Learning to Think, Not Just to Know

Learning Beyond Memorization

Coming into this semester, I thought I had a solid understanding of what it meant to “learn” science. As a neuroscience major on a pre-med track, I’ve spent years studying pathways, mechanisms, and disorders. But this class challenged me to move beyond memorization and into something deeper—engagement.

One of the biggest shifts for me came from reading scientific papers and actually interacting with the concepts instead of just passively trying to understand them. At first, primary literature felt dense and overwhelming. But over time, I started to see patterns—how researchers ask questions, how they design experiments, and how they interpret results. More importantly, I began to connect those findings back to what I was learning in my other classes, especially biochemistry and neurochemistry.

That shift—from just learning content to actively engaging with it—was one of the most meaningful parts of this semester.

The Reality of Balancing It All

At the same time, this semester was not easy.

Balancing coursework, assignments, and everything else going on in my life was one of the biggest challenges I faced. There were moments where staying on top of deadlines felt overwhelming, and I had to be more intentional about managing my time and energy. This wasn’t just about academics—it was about learning how to show up consistently, even when I didn’t feel fully prepared.

In a way, this challenge was its own form of learning. It forced me to develop discipline, resilience, and a better understanding of how I work under pressure. These are skills that go beyond the classroom and will definitely carry into my future career.

Finding My Voice in Science

If there’s one area where I saw clear growth, it was in how I communicate science.

Through blog posts and artstracts, I learned how to take complex neurochemical and biochemical concepts and present them in a way that is accessible and engaging. Writing for a general audience pushed me to simplify without losing meaning, which is much harder than it sounds. It made me think carefully about what really matters in a concept and how to explain it clearly.

I also saw this growth during oral exams and class discussions. Being able to explain neurochemical concepts in conversation—with my professor and peers—was something I became more confident in over time. There’s something different about speaking your understanding out loud. It reveals what you truly know and where your gaps are.

Looking back, I’m proud of how much more comfortable I’ve become in these moments. Instead of feeling intimidated, I now see them as opportunities to think through ideas in real time.

Connecting Knowledge to My Future

As someone interested in going into healthcare, particularly in a patient-centered role, the skills I developed this semester feel very relevant.

Healthcare is not just about knowing information—it’s about communicating it clearly and compassionately. Patients don’t think in terms of biochemical pathways or signaling cascades. They need explanations that make sense to them, especially when they are already dealing with stress or uncertainty.

This class helped me practice that skill in a meaningful way. Whether I was writing a blog post or explaining a concept during an oral exam, I was constantly thinking about clarity, structure, and understanding.

I also developed a deeper appreciation for how interconnected different areas of science are. Taking biochemistry and neurochemistry at the same time allowed me to see how molecular processes translate into brain function and behavior. That kind of integrative thinking is essential in healthcare, where problems are rarely one-dimensional.

What Liberal Learning Means to Me

Before this semester, I understood liberal arts education as being “well-rounded.” But now, I see it more as being connected.

At Concordia, I’ve had the opportunity to explore different disciplines, but more importantly, I’ve learned how to see the relationships between them. This semester really highlighted that for me. Concepts I learned in biochemistry directly supported my understanding of neurochemical pathways, and together, they gave me a more complete picture of how the body works.

Liberal learning, to me, means being able to move between perspectives—scientific, social, and personal—and understanding how they inform each other. It’s not just about depth in one area, but about the ability to integrate knowledge across fields.

This approach has also encouraged me to think more broadly about real-world issues, especially in health and disease.

A Skill Worth Highlighting

If I were to highlight one skill I improved this semester on my resume, it would be:

Science Communication and Concept Integration

I’ve developed the ability to explain complex scientific ideas in a clear and accessible way, while also connecting concepts across disciplines. This includes writing for a general audience, engaging in discussions, and thinking critically about how different areas of knowledge overlap.

This is a skill that will be valuable not only in healthcare, but in any setting where clear communication and interdisciplinary thinking are important.

Understanding Metabolic Syndrome Through Multiple Lenses

One example that stands out to me in terms of interdisciplinary problem-solving is metabolic syndrome.

At first, metabolic syndrome might seem like a purely biological issue—something explained by insulin resistance, lipid metabolism, and hormonal regulation. And while those factors are important, this class helped me see that the problem is much more complex.

From a biochemical perspective, we can analyze pathways involving glucose regulation, fatty acid metabolism, and inflammation. From a neuroscience perspective, we can consider how the brain regulates appetite, reward, and stress responses. These systems influence behaviors like eating patterns and physical activity.

But we also have to think about psychological and social factors. Stress, mental health, access to healthy food, cultural dietary habits, and socioeconomic status all play a role in the development and progression of metabolic syndrome.

By integrating these perspectives, the problem becomes more complete. It also changes how we think about solutions. Instead of focusing only on medication or biological interventions, we can consider lifestyle changes, education, and community-level support.

This kind of interdisciplinary thinking reflects the goals of liberal learning – it allows us to approach complex issues in a way that is both informed and meaningful.

Growth That Extends Beyond the Classroom

Looking back, this semester was not just about what I learned, but how I learned.

I became more comfortable engaging with difficult material, more confident in expressing my understanding, and more aware of the connections between different areas of knowledge. I also learned how to navigate challenges and keep moving forward, even when things felt overwhelming.

These are lessons that go beyond any single class.

Moving Forward

As I reflect on this experience, I realize that learning at a liberal arts institution is not just about preparing for a career—it’s about developing the ability to think, connect, and engage with the world in a meaningful way.

