway supports cell proliferation, survival, and metabolic reprogramming such as promoting glucose dependency. Glioblastoma cells leverage PI3K/AKT signaling to enhance glucose metabolism, which facilitates rapid growth while protecting them from apoptosis. A hyper-activation of PI3K, often combined with the loss of PTEN function, drives this process. The frequent occurrence of PI3K hyper-activation, PTEN loss, and AKT mutations underscores the central role of this pathway as a key driver of oncogenesis and treatment resistance in GBM.[3]

WHY YOU SHOULD CARE!

Understanding the complex signaling pathways involved in GBM is crucial because it explains the underlying reasons for its aggressiveness and resistance to therapy. With GBM being one of the deadliest cancers and given its ability to rewire neuronal networks and activate multiple survival pathways simultaneously, finding effective treatments remains one of the greatest challenges in oncology. Overcoming these challenges could lead to significant advancements in therapeutic strategies and ultimately improve the survival rate and quality of life for patients with this devastating disease.

REFRENCES

[3] Barzegar Behrooz, A., Talaie, Z., Jusheghani, F., Łos, M. J., Klonisch, T., & Ghavami, S. (2022). Wnt and PI3K/Akt/mTOR Survival Pathways as Therapeutic Targets in Glioblastoma. International journal of molecular sciences, 23(3), 1353. https://doi.org/10.3390/ijms23031353

[2] Fung NH;Grima CA;Widodo SS;Kaye AH;Whitehead CA;Stylli SS;Mantamadiotis T; (n.d.). Understanding and exploiting cell signalling convergence nodes and pathway cross-talk in malignant brain cancer. Cellular signalling. https://pubmed.ncbi.nlm.nih.gov/30710631/

[1] Wu, L., Chai, R., Lin, Z., Wu, R., Yao, D., Jiang, T., & Wang, Q. (2023). Evolution-driven crosstalk between glioblastoma and the tumor microenvironment. Cancer biology & medicine, 20(5), 319–324. https://doi.org/10.20892/j.issn.2095-3941.2022.0771

Disease/Health/Uncategorized

Untangling the Deadliest Brain Tumor: Why We Must Care About Glioblastoma Research

Posted on April 29, 2025 by ttiongso / 0 Comment

Glioblastoma (GBM) is the deadliest form of brain cancer, and despite decades of effort, survival rates have barely improved. While we’ve learned a lot about cancer pathways, glioblastoma remains particularly elusive because of its complex, tangled web of signaling networks. New research has revealed how major pathways like PI3K, MAPK, and cAMP interact and offer potential new targets for therapy. Therefore, understanding these pathways could be the key to finally outsmarting this brutal disease.

Why Glioblastoma Matters

GBM isn’t just another cancer—it’s an aggressive, invasive, and heterogeneous beast. After initial surgery, chemotherapy (typically temozolomide), and radiation, tumors almost always return within months. Median survival is just 14 months, with a 5-year survival rate of less than 5%[1].

What the Science Shows Us

The article, Understanding and Exploiting Cell Signalling Convergence Nodes and Pathway Cross-Talk in Malignant Brain Cancer, explores three crucial pathways:

PI3K pathway: Promotes cell survival, proliferation, and invasion. Mutations in genes like PTEN often hyperactivate this pathway in GBM.
MAPK pathway: Drives cell division and survival. EGFR mutations, common in GBM, turbocharge this cascade.
Figure 1 [1]
cAMP pathway: Normally suppresses tumor growth, but GBM often has abnormally low cAMP activity.

Each of these pathways individually promotes tumor growth.. PI3K and MAPK can activate each other, bypassing single-drug therapies. Meanwhile, cAMP can suppress parts of MAPK and PI3K, offering a potential therapeutic counterbalance.

How This Could Change Treatment

Glioblastoma (GBM) is hard to treat because it can quickly find new ways to grow when one path is blocked. It’s like cutting off one road, only to have the tumor take a different route. That’s why treating just one pathway at a time often doesn’t work for long. But new research suggests smarter ways to attack the tumor:

Combining Treatments

Instead of blocking just one pathway, scientists are now trying to block two or more at the same time, like PI3K and MAPK. These pathways often work together, so stopping both may prevent the tumor from finding a new route to grow [2].

Targeting Key Hubs

Some proteins, like CREB, sit at the center of many important growth signals. By targeting CREB, we could shut down several tumor pathways at once. This might make it harder for the tumor to adapt and could also target the cells that help tumors grow back [1,3].

Restoring Natural “Off” Signals

Healthy brain cells use cAMP signaling to control growth and trigger cell death. GBM cells often shut this down. Some drugs can boost cAMP, pushing the cancer cells back toward normal behavior or even killing them. But if MAPK is too active, the tumor resists this effect, so blocking MAPK at the same time could make these drugs work better [4].

So Why Should the Public Care?

