Cobbers on the Brain – Page 115 – Student Commentary on the Neurological Sciences

Risk Factors of Alzheimer’s Disease

Posted on October 3, 2016 by / 0 Comment

Alzheimer’s is the most common type of dementia and the sixth leading cause of death. The disease is characterized by mental deterioration that affects the memory, thinking, and behavior. It is estimated that 5.4 million Americans have Alzheimer’s. The number of individuals diagnosed with Alzheimer’s disease has shot up in the last years and is believed to continue to spike into the next few decades expecting the occurrence to triple. There is no cure for Alzheimer’s, but the treatment that slows the progression of the disease. This brings into question what risk factors are associated with Alzheimer’s disease? Some of the most talked about risk factors are age, obesity, diabetes, and genetics.
Age is the ultimate risk factor. According to Alzheimer’s Association, the majority of individuals with Alzheimer’s disease are above the age of 65. Only 5% of people diagnosed have early onset Alzheimer’s which occurs at a younger age within their 40s and 50s. It is thought that if an individual could live “forever” they would ultimately get Alzheimer’s because it is caused by the natural process of neurons not working correctly. Therefore, age is a major risk factor because of the natural process of the body and how the neurons get weaker as we grow older. However, it is still unknown as to why and what exactly happens that makes age the major risk factor.
Obesity has been shown to be a risk factor for Alzheimer’s as well. An obese individual is three times more likely to development Alzheimer’s. Eating healthy and exercise has been shown to decrease the effects and prevent neurodegenerative diseases, like Alzheimer’s. They prevent diseases through growth factors, such as BDNF and insulin growth factor (IGF1), which affect pathways, like ATK and GSK-3beta, that cause Alzheimer’s. Therefore, maintaining a healthy lifestyle decreases the risk of developing neurodegenerative diseases like Alzheimer’s.

Type III diabetes has recently become a nickname for Alzheimer’s disease. It is also referred to as a brain-specific form of diabetes. Insulin and insulin-like growth factors are essential for cell survival within the brain. The new name comes from the buildup of resistance to insulin or decreased the number of insulin receptors within the brain. If an individual has Type II diabetes that does not mean they will development Alzheimer’s because insulin resistance can vary between different organs. However, an individual with Type II diabetes is at a 50 to 65% higher risk of developing Alzheimer’s disease.
Genetics play a role as being a risk factor for two different types of genes; risk genes and deterministic genes, each can be heritable. Risk genes are genes linked to increasing the odds of developing the disease, but the presence of them do not cause the disease. An example would be if an individual inherits the gene APOE-e4, which is estimated to be present in 20-25% of cases. Deterministic genes cause the disease. If an individual inherits deterministic genes they will get Alzheimer’s, also called autosomal dominant Alzheimer’s disease (ADAD). An example would be the genes responsible for three proteins: amyloid precursor protein (APP), presenilin-1 (PS-1), and presenilin-2 (PS-2).

Disease/Health/Hot topics

A New Focus for Alzheimer’s Disease Treatment: Tau Protein

Posted on October 3, 2016 by / 0 Comment

Alzheimer’s is the only disease among the top 10 causes of death in America that cannot be prevented, cured or even slowed. Current treatments have varying effectiveness for different people, of course, however, in general, the average patient cannot find relief or delay in the progression of the disease. With 1 in 3 seniors dying from Alzheimer’s or another dementia and AD (Alzheimer’s Disease) being the 6th leading cause of death in the United States, it makes sense that this is a very active area of research. A new promising target for future AD treatment targeting is the protein Tau.
Before we get into Tau and its relevance, we should set up how AD changes the brain. The main characteristic of AD is dementia, memory loss. Dementia is caused by blockage of neuronal signaling and neuronal death, especially in the Hippocampus, which is the area of the brain that memory is associated with. There are two major players, Beta Amyloid and Tau. Both are proteins with necessary functions, but incorrect cutting or modifying leads to negative consequences. Beta Amyloid Plaque is the classic attribute of AD. What happens is Amyloid is cut incorrectly and begins to clump together. These clumps occur between cells and continue to grow over time. The plaque can cause Dementia in two ways, it can block neuronal communication which wouldn’t allow memory formation or recall, and it can also cause an inflammatory response leading to cell death, like when you puff up from a bug bite. Most treatment has been focused on Beta Amyloid Plaques because of how visible they are in the brain in AD patients, so naturally, they would be seen as a target for treatment.