This class pushed me to grow in those areas. It challenged me, but it also helped me see my own progress.

And while this may be the final blog post of the semester, the skills and perspectives I’ve gained will continue to shape how I approach learning in the future.

In that sense, this is not really an ending – it’s a continuation of the kind of learner I am becoming.

Feeding the Brain, Not Just the Body: How Omega-3s Rewire Metabolic Syndrome

Feature Image Credit: Created by Jackline Peace Nanyonga using ChatGPT.

Introduction: When Energy Balance Breaks Down

We eat to fuel our bodies and to maintain balance – between hunger and satiety, storage and use, health and disease. But in metabolic syndrome, this balance is disrupted. The body stores more, burns less, and signals get crossed. Therefore, what we eat doesn’t just add calories – it rewires the systems that control metabolism itself.

Metabolic syndrome – characterized by obesity, insulin resistance, dyslipidemia, and cardiovascular risk – is now understood as a disease of chronic, low-grade inflammation. Importantly, this inflammation isn’t just in fat tissue – it starts in the brain.

The Brain on Inflammation

At the center of metabolic regulation is the hypothalamus – a small but powerful brain region that integrates signals like insulin and leptin to regulate hunger and energy expenditure. Under normal conditions, this system maintains balance.

However, in obesity and metabolic syndrome, this system becomes inflamed.

Research shows that even a few days of a high-fat diet can trigger hypothalamic inflammation, activating pathways like JNK and NF-κB before significant weight gain even occurs.[1]  This inflammation disrupts signaling:

  • Insulin and leptin stop working effectively
  • Hunger signals override satiety
  • Energy expenditure drops

The result? A vicious cycle of overeating and metabolic dysfunction.

Figure 1: In metabolic syndrome, inflammation disrupts communication between hunger(AgRP) and satiety(MSH) pathways.

Not All Fats Are Equal

Here’s where diet becomes critical.

Saturated fatty acids (SFAs), commonly found in processed and high-fat diets, actively promote inflammation. They cross into the brain, activate immune-like pathways (like TLR4 signaling), and impair insulin and leptin signaling.[1]

In contrast, unsaturated fats – especially omega-3 fatty acids—do something different.

Instead of activating inflammation, they help reverse it.

Omega-3s as Metabolic Regulators

Omega-3 fatty acids (like EPA and DHA, found in fish, flaxseed, and walnuts) don’t just support heart health—they directly influence brain metabolism.

Studies show that omega-3s can:

  • Reduce hypothalamic inflammation
  • Restore insulin and leptin sensitivity
  • Improve signaling in appetite-regulating neurons

In fact, experimental evidence demonstrates that unsaturated fatty acids—including omega-3s—can reverse diet-induced hypothalamic inflammation and restore metabolic signaling.[1]

Mechanistically, omega-3s:

  • Inhibit pro-inflammatory pathways like NF-κB
  • Reduce cytokine production
  • Improve neuronal signaling related to energy balance

This essentially helps “reset” the system that metabolic syndrome disrupts.

Figure 2(right): Omega-3s counteract inflammatory pathways that drive insulin resistance.

 

 

From Brain to Body—Systemic Effects

What happens in the brain doesn’t stay in the brain.

Hypothalamic inflammation affects:

  • Glucose production in the liver
  • Fat storage in adipose tissue
  • Insulin secretion from the pancreas

This means improving brain inflammation can improve whole-body metabolism through the brain-body metabolic axis.

Omega-3s, by targeting this central control system, help:

  • Lower blood glucose
  • Improve lipid profiles
  • Reduce overall metabolic risk

In other words, they don’t just treat symptoms—they target the control center.

Rebalancing the System

Metabolic syndrome isn’t simply a matter of eating too much – it’s a failure of regulation. And that failure is deeply rooted in inflammation, especially in the brain. But not all nutrients worsen this process. Therefore, incorporating omega-3 fatty acids offers a way to actively restore balance.

By calming inflammation, improving signaling, and reconnecting the brain to the body, omega-3s shift metabolism from dysfunction back toward regulation.

Bibliography

[1]

Jais and J. C. Brüning, “Hypothalamic inflammation in obesity and metabolic disease,” J Clin Invest, vol. 127, no. 1, pp. 24–32, Jan. 2017, doi: 10.1172/JCI88878.

When Reward Feels Different: Dopamine and the Autism Brain

Introduction: The Signals That Shape Us

Every day, we are guided by invisible signals that tell us what matters. A smile from a friend, a good grade, even the satisfaction of finishing a task – these experiences feel meaningful because our brain marks them as worth it.

But what if those signals were quieter? Or different?

Autism Spectrum Disorder (ASD) is often described through behavior – differences in social interaction, communication, and patterns of repetitive actions. Yet beneath these outward traits lies something deeper: a brain that may be processing value and reward in a fundamentally different way. At the center of this idea is dopamine, a neurotransmitter that does far more than simply make us feel good.

Dopamine: More Than a “Feel-Good” Chemical

Dopamine is often misunderstood as the brain’s “pleasure chemical,” but its real role is more precise. It acts as a kind of internal currency, helping the brain decide what is worth attention, effort, and repetition. When dopamine is released, especially in pathways connecting areas like the ventral tegmental area and the nucleus accumbens, it sends a powerful message: this matters—remember it, seek it again.

This system shapes how we learn from our environment, how we stay motivated, and how we engage with others. It quietly influences everything from studying for an exam to forming friendships.