Glioblastoma is deadly because it quickly adapts to treatments by switching between different growth pathways. These new strategies focus on combining therapies, targeting key control points like CREB, and restoring natural tumor-blocking signals like cAMP.
By attacking multiple weak spots at once, we could finally slow tumor growth, prevent resistance, and improve survival. Instead of reacting to the tumor’s changes, we could stay one step ahead.

[1] Fung NH, Grima CA, Widodo SS, Kaye AH, Whitehead CA, Stylli SS, Mantamadiotis T. Understanding and exploiting cell signalling convergence nodes and pathway cross-talk in malignant brain cancer. Cell Signal. 2019 May;57:2-9. doi: 10.1016/j.cellsig.2019.01.011. Epub 2019 Jan 30. PMID: 30710631.

[2]Julien, L. A., Carriere, A., Moreau, J., & Roux, P. P. (2010). mTORC1-activated S6K1 phosphorylates Rictor on threonine 1135 and regulates mTORC2 signaling. Molecular and cellular biology, 30(4), 908–921. https://doi.org/10.1128/MCB.00601-09

[3] Mantamadiotis T, Papalexis N, Dworkin S. CREB signalling in neural stem/progenitor cells: recent developments and the implications for brain tumour biology. Bioessays. 2012 Apr;34(4):293-300. doi: 10.1002/bies.201100133. Epub 2012 Feb 13. PMID: 22331586.

[4] Daniel PM, Filiz G, Mantamadiotis T. Sensitivity of GBM cells to cAMP agonist-mediated apoptosis correlates with CD44 expression and agonist resistance with MAPK signaling. Cell Death Dis. 2016 Dec 1;7(12):e2494. doi: 10.1038/cddis.2016.393. PMID: 27906173; PMCID: PMC5261024.

Community

Final Reflection: Connecting the Dots

Posted on April 26, 2025 by gsparks1 / 0 Comment

As I wrap up my time at Concordia, I find myself reflecting on just how much this experience brought together the skills and knowledge I’ve developed over time. Majoring in Chemistry with an ACS certification and minoring in Biology and Mathematics, I have spent the last few years diving deep into the world of science, but this class pushed me to connect all of that in new ways. It challenged me to think differently, apply information creatively, and communicate complex ideas in ways that make sense beyond a lab setting.

This course reminded me why the liberal arts education model matters. It gave me the tools to see beyond just facts and equations and to ask deeper questions about how science fits into the broader world and how I can use that knowledge responsibly and meaningfully moving forward.

Expanding My Knowledge: Learning in New Ways

Throughout the semester, I gained a deeper understanding of key signaling pathways in the brain, such as MAPK, PI3K, and cAMP. These pathways are vital not just for understanding basic brain function but also for grasping how diseases like glioblastoma, anxiety, and obesity develop. I had learned about chemical signaling before, but this class pushed me to think about it on a systems level and to consider how disruptions ripple outward and cause real-world disease.

One of the most valuable things I took away from this class was improving my ability to read and process scientific articles. Academic research papers can be intimidating, even for students deep into their majors. However, this course pushed me to work through dense information, pull out key ideas, and translate them into my own words. Especially through writing weekly blogs aimed at a general audience.

Another important area of growth for me was learning to form hypotheses based on given data and to interpret new information critically. The signal interpretation tasks were some of my favorite assignments because they required me to predict outcomes based on pathways we had studied by not just memorizing but truly applying what I knew. This kind of thinking will be crucial as I move forward toward my future goals in graduate school and research.

Building Skills for the Future

The skills I developed this semester directly relate to the career I hope to pursue. After graduation, I plan to attend graduate school for chemistry, focusing on research. In that world, critical thinking, problem-solving, and the ability to communicate scientific ideas clearly are absolutely essential.

Through this class, I have become better at not just analyzing scientific data, but also connecting concepts across fields such as chemistry, biology, neuroscience, and even broader societal issues. Being able to see those connections will help me think more creatively and innovatively as a researcher.

If I were to highlight one major skill I’ve strengthened this semester on my resume, it would be critical thinking and problem-solving. Whether through analyzing a faulty signaling pathway, understanding a complicated article, or explaining a disease mechanism in simple language, this course constantly pushed me to solve problems from multiple angles and with multiple tools.

Liberal Arts Learning: Why It Matters

Studying at a liberal arts college like Concordia has been a huge part of shaping the way I think. Instead of focusing only on one narrow specialty, I have been exposed to a variety of disciplines ranging from science and math to history, philosophy, and the arts.

That exposure helped me understand that real-world problems are complex and interconnected. Diseases like glioblastoma or conditions like anxiety are not just chemical issues; they involve psychology, sociology, ethics, healthcare policy, and more. Liberal arts learning has taught me how to bridge those gaps, to ask better questions, and to think critically about the world around me.

In many ways, this class embodied the spirit of Concordia’s liberal learning goals. It reinforced a love for learning by encouraging curiosity about brain function and disease. It built on my foundational skills of analysis and communication. It gave me new interdisciplinary insights by combining neuroscience, psychology, chemistry, and even public health ideas. It asked me to think about the cultural and ethical implications of diseases and treatments. And most importantly, it prepared me to engage responsibly with the world as a future scientist.