Beta Amyloid Plaque accumulating outside the cell

Amyloid Plaques certainly do contribute to AD, however, recent research has shown that Tau levels and clumping together may better mirror AD development and symptoms. This is exciting news since current treatments aren’t very effective and a new drug target may be exactly what we need. Tau’s regular functions are much more important to understand for its role in AD. Tau helps stabilize something in the cell called the cytoskeleton. The cytoskeleton works much like our own, holding the cell in its form, but it also serves as the highway system of the cell to move nutrients, proteins, and organelles around. What happens in AD is that Tau is changed incorrectly so that it can’t stabilize the cytoskeleton. This leads to a dysfunctional skeleton and left-over Tau. The breakdown of the highway system leads to less efficient communication between cells and ultimately cell death, both contribute to dementia. Then, much like the plaques, Tau aggregates (groups together) at first in small clumps, but then eventually large groups that no longer dissolve in water (insoluble), same as plaques. These groupings are within the cell at first, however, they eventually burst out of the cell creating Neurofibrillary Tangles. This causes cell death and then the tangles continue to spread with the progression of the disease.

Tau breaking away from microtubules (cytoskeleton).

Tau is an exciting prospect for AD treatment, not only because any new treatment could help, but because we’re finding out that it may be the major agent causing AD, not the classically understood Beta Amyloid Plaques. This discovery follows the development of imaging techniques to the point where a PET scan can observe the levels of Tau, Beta Amyloid, and rate of metabolism in cells (energy burning). These new imaging techniques have allowed us to see that in patients with AD, increased Tau levels associate more closely with the progression of the disease and cell death than Amyloid. It has even been presented that Tau might be one of the first players in AD, well before Amyloid, possibly even causing Beta Amyloid Plaque formation. In light of the ineffectiveness of AD treatment, this new target offers hope of managing and maybe even preventing Alzheimer’s disease. Future treatment will focus on stopping the wrong modification of Tau and not allowing aggregation, targeting pathological tau proteins for degradation along with dissolving aggregations of Tau. Hopefully, these new avenues bring hope to those with AD, however, this is a very recent discovery and drug development and refinement will take some time.

Disease/Health

Common Misconceptions of Alzheimer’s

Posted on October 2, 2016 by / 0 Comment

Alzheimer’s disease (AD) is characterized by gradual memory loss, which can eventually lead to the impairment of simple every day tasks for an individual. It is also the leading cause of dementia in elderly individuals, which highlights the importance in finding an effective treatment method for the disease. The increasing prevalence of AD in our society has made it a common household name. What is important though, is for individuals to thoroughly understand the disease and step away from the common misconceptions that come with the name.

Yes, AD and dementia are NOT the same thing.

According to the National Institute on Aging (NIA), dementia is a brain disorder that affects communication and performance of daily activities and AD is a form of dementia that specifically affects parts of the brain that controls thought, memory and language. While dementia is used as an “umbrella term”, AD constitutes one of the very many causes that leads to dementia. Therefore, it is important for one to understand that there is in fact a difference between the two terms.
2. Memory loss comes with aging.
While memory loss does in fact happen with aging, the type of memory loss that comes with AD is quite different. Occasionally forgetting to take out the trash or call a friend is normal as a person ages, but forgetting names of people or not remembering a location that was once dear to an individual is a more severe form of memory loss. This type of memory loss is not normal to exhibit during old age. Being able to distinguish between “normal” memory loss and more severe memory impairment is critical to understand in order to take proper action in helping an individual exhibiting signs of AD.
3. Alzheimer’s is only meant for old people.
Yes, the elderly make up 5.2 million Americans with AD, but 200,000 individuals under the age of 65 also exhibit Alzheimer’s. This is termed early onset Alzheimer’s, which is caused by inheritance of certain genetic factors. The most common risk factor for early onset AD is a chromosomal mutation which induces incorrect folding of a protein called APP. APP is a very important protein in signaling pathways involved with memory formation.
4. Aluminum leads to AD.

One of the common myths, that has since been disproven, is that aluminum can contribute to the formation of AD. After extensive studies, it has been proven that aluminum does not have any negative effects which contribute to the development of the disease.
5. Alzheimer’s does NOT lead to death.
Alzheimer’s is the sixth leading cause of death in the United States. The loss of synapse formation and increase of plaque formation within the brain can contribute to death from AD. Also, memory loss can lead to a loss of nutrient intake or may also increase risky behavior which can put an individual at risk for death.

These are just a few of the common misconceptions of AD. It is very important to thoroughly understand the basics of Alzheimer’s not only to be well-educated on the disease, but also to be able to properly care for someone who has been diagnosed with the disease.

Disease

What’s the Deal With Alzheimer’s?

Posted on October 2, 2016 by / 1 Comment

Your brain is your most powerful organ, yet weighs only about three pounds. It has a texture similar to firm jelly. It uses 20% of the total oxygen in your body and generates 10 to 23 watts of power: enough to power a light bulb.