Figure 1(left): Dopaminergic pathways connecting key brain regions involved in reward and motivation. [1]

Autism: A Spectrum, Not a Single Story

One of the most important things to understand about ASD is that it is not caused by a single gene, pathway, or brain difference. Instead, it represents a wide spectrum of neurobiological variations. Researchers now recognize that there may be multiple subtypes of ASD, each shaped by different underlying mechanisms. [1]

Among these possibilities, dopamine dysfunction stands out as a compelling explanation for some individuals. Since dopamine is central to reward processing and behavioral learning—both of which are often altered in ASD – it offers a way to connect brain chemistry with lived experience.

When the Reward System Shifts

In a typical brain, social interactions are naturally rewarding. Eye contact, shared laughter, or conversation can trigger dopamine release, reinforcing those behaviors over time. However, in some individuals with ASD, these same social cues may not produce the same internal response.

If social interaction does not feel rewarding, the motivation to seek it out may be reduced—not because of disinterest, but because the brain is assigning value differently. At the same time, predictable and repetitive behaviors may provide a more reliable or satisfying signal, making them more appealing.

This perspective helps reframe common features of ASD. Reduced social engagement and repetitive actions are not simply deficits; they may reflect a brain that is responding to a different set of internal rewards. As the research suggests, disruptions in dopamine signaling can directly affect reward processing and learning patterns in ASD.[1]

Figure 2: Differences in dopamine signaling may shape how social interactions and repetitive behaviors are experienced in autism.[2]

Repetition, Motivation, and Control

Dopamine also plays a key role in shaping habits and repetitive behaviors. When dopamine signaling is altered, the balance between flexible behavior and repetition can shift. Interestingly, this is not unique to autism. In conditions like Parkinson’s disease, where dopamine levels are medically adjusted, individuals can develop intense, repetitive behaviors—highlighting how powerful this system is in driving what we do again and again.

This connection suggests that repetition in ASD may not simply be a behavioral trait, but a reflection of deeper neurochemical patterns influencing motivation and control.

Conclusion: Rethinking Behavior Through the Brain

Understanding autism through the lens of dopamine invites a shift in perspective. Instead of asking why certain behaviors occur, we begin to ask how the brain is assigning value to the world.

If dopamine signals are altered, then the meaning of everyday experiences changes. Social cues may feel less compelling, while structured patterns may feel more grounding. This is not a failure of the system, but a difference in how it operates.

Recognizing these differences is important, not only for understanding ASD, but for shaping more thoughtful and personalized approaches to support. Because ultimately, behavior is not just what we see—it is the reflection of how the brain experiences the world.

Bibliography

[1]

E. DiCarlo and M. T. Wallace, “Modeling dopamine dysfunction in autism spectrum disorder: From invertebrates to vertebrates,” Neuroscience & Biobehavioral Reviews, vol. 133, p. 104494, Feb. 2022, doi: 10.1016/j.neubiorev.2021.12.017.

[2]

“What is autism? | AUsome Training | Autism explained by Autistics.” Accessed: May 05, 2026. [Online]. Available: https://ausometraining.com/what-is-autism/

[Feature image]

“Is There an Autism Epidemic? | Johns Hopkins | Bloomberg School of Public Health.” Accessed: May 05, 2026. [Online]. Available: https://publichealth.jhu.edu/2025/is-there-an-autism-epidemic

From Signal to Gene: How β-Catenin Controls Transcription in the Brain

Feature Image Credit: Created by Jackline Peace Nanyonga using ChatGPT.

Feature Image Credit: Created by Jackline Peace Nanyonga using ChatGPT.

Introduction: Why Gene Transcription Matters

Your brain is constantly interpreting signals and translating them into changes in gene expression. One of the most important pathways involved in this process is Wnt signaling, a highly conserved system that plays a central role in brain development and neural function.

What makes this pathway especially powerful is not just the signal itself, but how it ultimately influences gene transcription. At the center of this process is β-catenin, a protein that acts as the final decision-maker – determining whether specific genes are turned on or off.

Understanding how β-catenin regulates transcription provides insight into how disruptions in signaling pathways may contribute to neurodevelopmental disorders such as schizophrenia.

When the Pathway is Off: Controlling β-Catenin

In the absence of a Wnt signal, β-catenin is tightly regulated and continuously broken down. This is achieved through a “destruction complex” composed of proteins such as GSK3β, Axin, APC, and CK1α. This complex phosphorylates β-catenin, targeting it for degradation and preventing it from accumulating in the cell (Singh, 2013).[1]

As a result, β-catenin cannot enter the nucleus, and Wnt target genes remain inactive. In this state, the pathway is effectively turned off, and no transcriptional response occurs.

 Turning the Switch On: β-Catenin and Gene Activation

When Wnt ligands bind to their receptors, the destruction complex is disrupted. This allows β-catenin to escape degradation and accumulate in the cytoplasm. As levels rise, β-catenin translocates into the nucleus, where it interacts with TCF/LEF transcription factors to activate gene expression programs involved in neural development, cell proliferation, and synaptic plasticity (Singh, 2013).[1]

Figure 1: Canonical Wnt signaling pathway showing β-catenin degradation (left) versus nuclear translocation and transcriptional activation (right).[1]

Importantly, β-catenin does not bind DNA directly. Instead, it acts as a co-activator, helping transcription factors initiate gene expression. This makes it a crucial link between extracellular signals and long-term cellular changes.