Solving Problems Across Disciplines

One specific example of using several disciplinary perspectives came when we discussed treatments for diseases like obesity. Understanding obesity is not just a question of biology, it also involves chemistry (how molecules interact in the body), neuroscience (how the brain regulates hunger and reward), psychology (how behaviors and emotions influence eating), and sociology (how social environments shape habits).

By looking at the issue from all those angles, we could better understand why obesity is so difficult to treat and why a one-size-fits-all solution won’t work. This kind of interdisciplinary thinking will be critical in any future research I do, especially if I want my work to have real-world impact.

Looking Ahead

As I move forward toward graduate school and a future career in chemistry, I know the skills and experiences I gained in this course will stay with me. Being able to critically analyze information, synthesize ideas across disciplines, communicate clearly, and solve problems creatively are skills that matter in every field but especially in science, where the challenges we face are rarely simple.

This class helped remind me that the ultimate goal of education isn’t just to learn facts. It’s to become someone who can take knowledge and use it to make a difference. Whether through research, communication, or collaboration, I hope to keep building on what I’ve learned here at Concordia and to always keep growing as a learner, a thinker, and a responsible global citizen.

I also want to take a moment to express my gratitude for the dedicated professors here at Concordia. Throughout my time as a student, and especially in this course, I have been consistently supported and challenged by faculty who truly care about their students’ success. Their passion for teaching and commitment to helping us grow not just academically, but also personally, has made a lasting impact on me. I am incredibly thankful for their guidance, encouragement, and the countless ways they have helped me become a more thoughtful learner and a more prepared future scientist.

Disease/Health

Cracking the Code of Brain Cancer: How Glioblastoma Outsmarts Us and How We’re Fighting Back

Posted on April 26, 2025 by gsparks1 / 0 Comment

abstract created by Gabe Sparks.

Cancer is one of the most recognized and feared diseases in our society. It has been the focus of decades of research, with countless efforts dedicated to finding a cure. Thanks to these advances, we now have a range of treatments that can successfully target many types of cancer. However, there is still much we don’t understand, and some forms of cancer continue to cause trouble for even our best therapies. While breast cancer and skin cancer are commonly known, one of the most aggressive and deadly forms often goes overlooked: glioblastoma (GBM). This malignant brain tumor is notorious for its poor survival rates, with most patients living only months after diagnosis. Despite aggressive treatment with surgery, radiation, and the chemotherapy drug temozolomide, glioblastoma remains devastatingly difficult to control.¹

But new research is beginning to crack the code of how GBM survives and thrives. Potentially offering hope for smarter, more effective ways to fight back.

Understanding the Science

To understand the development of glioblastoma (GBM), it’s essential to look closely at three major signaling pathways: MAPK, cAMP, and PI3K. These pathways are critical for regulating key cellular functions, including metabolism, proliferation, survival, invasion, and stemness.¹ Under normal conditions, they work together in a carefully balanced system to maintain healthy cell growth and tissue stability. However, when these signaling networks become disrupted or unbalanced, they can trigger uncontrolled cell growth which sets the stage for the development of GBM.

The MAPK pathway begins with the activation of a receptor tyrosine kinase (RTK) on the cell surface. Once the receptor binds its specific ligand, it triggers a cascade of intracellular events: adaptor proteins like GRB2 and SOS activate Ras, which in turn activates RAF. RAF then phosphorylates MEK, which subsequently activates MAPK. Activated MAPK moves into the nucleus, where it phosphorylates transcription factors such as CREB, leading to the recruitment of additional regulatory proteins and RNA polymerase to initiate the expression of genes that promote growth and survival.¹Under normal conditions, this pathway is regulated by negative feedback mechanisms, including the tumor suppressor NF1.¹ However, in GBM, NF1 is often deleted or inactivated, allowing the pathway to remain unchecked.

The PI3K pathway also starts with the activation of an RTK. Activation of PI3K leads to the conversion of PIP2 to PIP3, which then recruits and activates PDK1. PDK1 then activates AKT which is a key regulator that can translocate into the nucleus and promote gene expression that drives survival, growth, and metabolic activity.¹ This pathway is normally kept in balance by PTEN (phosphatase and tensin homolog), a tumor suppressor that dephosphorylates PIP3 back to PIP2.¹ In GBM, PTEN is frequently mutated, deleted, or silenced, resulting in hyperactivation of PI3K signaling.

The cAMP pathway operates through a different mechanism. It begins with the binding of a ligand to a G-protein-coupled receptor (GPCR), leading to activation of adenylyl cyclase. This enzyme catalyzes the conversion of ATP to cAMP, which activates protein kinase A (PKA). PKA serves as an important modulator by inhibiting signaling at the RAF step of the MAPK pathway, thus helping to regulate cell growth. In GBM, cAMP levels are often reduced, weakening this inhibitory control and further contributing to the imbalance among pathways.