This week we took a look into the brains’ signaling pathway of people living with Alzheimer’s Disease (AD).

“Today, 47 million people live with dementia worldwide, more than the population of Spain. This number is projected to increase to more than 131 million by 2050, as populations age. Dementia also has a huge economic impact. Today the total estimated worldwide cost of dementia is US$818 billion and it will become a trillion dollar disease by 2018.”

What exactly does Alzheimers do to the brain? Can I prevent this disease from happening to me? These were some of the questions that we asked but the more we learned the more questions we had!

The main signaling pathway that we associated with AD was the P13K or phosphatidylinositide 3-kinases. This pathway is activated by insulin, or insulin like growth factor.

Wait insulin in the brain? I thought insulin was used to regulate blood sugar?

You’re right it does regulate blood sugar in the kidneys but it also is used to activate neurons in the brain. This pathway regulates cell survival, growth and death. This means that homeostasis of this pathway is vital for healthy cognitive function.

When this pathway goes unchecked, somewhat like defective stoplights at a busy intersection during rush hour, this is where Alzheimer’s disease begins to show. Many different things can go wrong like over activation of the P13K pathway; insulin resistance so the pathway doesn’t get activated at all; or specific proteins being turned off/on at the wrong times. There were so many opposing forces we couldn’t even get good grasp on all of them. However, the main picture was it is all about balance and things happening at the right time.
If you want more clarification, here is a link to a slide show that Alzheimers.org has that shows step by step what happens to the brain of someone suffering from Alzheimer’s disease.
http://www.alz.org/braintour/severe_stage.asp

Prevention. Everyone wants to know what they can do to prevent a disease that harms them and the people surrounding them. The hard part is there is no set prescription that will guarantee a person will not develop the disease.

We often look to genetics to find if we are going to develop a disease, but only 1% of the population has the genetic predisposition for the disease. This means that outside environmental factors are a more likely cause, and taking the extra steps to slow or stop the disease is the best advice.

The prescription for decreasing your chances of getting Alzheimer’s Disease.

Regular Exercise
Eating Healthy
Quality Sleep
Stress Management
Active Social Life
Metal Stimulation

Do these sound like the prescription for other types of disease? Yep! The key to AD is a healthy lifestyle. There is no one drug or vitamin that can eliminate this disease from the lives of many people, but doing your best to be healthy can greatly improve your outlook.

Since this is such an expensive and devastating disease for patients and their families, why not try to do your best to prevent it.

“What the mind can’t remember the heart never forgets” -Unknown

Disease/Health

Alzheimer’s Disease and You: Can It Be Prevented?

Posted on October 2, 2016 by Joseph Kennedy / 0 Comment

Alzheimer’s disease is an irreversible progressive brain disorder that slowly destroys memory and thinking skills. In most people with Alzheimer’s, the symptoms first start appearing in their mid-60’s. Although estimates vary, there are an estimated 5 million Americans that may have the disease.
If after reading that you say “but I’m only 25, should I even worry about it?”, the thing is that you should at least be paying a little attention to it. A lot of the steps to preventing the disease will even improve your quality of life now! Even younger people can be affected by the disease, and if you have ever had an older loved one that has had it you can know the struggle.
In people with Alzheimer’s disease, there are a few things that are consistent with all patients. The first thing is that there are “Plaques” that have developed between drying brain cells. Another thing that goes wrong is that there are “tangles” in the brain neurons that form from a protein called tau.
Now that you have a little bit of background information on the disease, how can you at least try to prevent it? I am not going to say that following this will completely prevent the disease, as there is currently no way that will lead to a 100% prevention, but we can at least slow it down or make it so that it is not as serious. Well, there are a few unavoidable risk factors such as age, family history with the disease, and having a few specific genes. But, there are also some avoidable or modifiable factors which I am here to tell you about today!
These factors are “avoidable” or “modifiable” because changes in lifestyle can lead to improved resistance to the disease.
1.) Regular Exercise
According to the Alzheimer’s Research and Prevention Foundation, regular physical exercise has been shown to reduce the risk of developing th disease by up to 50 percent. Not only will regular exercise decrease your chances of the disease, you’ll look good and feel good doing it as well!

2.) Healthy Diet
The lifestyle change that you always here about going hand in hand with exercise, eating healthy is next on the list. Alzheimer’s is sometimes called “Type 3 Diabetes” and there is strong research to show eating healthier can reduce inflammation and protect your brain.