Regulation and Relevance: Why β-Catenin Matters in the Brain

The activity of β-catenin is closely tied to GSK3β, a kinase that determines whether β-catenin is degraded or stabilized. When GSK3β is active, β-catenin is broken down. However, when GSK3β is inhibited – such as by lithium – β-catenin accumulates and transcription is enhanced (Singh, 2013).[1]

This regulation becomes especially important in the context of schizophrenia. The paper highlights that multiple pathways, including dopamine signaling and Akt/GSK3β signaling, converge on β-catenin. Additionally, genetic factors such as the DISC1 gene can inhibit GSK3β, leading to increased β-catenin stability and greater activation of transcription (Singh, 2013).[1]

Figure 2 (left): Integration of dopamine, Akt/GSK3β, and Wnt signaling pathways converging on β-catenin-mediated transcription.[1]

These findings suggest that β-catenin is not just part of one pathway, but a central hub where multiple signals influence gene expression.

Conclusion: A Small Protein with Big Consequences

β-catenin represents the point where signaling pathways are translated into changes in gene expression. By controlling TCF/LEF-mediated transcription, it plays a key role in shaping how neurons develop, connect, and function.

Because of this, even subtle disruptions in β-catenin regulation can have significant downstream effects. In disorders like schizophrenia, these disruptions may alter gene expression patterns during critical stages of brain development, contributing to long-term changes in neural circuitry.

Ultimately, studying β-catenin helps shift our understanding of psychiatric disorders—from focusing only on neurotransmitters to considering how gene transcription itself is regulated.

Bibliography

                                                                                                                                                                   [1]

K. K. Singh, “An emerging role for Wnt and GSK3 signaling pathways in schizophrenia,” Clin Genet, vol. 83, no. 6, pp. 511–517, Jun. 2013, doi: 10.1111/cge.12111.

 

A Final Reflection on Neurochemistry

Neurochemistry was one of those classes I was not totally sure what to expect from going in. I knew it would be challenging, but I did not anticipate how different it would feel from most science courses I had taken here at Concordia. Finishing this semester feels like a good time to actually reflect on what happened over the last few months, not just in terms of what I learned, but how I learned it, and what I am taking with me.

Looking back at the semester, I can honestly say that this class pushed me more than a lot of courses in my four years here at Concordia. Not because of exams or the amount of material, but because of the way it was structured. Every week, we were reading real scientific papers, not textbook summaries of them. We had to understand them, pull out what mattered, and then find a way to explain it to someone who had never taken a biology class in their life. That process forced a level of understanding that I had not really experienced before.

What Learning Actually Looked Like This Semester

Most classes I have taken follow a pretty predictable pattern. You show up, you take notes, you study, you get tested. Neurochemistry did not work that way, and I think that is what made it stick. The learning here felt more applied. Reading a paper and then having to write a blog post about it for a general audience meant I could not just skim the surface. If I did not actually understand what the researchers were doing and why it mattered, it would come through immediately in the writing.

The Friday discussions were another big part of this. Sitting around and actually talking through the science, bouncing off ideas with classmates, and hearing different takes on the same paper helped me realize that understanding science is rarely a solo process. A lot of my best thinking in this class happened during those conversations.

The blog posts themselves were probably the most challenging and most rewarding part of the whole semester. There is a real difference between knowing something and being able to communicate it well. I learned that the hard way on my first few posts, and I think by the end I had genuinely improved.

Connecting to Concordia’s Goals for Liberal Learning

Concordia talks a lot about BREW, becoming responsibly engaged in the world, and about the five goals for liberal learning. Honestly those phrases were something I had not really heard or at least not paid much attention to, but this class definitely made them feel a little more real to me.

The goal of instilling a love for learning showed up in a way I did not expect. When you are reading primary literature on topics like how signaling pathways go wrong in disease, or how certain psychiatric conditions change the chemistry of the brain, it is hard not to get pulled in. There were weeks where I genuinely kept reading past what I needed to because I wanted to know what came next. That does not always happen in a science course.

Developing interdisciplinary perspectives was also a big piece of this class. Neurochemistry sits at this intersection of biology, chemistry, psychology, and public health, and none of those fields can fully explain the conditions we studied on their own. I found myself thinking about things from a bunch of different angles at once, which is a skill I think I will carry forward regardless of where I end up.

There is also responsible participation in the world. Writing blog posts that are publicly available to anyone forced me to take that seriously. If someone outside of Concordia reads what I wrote and comes away with a misunderstanding, that is on me. Getting that right felt like it mattered.

Skills I Am Taking With Me

If I were going to highlight one thing on a resume from this semester, it would be science communication. Before this class, I would have said I was a decent writer. Now I think I am a much more intentional one. There is a specific skill in taking something complicated and finding the clearest, most honest way to explain it to someone who does not share your background. I feel like I have actually developed that this semester, not just practiced it.

Critical reading is another one. I can look at a paper now and have a real conversation about its limitations, its methodology, and what the findings actually do and do not tell us. That felt pretty new to me at the start of the semester.

Using Multiple Perspectives to Understand a Problem

One of the things this class did really well was show how rarely a single discipline can fully explain something. Whether we were looking at neurodegenerative disease, psychiatric conditions, or addiction, the chemistry alone never told the whole story. You also had to think about behavior, environment, access to treatment, and the ethical questions around intervention and research.

A good example of this is how we approached addiction throughout the semester. From a neurochemistry standpoint, you can map out exactly what dopamine is doing in the reward pathway and how repeated substance use rewires those circuits over time. But that only explains part of the picture. Psychology brings in behavioral patterns and how stress and trauma shape vulnerability. Sociology asks who has access to treatment and who does not, and why. None of these perspectives are complete on its own, and learning to hold all of them at once is something I genuinely got better at this semester. That kind of thinking is what I would consider one of the more transferable things I am leaving this class with.