In glioblastoma, the MAPK and PI3K pathways are often hyperactivated, driving rapid and uncontrolled tumor cell proliferation, while the regulatory influence of the cAMP pathway is diminished.¹ This imbalance between growth-promoting and growth-suppressing signals creates an environment where cancer cells can thrive. Figure 1 is a pictural representation of the three pathways and how they interact with one another. Here is a link to an article that goes into great detail on how these pathways play a role in GBM.

Figure 1. Pictorial representation of the multiple pathways involved in GBM.

Fortunately, recent advances in research are uncovering new strategies to target these disrupted signaling networks and bring new hope in the fight against GBM.

Emerging Treatments

Despite the major challenges presented by glioblastoma’s complexity and resistance to treatment, several promising new therapies are under active investigation. One major area of focus is immunotherapy, which aims to help the body’s own immune system recognize and attack tumor cells. Immune checkpoint inhibitors that target proteins like PD-1, PD-L1,and CTLA-4 are being tested, often in combination, to boost immune activation against GBM.² Another exciting strategy is CAR T-cell therapy, where a patient’s T cells are genetically engineered to recognize specific tumor markers such as EGFRvIII and IL13Rα2.² While these approaches show great promise, challenges like tumor relapse and immune evasion remain, highlighting the need for further investigation.

Nanocarrier-mediated therapy is another cutting-edge field. Researchers are developing nanoparticles designed to cross the blood-brain barrier and deliver drugs directly to tumor cells.² By targeting cancer cells more precisely, these nanocarriers hope to improve treatment effectiveness while minimizing side effects. Magnetic nanoparticles, in particular, are entering clinical trials and may offer a new solution for delivering therapies deep within the brain.²

While many of these new therapies are still in early stages of development, they are already showing encouraging results. Together, they represent an exciting shift in how we approach one of the most challenging cancers. Here is a link to an article that explores many of the new treatments being developed.

Conclusions

GBM is a devastating form of cancer that too often goes overlooked. While more common cancers like breast and skin cancer receive widespread attention, it’s crucial that we shine a light on all forms of cancer especially those as aggressive and lethal as GBM. Increasing public awareness can drive not only a deeper understanding of this disease but also greater support for the research needed to develop new, life-saving treatments. By broadening the conversation around cancer, we can help accelerate progress and offer hope to those affected by glioblastoma and other under-recognized cancers.

References

(1) Fung, N. H.; Grima, C. A.; Widodo, S. S.; Kaye, A. H.; Whitehead, C. A.; Stylli, S. S.; Mantamadiotis, T. Understanding and Exploiting Cell Signalling Convergence Nodes and Pathway Cross-Talk in Malignant Brain Cancer. Cellular Signalling. Elsevier Inc. May 1, 2019, pp 2–9. https://doi.org/10.1016/j.cellsig.2019.01.011.

(2) Angom, R. S.; Nakka, N. M. R.; Bhattacharya, S. Advances in Glioblastoma Therapy: An Update on Current Approaches. Brain Sciences. Multidisciplinary Digital Publishing Institute (MDPI) November 1, 2023. https://doi.org/10.3390/brainsci13111536.

Uncategorized

Final Reflection: My Capstone Experience

Posted on April 26, 2025 by jdeitz1 / 0 Comment

Every ending is also a beginning — and as I close this chapter at Concordia, I find myself reflecting on how this journey has shaped who I am and how I see the world. As I reflect on my experience in this course and my broader education at Concordia, I realize how much the CORE curriculum and the philosophy of liberal learning — to Become Responsibly Engaged in the World (BREW) — have truly shaped my academic and personal growth. This class served as a culmination of the many skills, competencies, and perspectives I have gained during my time at Concordia, allowing me to not only apply what I have learned across disciplines but also to better understand my role in the larger global community.

Throughout the semester, the knowledge I gained from participating in this class was both academic and personal. Academically, I strengthened foundational skills such as critical thinking, comprehension and processing of research articles in a variety of fields, communication, and collaboration. Each of our weekly assignments not only made me better understand the topics discussed in each of the articles, but also it challenged me to think beyond surface-level understanding, encouraging me to connect theoretical knowledge to real-world applications. Personally, the group discussion aspect of this course pushed me to reflect more deeply on my values, my approach to problem-solving, and my ability to engage with diverse perspectives. Learning, for me this semester, was an active process of integration — weaving together threads from different courses, disciplines, and experiences into a cohesive understanding of complex issues.

The skills and competencies I gained this semester are directly aligned with my future goals. As I look toward a career in the field of chemistry that requires not only technical knowledge but also the ability to think critically, adapt, and lead ethically, I am grateful for the emphasis Concordia has placed on transferable skills. Whether it is analyzing data, finding and researching scientific topics of interest, creating stories and communicating them in a way that fit my audience, navigating intercultural communication, or leading a team with empathy and responsibility, the liberal learning goals have prepared me to meet these challenges. In particular, developing interdisciplinary perspectives has been invaluable. Problems in the real world are rarely isolated within one field, and my education has trained me to draw from multiple disciplines to find creative and effective solutions.

Learning at a liberal arts institution like Concordia has meant more than simply mastering content; it has meant developing a mindset of lifelong curiosity and responsibility. It has taught me to ask not just “How?” but also “Why?” and “For whom?” Concordia’s commitment to cultivating an examined self — culturally, ethically, physically, and spiritually — has encouraged me to be mindful of the broader impact of my actions. It has challenged me to think about my place in society and to recognize my responsibility to contribute positively to my community and beyond. In a world that is increasingly complex and interconnected, I believe this kind of education is more important than ever.

If I were to highlight a few skills I really strengthened this semester, I would definitely focus on communication, research and information literacy, and time management. Over the past few months, I had so many opportunities to practice different forms of communicating clearly — whether it was writing scientific based papers or blog posts, giving presentations, or simply explaining my thoughts and ideas in class discussions. I learned that good communication isn’t just about sharing information; it’s about telling a good story and making sure your message connects with your audience, and that’s something I know I’ll carry into my future work. I want to specifically highlight the opportunities that I have had to communicate in a public speaking manner. Public speaking or just clearly communicating my thoughts out loud to any size of audience has always been a struggle for me. I have gone through a lot of speech therapy throughout my life, especially in my childhood, and so public speaking is scary and difficult for me as I usually revert back to bad habits that make it hard to understand what I am trying to say. I have had plenty of practice with this over the years, but I think in this class as well as through senior chemistry seminar has been extremely influential in helping me feel more confident in my abilities and has given me hope that I can give solid scientific talks in the near future.

This semester also pushed me to become much more confident in my research skills. Finding reliable sources, evaluating information critically, and weaving different perspectives into a clear argument has become almost second nature. I realized how important it is not just to find information, but to understand and use it responsibly — a skill that’s incredibly valuable in any career path.

And finally, managing all the moving pieces of this semester really tested — and improved — my organizational skills. Being my fifth and final year here at Concordia came with some exciting opportunities to show off what I have done and learned such as senior chemistry seminar. This added to the process of balancing academic deadlines, looking for my next career step, and other outside commitments which forced me to plan ahead, stay focused, and adjust when things didn’t go exactly as planned. I struggled a lot with staying healthy this and last semester which really took me out of the flow that I have gotten used to being in during college. The previous semester showed it in terms of my academic performance and my struggles with bouncing back from being behind. However, I think I was able to learn from that experience, and even though I was dealing with similar issues this semester, I handled the situation much better and got back into the swing of things much more efficiently. I can honestly say I’m ending this semester more confident in my ability to stay organized and handle competing priorities, which will definitely help me moving forward.

Overall, this course — and my education at Concordia more broadly — has instilled in me a deep love for learning, an ability to think across disciplines, and a commitment to being a responsible, engaged participant in the world. I now see liberal learning not just as an academic ideal but as a lifelong practice — one that calls me to continue growing, questioning, and contributing, wherever my future may take me.

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Unlocking the Secrets of Cannabis: The Endocannabinoid System and the Future of Medicine

Posted on April 26, 2025 by jdeitz1 / 0 Comment

Cannabis has captivated human attention for centuries, from ancient herbal remedies to its modern role as a controversial therapy. But beyond the cultural conversation, modern science has pulled back the curtain to reveal a fascinating biological system deeply woven into the human body: the endocannabinoid system (ECS). Understanding this system—especially the cannabinoid receptors CB1 and CB2—is key to unlocking cannabis’s full therapeutic potential.

What Is the Endocannabinoid System (ECS)?

The ECS is a vast and complex network within our bodies that helps regulate vital functions like synaptic plasticity, homeostasis, pain perception, memory, mood, and even immune responses. At the heart of this system are two major players: CB1 and CB2 receptors.

CB1 receptors are mostly found in the central nervous system (CNS). These receptors are responsible for the majority of psychoactive effects associated with cannabis, especially those triggered by THC (tetrahydrocannabinol). They influence the release of neurotransmitters, modulate synaptic activity, and play key roles in memory formation, mood regulation, and motor control.
CB2 receptors, on the other hand, are typically associated with immune cells, though they also appear in the CNS, particularly during times of injury or disease. These receptors contribute to regulating inflammation and may provide neuroprotection in conditions like multiple sclerosis and Alzheimer’s disease.