What Liberal Learning Means to Me

Being in Concordia and now graduating I have thought about this question in different ways at different times. Right now, at the end of my last semester, I think liberal learning means being trained to keep learning after you leave. It is not just about what you know when you walk across the stage, it is about whether you know how to figure things out, ask good questions, and communicate clearly once you are out in the world.

Neurochemistry, more than almost any other class I have taken here, felt like it was doing exactly that. I am finishing this semester with more questions than I started with, which is maybe the best sign that something actually worked.

 

[1]       “neuroscience cartoon,” Bing. Accessed: May 03, 2026. [Online]. Available: https://www.bing.com/images/search?q=neuroscience+cartoon&qs=n&form=QBIR&sp=-1&lq=0&pq=neuroscience+cartoon&sc=2-20&sk=&cvid=04B1F41362D14FD7B9701B8121A6BCA5

Final Reflections

This course was not just another requirement to complete. It became a space where I could actively integrate the skills, perspectives, and habits of mind I have been developing throughout my time at Concordia. In many ways, it helped me understand what liberal learning truly means and how it prepares me to be a responsibly engaged participant in the world.

My Relationship with Learning Changed

In terms of the types of learning that occurred this semester, I experienced a combination of academic, reflective, and applied learning. Academically, I deepened my understanding of complex topics and improved my ability to analyze information. Reflectively, I became more aware of my own learning process, strengths, and areas for growth. Applied learning came through translating knowledge into blog posts and discussions that required me to think beyond the classroom and consider real-world relevance.

Looking ahead, I can see how everything I’ve gained this semester connects to my future goals. I want to go into neuroscience, potentially through a post-bacc program, and eventually work in research. The skills I’ve built, especially critical thinking, communication, and the ability to look at problems from multiple angles, are going to be essential. But beyond that, I think this class helped me develop a mindset that will matter just as much. Being curious, being reflective, and being aware of the bigger picture are things that will stay with me no matter what path I take.

If i had to put one skill on my resume from this semester, it would definitely be science communication. I feel so much more confident now in my ability to take complex ideas and explain them in a way that people can actually understand and connect with. That’s something I didn’t realize I needed to work on before, but now I see how valuable it is.

Neurochemistry Class 2026

At times during college, especially when balancing a heavy course load, work, and personal responsibilities, learning can start to feel unbearable. However, through this class, I was reminded that learning is not just about absorbing information but about curiosity, questioning, and growth. Whether I was writing blog posts, engaging with Wednesday speed learning, or reflecting on complex topics, I found myself becoming more genuinely interested in the “why” behind what I was studying. That curiosity is something I will carry forward beyond this semester.

I was pushed to think about not only what I am learning, but why I’m learning it. For instance, when considering the ethical implications of AI or scientific advancements, I had to confront my own beliefs about responsibility, human connection, and the role of technology in our lives. This process helped me develop a more thoughtful and intentional perspective on my future career path. This class emphasized that knowledge comes with responsibility. As a future professional in neuroscience, this means considering the ethical implications of research, advocating for equitable access to resources, and communicating information in a way that is accurate and compassionate. It also means being open to different perspectives and continuously learning from others.

This class also strengthened my foundational skills and transferable intellectual capacities, particularly in writing and critical thinking. Many of our assignments required us to take complex scientific or conceptual topics and translate them into accessible, engaging formats. This challenged me to think not only about what I know, but how I communicate it. I thought I was used to engaging with dense scientific literature, but this course pushed me to step back and consider how to make that information meaningful to a broader audience. That is a skill that will be valuable in my future, especially as I hope to pursue post-baccalaureate programs and eventually work in research where communication is essential.

By the end of this semester, I don’t just feel like I completed another course. I feel like I’ve grown into a more thoughtful, aware, and capable learner. And honestly, that feels a lot more important than any grade.

Images sourced from ChatGPT

A Reflection on the Semester

Most classes involve lecture, assignments, and then tests. The structure of this class was quite different than a traditional class, yet it works so well, and in my case better than traditional classes. I think the way this class is laid out makes it a poster child for liberal learning. It covers all five of Concordia’s goals for liberal learning and more classes should be structured in a similar way.

The Unique Way of Learning This Class Encourages

The way the class is structured encourages a very independent approach to learning and allows us, the students, to take advantage of a learning style that suits us best. By encouraging this independent learning, it not only helps us learn about the topic, but also about our own personal learning styles and how to solve problems in the future. Even if I never talk about anything I used in this class again, I will still use the skills I learned in it on a daily basis in whatever career I find myself in. These skills include finding information, applying outside information to the information presented in class, and developing our own questions about the topic. Additionally, I think this class encourages a learning style and class set up consistent with graduate school. As graduate school is a path many of us will follow, learning these skills before hand gives us that much of an advantage once we get to graduate school as well.

Credit: eSchool News (1)

The learning encouraged by the class also helped with developing a deeper understanding of the overall material of my majors. As a neuroscience and psychology major I have learned about most of the diseases talked about in the class, but I have never really gotten into the why. This class for me felt more like a more advanced extension of psychopathology, as I got to learn the ins and outs of all these diseases and this encouraged me to think deeper about these topics outside of class. This exemplifies one of the cores of liberal learning, developing an understanding of interdisciplinary perspectives. Without this class I would have not learned the ins and outs of these diseases I am so interested in nearly as well as I have. Especially since many of the papers we read are new perspectives on things and getting an understanding on new perspectives has allowed me to further my own understanding on the topics.