Our bodies produce their own “natural cannabis-like chemicals,” called endocannabinoids, such as anandamide (AEA) and 2-arachidonoylglycerol (2-AG). These molecules help fine-tune communication between cells, ensuring that our nervous and immune systems remain balanced. [1]

This figure depicts the cell signaling mediated by CB1 receptor activation. [2]

Cannabis, Disease, and the ECS

Research has shown that dysregulation of the ECS is associated with several neurological and autoimmune conditions:

In Alzheimer’s disease, CB1 receptor activity may offer neuroprotection by limiting inflammation and neuron death.
In Huntington’s disease, alterations in CB1 receptor signaling are thought to contribute to disease progression.
Multiple sclerosis (MS) patients may benefit from cannabinoid-based therapies that reduce spasticity and pain.
After a traumatic brain injury (TBI), endocannabinoid signaling often ramps up, which may help the brain cope with trauma.

Importantly, endocannabinoid signaling is tightly linked with intracellular calcium levels and synaptic plasticity, suggesting that targeting this system could have far-reaching implications for treating both chronic pain and mental health conditions. [1]

Pharmaceutical Advances: Sativex and Beyond

One of the most promising examples of cannabis-based therapy is Sativex, an oromucosal spray containing a roughly 1:1 ratio of THC and CBD (cannabidiol).

Key points about Sativex:

It’s primarily used for neuropathic pain, spasticity in MS, and opioid-resistant pain.
It mimics the body’s own natural pain-relieving mechanisms.
It shows mild physiological effects like slight heart rate increases and occasional anxiety, but no major adverse events.
Compared to smoked cannabis, it provides slower absorption and delayed onset (3–6 hours), allowing patients better control over dosing and minimizing the risk of severe psychoactive side effects.

Clinical relevance: Sativex represents a major step forward—offering a safer, controlled, and standardized way for patients to benefit from cannabinoids without many of the risks associated with traditional cannabis use. [3]

Ethics and the Future of Cannabinoid Research

As scientific curiosity around cannabis grows, an important question looms: Should we keep investing in cannabinoid research?

From a medical standpoint, the answer seems clear—yes. The ECS regulates many critical systems in the body, and deeper insights could lead to treatments for devastating illnesses like Alzheimer’s, multiple sclerosis, chronic pain, epilepsy, and even cancer. The possibilities for neuroprotection, immune modulation, and pain management are too great to ignore.

However, there are ethical considerations:

Risk of misuse: As cannabis-based treatments become more available, there is a danger of blurred lines between therapeutic use and recreational abuse, especially among vulnerable populations.
Access and equity: Will cannabis-based therapies be accessible to all patients, or will they be priced out of reach?
Long-term effects: We still don’t fully understand the long-term impact of chronic cannabinoid use, particularly on developing brains.
Stigma: The historical stigma surrounding cannabis could discourage both patients and doctors from exploring legitimate treatments.

Despite these challenges, the potential benefits outweigh the risks—especially when research is conducted thoughtfully, ethically, and with a focus on scientific rigor and patient well-being.

Conclusion

Cannabis is much more than a cultural phenomenon—it is a doorway into one of the body’s most fascinating regulatory systems. By unlocking the secrets of the endocannabinoid system, researchers are paving the way for safer, smarter therapies that could transform how we treat some of the most challenging diseases known to humankind.

The future of medicine may very well be green—but only if we continue the work with open minds, cautious hands, and a commitment to scientific excellence.

To learn more about this topic click here.

[1] D. A. Kendall and G. A. Yudowski, “Cannabinoid Receptors in the Central Nervous System: Their Signaling and Roles in Disease,” Front. Cell. Neurosci., vol. 10, Jan. 2017, doi: 10.3389/fncel.2016.00294.

[2] L. Tian et al., “Cannabinoid receptor 1 ligands: Biased signaling mechanisms driving functionally selective drug discovery,” Pharmacology & Therapeutics, vol. 267, p. 108795, Mar. 2025, doi: 10.1016/j.pharmthera.2025.108795.

[3] E. L. Karschner et al., “Subjective and physiological effects after controlled Sativex and oral THC administration,” Clin Pharmacol Ther, vol. 89, no. 3, pp. 400–407, Mar. 2011, doi: 10.1038/clpt.2010.318.

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Unraveling Glioblastoma: The Relentless Brain Cancer That Outsmarts Treatment

Posted on April 25, 2025 by jdeitz1 / 0 Comment

A Killer Hidden in the Brain

Glioblastoma (GBM) doesn’t knock—it crashes in. It’s the most aggressive form of brain cancer known to modern medicine. Often, it’s discovered late, grows fast, and responds poorly to therapy. Despite the best surgical tools and targeted drugs, GBM continues to outmaneuver treatment. But why?

Recent studies show that glioblastoma’s power lies not just in how fast it grows, but in how it hijacks our body’s signaling systems—the same molecular messages responsible for normal cell survival, growth, and repair. Understanding these hijacked pathways could be the key to stopping this formidable disease. [1]

What Is Glioblastoma?

Glioblastoma is a malignant brain tumor that originates from glial cells—the supportive tissue in the brain. It falls under the category of gliomas, and it’s the most severe type (WHO Grade IV). The standard treatment includes surgery, radiation, and chemotherapy, but even with aggressive therapy, recurrence is common. Survival time often averages just over a year.

GBM isn’t a single disease. It has multiple subtypes, each with different mutations, gene expressions, and levels of severity. Among the most significant genes involved are:

EGFR (epidermal growth factor receptor): Often mutated or overexpressed in GBM, leading to uncontrolled cell division.
TP53: A tumor suppressor gene frequently altered in many cancers, including GBM.
NF1 and PTEN: Genes that act as brakes in important signaling pathways; when these are disabled, the brakes are off—and cancer runs wild. [1]

The Pathways That Fuel GBM

To understand glioblastoma is to understand how it rewires the body’s normal growth signals.

MAPK Pathway (Mitogen-Activated Protein Kinase): This pathway normally helps cells grow and respond to stress. In GBM, it’s often hyperactivated, fueling relentless cell division.
PI3K Pathway (Phosphoinositide 3-Kinase): Like MAPK, this pathway is critical for survival and growth. In many GBM patients, the PI3K pathway is stuck in the “on” position, sometimes because of loss of PTEN, a gene that usually keeps it in check.
cAMP Pathway: Normally involved in signaling within the cell, cyclic AMP is found at reduced levels in GBM. It also interacts with the MAPK and PI3K pathways, creating a web of dysregulation that supports tumor growth.

Together, these altered signals allow glioblastoma to grow, invade, and resist treatment. [1]

Why Can’t We Just Cut It Out?

That’s a common and fair question. In most cancers, removing the tumor—and a little extra tissue around it—is a good strategy. But in the brain, the stakes are different. Removing too much can damage critical functions like speech, memory, or movement. Even when surgery is aggressive, microscopic tumor cells often remain behind—and they’re often the toughest.

The Role of Cancer Stem Cells

One of GBM’s most terrifying strengths is its ability to bounce back after treatment. A key reason? Cancer stem cells (CSCs).

These cells possess a trait called stemness—the ability to replicate endlessly and produce many different cell types. CSCs in GBM:

Survive therapy by activating stress responses
Repopulate tumors even after remission
Change form (a trait called plasticity) to resist drugs
Migrate and seed new tumor regions

Because they aren’t a single type of cell, but a flexible population, these CSCs create tumor diversity that’s very hard to treat. Even if one therapy works on some cells, others survive and adapt. [2]

Artstract by J. Deitz

A Glimmer of Hope: Targeting Signaling and Stemness

While there’s no cure yet, scientists are exploring therapies that:

Inhibit key signaling proteins in the MAPK and PI3K pathways
Restore function to tumor suppressor genes like PTEN
Target cancer stem cells to prevent tumor regrowth

Personalized medicine—tailoring therapy to an individual’s unique tumor profile—offers a promising future. Understanding the signaling chaos behind GBM is a big step in that direction. [3]

Conclusion: The War in the Brain

Glioblastoma is a master strategist. It hijacks signaling, outwits treatment, and hides behind the blood-brain barrier. But science is catching up. With deeper understanding of its pathways and the stubborn stem cells that fuel it, we may someday turn this killer into something we can fight—and win.

To find out more about glioblastoma click here.

[1] N. H. Fung et al., “Understanding and exploiting cell signalling convergence nodes and pathway cross-talk in malignant brain cancer,” Cellular Signalling, vol. 57, pp. 2–9, May 2019, doi: 10.1016/j.cellsig.2019.01.011.

[2] P. M. Aponte and A. Caicedo, “Stemness in Cancer: Stem Cells, Cancer Stem Cells, and Their Microenvironment,” Stem Cells International, vol. 2017, pp. 1–17, 2017, doi: 10.1155/2017/5619472.

[3] J.-J. Loh and S. Ma, “Hallmarks of cancer stemness,” Cell Stem Cell, vol. 31, no. 5, pp. 617–639, May 2024, doi: 10.1016/j.stem.2024.04.004.

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The Silent Fire: How the Brain’s Inflammation Fuels Metabolic Syndrome—and How Fasting Might Fight Back

Posted on April 25, 2025 by jdeitz1 / 0 Comment

It starts quietly.

You might notice your pants fitting tighter, or maybe you feel tired even after a full night’s sleep. Your doctor says your blood pressure’s creeping up, your blood sugar’s higher than it should be, and your cholesterol’s out of balance. These are the early whispers of metabolic syndrome (MS)—a cluster of symptoms that often snowballs into type 2 diabetes, cardiovascular disease, and even cognitive decline. [1]

But what if the root of it all isn’t just in your gut, muscles, or heart… but in your brain?

Artstract by J. Deitz

The Brain Behind the Body

For decades, scientists believed obesity was driven mostly by willpower and metabolism. But research now paints a far more complex picture. At the center of it all is a tiny region in the brain called the hypothalamus, which acts as your body’s internal thermostat for energy balance. It senses nutrients, hormones like insulin and leptin, and sends out signals to adjust your hunger, energy use, and hormone production.