Encouraging Responsible Participation in the World

While this class doesn’t involve actually going out into the community and getting us physically involved, it still encourages us to be engaged in the world. Simply by being informed about these things encourages us to be engaged, as the first step to fixing a problem is understanding the problem to begin with. The learning in this class encourages us to understand each individual part of the problem, as we all go out and learn a lot about thing and then share it. This is another way this class encourages us to participate in the world, it teaches us how to present information to others in a way that helps them understand the problem we are learning about. Additionally, the discussion questions every Friday encourage us to think deeper about the problem and share our own perspectives on the issue. This can help us think of potential future areas of research, that some of us may be interested in, issues involving that research, and also ethical problems about the problem in general.

Credit: Adobe (2)

The way this class encourages us to participate in the world the most is through these blog posts. Blog posts are available to anyone in the public, and a key part of making this information accessible is figuring out how to present it in a simplified way. Many people in the public aren’t going to know what cAMP is let alone a synapse, so figuring out how to present information in a way that is digestible to the general public is a key skill this class encourages us to develop. In order to make a difference in the world you need to get peoples attention and then you have to get them to understand it. If people can’t understand what you are saying, they aren’t going to care about the message you are trying to tell them. This is why I think this is the most valuable skill that this class teaches in relation to engaging with the world around us.

What Does Learning at a Liberal Arts Institution Mean to Me?

Learning at a liberal arts institution means learning how to become a well rounded individual in the modern world. This means teaching skills that enhances our ability to learn and understand the world around us, rather than just solely teaching us the information that we need to know about our major and future careers. I think Concordia does a great job at this and this class really exemplifies why. As stated earlier, most classes are simply lecture, assignment, and tests. For many classes, this is the only way to effectively teach the information, but for other classes, such as this one, there is much more effective ways to learn not just the information but learn in general. By requiring us to find our own information, putting it together, and presenting it in our own words, we learn much more than just the class content and it helps us become the well rounded individuals that Concordia aims to turn us into.

In the end, this class taught me much more than just neurochemistry. I was able to refine my problem solving skills permanently, and these skills will be very valuable moving forward. The refining of these skills have also helped me be more confident in my own abilities, as well as my ability to feel confident in not knowing something. Even when I wasn’t sure about something, I still felt confident enough in this class to give it my best shot. While this has been a year of growth in all aspects of my life, this class has been a large contributor in my growth as a student. In the end, maybe the neurochemistry was the friends we made along the way (credits role).

1.) https://www.eschoolnews.com/district-management/2017/07/20/classroom-redesign-achievement/

2.) https://stock.adobe.com/search?k=cartoon+earth

Feature Image: https://missiontolearn.com/make-reflection-daily-habit/

The Genetics behind Addiction

Do you ever wonder why addictions seem to run in families? A parent may struggle with alcohol, a sibling with pills, and suddenly the pattern becomes hard to ignore. This is not a coincidence, it’s biology. Research shows that genetics account for 40-60% of addiction risk, shaping how our brain processes reward, forms memories, and responds to substances.[1] But genetics alone don’t tell the whole story.

How our brains reward system is already wired differently

Every brain runs on dopamine, that “that felt good, do it again” chemical. Variants in genes like DRD2 (dopamine receptor) and DAT1/SLC6A3 (dopamine transporter) influence how sensitive our reward system is and how easily impulse control breaks down.[1] Some people are simply born with a reward system tuned louder than others. That genetic difference can tilt the odds toward addiction before a person ever takes a drug, however, dopamine is only half the story.

Glutamate: The Learning and Memory Problem

Addiction isn’t just about chasing a high, it’s about learning. Glutamate, the brain’s main excitatory neurotransmitter, drives synaptic plasticity, the process by which experiences get permanently wired into memory.[2] Genes regulating glutamate receptors, including GRM5 and GRM2 (metabotropic glutamate receptors), as well as NMDA and AMPA receptors, influence how deeply drug-associated memories get carved into the brain and how hard they are to erase.

Research found. What happens to the brains Glutamate system?

A 2023 review showed how metabotropic glutamate receptors (mGluRs) change across the brain’s reward circuit including; the nucleus accumbens, prefrontal cortex, and ventral tegmental area following cocaine, amphetamine, methamphetamine, and nicotine use. As shown in Figure 2 of the paper, mGluRs are strategically placed on both sides of the synapse: Group I receptors sit postsynaptically and drive learning-related plasticity (LTP/LTD), while Groups II and III act presynaptically as a brake on glutamate release.

Repeated drug use throws this balance off. Group I receptors become overactive, fueling relapse-seeking. Group II receptors lose function, removing the brain’s natural glutamate brake. In animal studies, blocking mGluR5 significantly reduced cocaine-seeking behavior. Rats with mGluR2 deleted showed increased cocaine self-administration. Your genes controlling these receptors directly influence whether your brain pushes toward or away from relapse.

Epigenetics: When Drugs Rewrite Your Gene Expression

Through epigenetics, which is changes in gene expression without changing DNA itself, drug use can chemically silence genes involved in impulse control via DNA methylation, and alter histone modification, changing how tightly DNA is wound around proteins.[3] These changes can outlast the drug use by years, helping explain why relapse risk stays high long after someone stops using.

Why This All Matters

There are currently no FDA-approved medications for psychostimulant use disorder.[4] That’s a staggering gap. However, understanding the genetic variation in glutamate and dopamine systems is exactly the kind of knowledge that could lead to targeted treatments. mGluR-based drugs are among the most promising candidates.