In a healthy system, this works beautifully. You eat, your body registers fullness, and energy is distributed efficiently. But under the influence of high-fat, high-sugar diets, this system begins to unravel.

The Fire Within: Hypothalamic Inflammation

New studies reveal that even a few days of eating a high-fat diet (HFD) is enough to trigger inflammation in the hypothalamus. Immune markers like IKK and NF-κB, key regulators of inflammation, become activated. Microglia—the brain’s immune cells—become hyperactive, and astrocytes (which usually support brain health) start to dysfunction.

This inflammation doesn’t just damage neurons; it disrupts the brain’s ability to respond to leptin and insulin, two hormones that help regulate appetite and metabolism. The result? A vicious cycle: your brain thinks you’re starving, even when you’re not. So it tells you to keep eating. And your body keeps storing. [1]

What’s even more fascinating is that this inflammation happens before noticeable weight gain. It’s not a symptom—it might be a cause.

Over Time: Chronic Chaos

With ongoing exposure to poor dietary choices, the inflammation worsens. Blood vessels in the hypothalamus begin to leak. Barriers that normally protect the brain—like the blood-brain barrier (BBB)—break down. Over time, glial cells like tanycytes and NG2-glia also join the chaos, further derailing energy regulation.

And it’s not just about food anymore. This dysfunction spreads: insulin resistance emerges in the liver, fat cells grow and become inflamed, and even your pancreas struggles to keep up. What began in the brain has now become a full-body metabolic mess.

The Maternal Link

Shockingly, the consequences don’t stop with you. A mother with metabolic syndrome or gestational diabetes can pass on a higher risk of obesity and metabolic dysfunction to her child—a phenomenon known as metabolic imprinting. It’s a generational echo of one person’s diet-induced inflammation.

Enter Fasting: A Possible Reset Button?

But there’s hope—and it might come from an ancient practice: fasting.

Intermittent fasting (IF), in its many forms—alternate-day fasting, time-restricted eating, or periodic fasts—has shown remarkable promise in combating metabolic syndrome. Multiple studies have found that even five weeks of intermittent fasting can improve blood pressure, reduce insulin resistance, and normalize glucose and lipid metabolism.

One recent study reported that IF led to measurable weight loss and even helped reverse metabolic symptoms in participants with impaired metabolism—all within just over a month. [2]

Fasting, Cancer, and Cognitive Health

Beyond metabolic benefits, IF may have anticancer effects. In a recent study, participants who fasted intermittently for four weeks showed a significant increase in tumor suppressor and DNA repair proteins. These protective effects weren’t seen in individuals following regular diets, suggesting fasting may have unique cancer-fighting properties. [3]

And it doesn’t stop at the body. Fasting also appears to benefit the brain. By influencing the gut-brain axis, IF supports healthier brain function and has been linked to better cognitive performance. Improved metabolic health from fasting was found to correlate with sharper thinking and reduced risk for central nervous system disorders, especially in people with MS. [4]

What Happens in the Brain During Fasting?

Fasting triggers the hypothalamus to switch gears. It downregulates inflammatory signals like IKK/NF-κB and improves leptin and insulin sensitivity. It also activates POMC neurons, which are responsible for telling your body to stop eating—restoring a function that is often impaired in obesity. Meanwhile, energy metabolism becomes more efficient, and fat stores are tapped more readily. [2]

The Road Forward

Metabolic syndrome is more than just a warning sign—it’s a flashing red light from your body and brain. But by understanding how diet-induced inflammation in the hypothalamus drives this condition, we gain powerful tools for prevention and healing.

Intermittent fasting, when done safely and sustainably, offers one such tool. It may not only reset the body but restore harmony in the brain’s control centers—quenching the silent fire and turning metabolic chaos into balance.

To learn more about metabolic syndrome click here.

[1] A. Jais and J. C. Brüning, “Hypothalamic inflammation in obesity and metabolic disease,” Journal of Clinical Investigation, vol. 127, no. 1, pp. 24–32, Jan. 2017, doi: 10.1172/JCI88878.

[2] X. Yuan et al., “Effect of Intermittent Fasting Diet on Glucose and Lipid Metabolism and Insulin Resistance in Patients with Impaired Glucose and Lipid Metabolism: A Systematic Review and Meta-Analysis,” International Journal of Endocrinology, vol. 2022, pp. 1–9, Mar. 2022, doi: 10.1155/2022/6999907.

[3] A. L. Mindikoglu et al., “Intermittent fasting from dawn to sunset for four consecutive weeks induces anticancer serum proteome response and improves metabolic syndrome,” Sci Rep, vol. 10, no. 1, p. 18341, Oct. 2020, doi: 10.1038/s41598-020-73767-w.

[4] J. Gudden, A. Arias Vasquez, and M. Bloemendaal, “The Effects of Intermittent Fasting on Brain and Cognitive Function,” Nutrients, vol. 13, no. 9, p. 3166, Sep. 2021, doi: 10.3390/nu13093166.