Addiction isn’t a moral failure. It’s genetics, molecular neuroscience, and experience colliding in the brain. The more precisely we understand that collision, the closer we get to stopping it.

 

 

 

[1]       “Is Addiction Genetic?,” Cleveland Clinic. Accessed: May 01, 2026. [Online]. Available: https://health.clevelandclinic.org/is-addiction-genetic

[2]       P. W. Kalivas, “The glutamate homeostasis hypothesis of addiction,” Nat Rev Neurosci, vol. 10, no. 8, pp. 561–572, Aug. 2009, doi: 10.1038/nrn2515.

[3]       A. S. Koijam, K. D. Singh, B. S. Nameirakpam, R. Haobam, and Y. Rajashekar, “Drug addiction and treatment: An epigenetic perspective,” Biomedicine & Pharmacotherapy, vol. 170, p. 115951, Jan. 2024, doi: 10.1016/j.biopha.2023.115951.

[4]       R. Mozafari, S. Karimi-Haghighi, M. Fattahi, P. Kalivas, and A. Haghparast, “A review on the role of metabotropic glutamate receptors in neuroplasticity following psychostimulant use disorder,” Progress in Neuro-Psychopharmacology and Biological Psychiatry, vol. 124, p. 110735, Jun. 2023, doi: 10.1016/j.pnpbp.2023.110735.

 

Who is at risk? Hidden Risk factors behind a deadly Brain Cancer

Can you image being told you have a brain tumor and that the median survival time is around 14 months. Unfortunately, that is the reality for patients diagnosed with Glioblastoma (GBM), the most common and deadly form of malignant brain cancer. And for many people, cancer feels like a random role rolling of dice. But researchers have been able to pinpoint some specific risk factors including genetic, environmental, and even immunology, that can help determine who is most vulnerable. Understanding these risk factors isn’t just fascinating science, it may get us one step closer, saving lives.

A brain tumor built from bad signals

A 2019 review discussed how GBM hijacks the body’s own cellular communication systems. Signaling pathways like PI3K, MAPK, and cAMP are responsible for telling our cells when to grow, divide, and die. However, in GBM, these first 2 are cranked up to full blast, while the third (cAMP, which suppresses tumors) is suspiciously quiet. This results in cells dividing out of control, invading neighboring brain tissue, and becoming almost impossible to treat.[1]

Who can get GBM?

GBM isn’t an equal-opportunity disease. Most diagnoses happen in adults between ages 45 and 70, with the average age at diagnosis hovering around 64.[2] Younger patients do get it, especially the “Proneural” subtype, which is discussed in the research as more common in younger individuals, however, it’s predominantly a disease of middle and older age. Sex also plays a role, as men are slightly more likely to develop GBM compared to women, though researchers are still trying to understand why. [3]

Environmental risks

The environment around us can quietly rewrite our DNA. The most known environmental risk factor for GBM ionizing radiation exposure. This is the same radiation that is sometimes used to treat other cancers.[4] Radiation can cause point mutations, DNA double-strand breaks, and chromosomal rearrangements in brain cells, potentially sparking the cascade that leads to GBM. Besides radiation, prolonged exposure to certain chemicals like pesticides, petroleum products, synthetic rubber, and vinyl chloride, has also been linked to elevated risk. These aren’t rare exposures; some people encounter them regularly in industrial or agricultural jobs.

It is not usually inherited, but sometimes it is

Most people don’t know that inherited glioblastoma is actually pretty rare. The vast majority of GBM- causing mutations happens suddenly during a person’s lifetime, not from one’s parents.[3] However, it is important to note that there is a handful of hereditary syndromes that drastically raise the odds including:

  • Li-Fraumeni syndrome: involves inherited TP53 mutations, one of the most mutated genes in GBM tumors overall
  • Neurofibromatosis type 1 (NF1): loss of this tumor suppressor is found in roughly 14% of all GBM cases, especially the mesenchymal subtype (as described in the article)
  • Turcot syndrome: a mismatch repair disorder that predisposes people to both colorectal cancers and brain tumors including GBM

What is actually mutated in GBM tumors?

Top mutated genes in GBM

TP53- 34.4%

EGFR- 32.6%

PTEN- 32%

NF1- 13.7%

PIK3CA- 12%

The Cancer Genome Atlas (TCGA), a massive project cataloguing cancer-causing genomic alterations across thousands of patient tumors, has shown that GBM is essentially a disease of broken signaling.[5] The top mutated genes all tie directly back to the PI3K and MAPK pathways that the article described. This confirms that these signaling highways aren’t just academic curiosity, but the actual biological machinery that goes haywire in almost every GBM patient.

Could Asthma be Protecting you?

In what may be one of the most interesting findings, people with asthma and allergic conditions actually appear to have a lower risk of developing GBM. The immune activity associated with allergic responses may somehow create a microenvironment that’s hostile to tumor development.[2] This lines up with the broader picture in the review, which discusses how the tumor microenvironment and immune checkpoint pathways like PD-L1 are deeply intertwined with GBM progression.

Takeaway

GBM is not a simple disease with a single cause. Age, sex, radiation, chemical exposure, inherited syndromes, and spontaneous mutations in the wrong genes at the wrong time can all have a possibility of leading to glioblastoma. As the article remind us, once those PI3K and MAPK signals go haywire, they’re incredibly difficult to shut back down.

 

 

 

 

[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]       A. F. Tamimi and M. Juweid, “Epidemiology and Outcome of Glioblastoma,” in Glioblastoma, S. De Vleeschouwer, Ed., Brisbane (AU): Codon Publications, 2017. Accessed: Apr. 30, 2026. [Online]. Available: http://www.ncbi.nlm.nih.gov/books/NBK470003/

[3]       “Risk Factors and Symptoms of Glioblastoma – Brigham and Women’s Hospital.” Accessed: Apr. 30, 2026. [Online]. Available: https://www.brighamandwomens.org/cancer/glioblastoma/risk-factors-and-symptoms

[4]       “Glioblastoma: GBM Symptoms, Causes and Survival Rate.” Accessed: Apr. 30, 2026. [Online]. Available: https://www.cityofhope.org/clinical-program/brain-tumors-cancers/types/glioblastoma

[5]       P. Zhang, Q. Xia, L. Liu, S. Li, and L. Dong, “Current Opinion on Molecular Characterization for GBM Classification in Guiding Clinical Diagnosis, Prognosis, and Therapy,” Front. Mol. Biosci., vol. 7, Sep. 2020, doi: 10.3389/fmolb.2020.562798.

Glioblastoma Explained: Inside the Most Aggressive Brain Tumor

Featured image (Artstract) created by Cayley Borrud with ChatGPT

Glioblastoma (GBM) is the most aggressive and most common type of brain cancer that originates in astrocytes. Currently, there is no cure for glioblastoma but there are treatments that can slow growth and make a more comfortable life. The main symptom is headaches that are very frequent and worsening [2]. Unfortunately, by the time symptoms show up, the tumor may have likely already degraded healthy brain matter and started growing rapidly. These poses the question; how does glioblastoma grow?

Understanding the step-by-step development of glioblastoma is important because each stage of tumor growth reveals a potential point for treatment.

Image sourced from Cleveland Clinic

Tumor growth and development:

Glioblastoma can develop from one of two origins. The first way GBM can develop is very quick and develops within months without any pre-existing gliomas (Primary GBM).  The second way it can develop is from a preexisting glioma (Secondary GBM). Secondary GBM develops very slowly over the course of years [2].

Despite the origins, glioblastomas arise from the same activations of pathways. The cancer would start out benign with its cAMP pathway being increased. The increase of this pathway is a good thing since it’s a suppressor of cancer cell growth [3]. Unfortunately, it can quickly become malignant where it mutates further and becomes aggressive. According to the article by Fung et al., in a malignant cancer, the cAMP pathway is suppressed while the MAPK and PI3K pathways become hyperactive [1]. The MAPK and PI3K pathways drive the cancer cell spread and growth.

While the GBM cells are multiplying, they are also producing enzymes called Matrix-metalloproteinases (MMPs) that break down the healthy brain tissue to make more room for it to spread [5]. Additionally, while the cancer cells are multiplying, they are creating new blood vessels that provide vital nutrients for the growth of the cancer. This process is called angiogenesis [6].

Then, the tumor progresses into a multiforme state. This means that the cells would develop different genetic traits. In Glioblastoma multiforme, the cells accumulate additional mutations and changes over time. This is how the cancer can become resistant to gene targeted therapies [4].

image sourced from biorender

Takeaways:

Glioblastoma is not a single event but a multistep evolutionary process where cells mutate, invade, recruit blood supply and adapt to survive. Understanding each developmental step may help researchers design better therapies. In addition, the genetic diversity within GBM allows some cells to resist targeted therapies and continue progressing. Knowing how GBM invades healthy brain tissue can help scientists create drugs that block enzymes such as MMPs and slow tumor spread. Also, understanding how the tumor forms new blood vessels may improve anti-angiogenic therapies that cut off its nutrient supply.

As scientists continue to understand the molecular pathways behind GBM development, including MAPK, PI3K, and cAMP signaling, new treatment strategies may emerge. While glioblastoma remains devastating, advances in research offer hope for more effective and personalized therapies in the future.

Sources:

1. 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 Signalling, 57, 2–9. https://doi.org/10.1016/j.cellsig.2019.01.011

2. Mayo Clinic Staff. (2026, March 5). Glioblastoma: Symptoms and causes. Mayo Clinic. https://www.mayoclinic.org/diseases-conditions/glioblastoma/symptoms-causes/syc-20569077

3. Xing, F., Luan, Y., Cai, J., Wu, S., Mai, J., Gu, J., Zhang, H., Li, K., Lin, Y., Xiao, X., Liang, J., Li, Y., Chen, W., Tan, Y., Sheng, L., Lu, B., Lu, W., Gao, M., Qiu, P., … Yan, G. (2017). The anti-Warburg effect elicited by the cAMP-PGC1α pathway drives differentiation of glioblastoma cells into astrocytes. Cell Reports, 18(2), 468–481. https://doi.org/10.1016/j.celrep.2016.12.037

4.Li, X., Wang, Y., Zhang, H., Chen, J., & Zhao, Q. (2025). Applications and emerging challenges of single-cell RNA sequencing technology in tumor drug discovery. Drug Discovery Today, 30(2), 104290. https://doi.org/10.1016/j.drudis.2025.104290

5. Aitchison, E. E., Dimesa, A. M., & Shoari, A. (2025). Matrix metalloproteinases in glioma: Drivers of invasion and therapeutic targets. BioTech, 14(2), 28. https://doi.org/10.3390/biotech14020028

6. Barresi, V., Christopoulou, M.-E., Karamani, V., Aletras, A. J., & Gatzounis, G. (2015). p-CREB expression in human meningiomas: Correlation with angiogenesis and recurrence risk. Journal of Neuro-Oncology, 122(1), 87–95. https://doi.org/10.1007/s11060-014-1706-9

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