3.) Mental Stimulation
Those who continue learning things throughout their life are less likely to develop Alzheimer’s disease or dementia. So, start learning something new! Study a foreign language, learn an instrument, or start up a new hobby in general. Who say’s that you can’t have fun while protecting your brain? It doesn’t all have to be about diet and exercise!

4.) Quality Sleep
You’ve got to sleep! It is not uncommon for people with Alzheimer’s to suffer with a sleeping disorder or have other sleep problems alongside with it. Establishing a regular sleep schedule will not only help prevent the disease, it will also keep you healthy and alert now!

5.) An Active Social Life
We are highly social creatures, and nobody does great in isolation. Our brains are the same way. Being socially involved in things may prevent Alzheimer’s later in life, but it will also improve life as it is now! Being active and social can make us feel more connected and may even develop new friendships. So get out there and participate in something!

Now I know that it takes a lot to have a change of lifestyle, and a lot of what I just said gets repeated so much in so many situations that you might not take it to heart, but I hope you’ll at least consider it! Following these steps will not only lead to a healthier lifestyle today, it will also help prevent a terrible disease like Alzheimer’s in the future.

Disease/Health

Alzheimer’s Research to Amount to a “God Complex”

Posted on October 2, 2016 by / 0 Comment

The Issue
More than 5 million Americans are living with Alzheimer’s Disease (AD), and 1 in 9 Americans over the age of 65 has the disease, according to the Alzheimer’s Association (2016). Statistics like these support the national claim of an “Alzheimer’s Epidemic.” This is a regional crisis as well, with North Dakota having the highest AD death rate in America (Alzheimer’s Association, 2016).
The increasing prevalence rates of AD have led scientists to investigate the causes of such a detrimental disease.

The Research
Persistent brain research has led to developments in understanding the fundamental causes of AD. In a 2013 article in Experimental Gerontology, biochemist Dr. Cora O’ Neill details the importance of a biochemical pathway called the PI30K/Akt pathway in determining the primary causes of AD.
According to O’ Neill, sustained and abnormal activation of PI3-K/Akt signaling is an early feature of AD. More specifically, dysfunction of this pathway is characterized by progressive resistance to insulin in the brain, abnormal levels of beta-amyloid protein and tau protein, and loss of synaptic transmission.
Synaptic loss can be caused by long term depression (LTD), according to a 2012 review article by Bradley et. al in Frontiers in Molecular Neuroscience. LTD results in synaptosis, a process that retracts synapses at the neuromuscular junction, which is important for pruning unwanted synaptic connections during early development.
However, up-regulation of LTD, as a result of over-expression by the protein GSK-3 in the PI3K-Akt pathway, leads to pathological plasticity in an adult brain. So instead of neural connections being made stronger, synaptic connections are being lost, which results in cognitive deficits, memory loss, and other symptoms of AD.
The discoveries of synaptic loss, beta-amyloid protein, tau protein, and insulin resistance as indicators of AD are primarily due to research on post-mortem AD-diagnosed brains. As a result, physicians are not yet able to proactively detect these warning signs to preventatively treat their patients for AD.
But what if they were?

The Complex
Would you want to know 10 or 20 years prior to a diagnosis of Alzheimer’s Disease that you would be contracting the disease within a decade or two?
Researchers at Sweden’s Karolinska Institute and the Uppsala University discovered that inflammation, a recognized indicator of protein-dysfunction, can be detected decades before the first appearance of symptoms (2016).
Many believe that knowing in advance would be advantageous, as it would provide opportunity to make lifestyle changes or take prescription medication to slow down the disease.
According to Dr. Elena Rodriguez-Vieitez, first author of the 2016 study at Karolinska Institute, current therapies for AD only mitigate symptoms and don’t actually change the course of the disease.
But what if they did?
The advancements in brain research specific to the “Alzheimer’s Epidemic” has resulted in many implications. However, it seems that as more findings continue to be reported by the scientific community, the general public will be left with more ethical questions. And the study of diseases like AD may be preparing people for a day when they may face their own “God Complex,” being faced with negatively foreshadowing news, having the ability to remedy the condition, and choosing to do something about it, or not.

Disease

Autism Spectrum Disorder: Neurexin Proteins

Posted on May 1, 2016 by / 0 Comment

Autism spectrum disorder (ASD) is a group of developmental disabilities characterized by abnormal social interaction, communication, and stereotyped behaviors.
The diagnosis of autism is mainly based on the presence of two major symptoms: social-communication deficits, and restricted and repetitive interests/behaviors.
A 1996 study showed the prevalence of Autism to be 4.5 in 10,000 children. The prevalence increased to 19 in 10,000 American children in 1992 and rose to 1 in 150 in 2002 and 1 in 110 in 2006. The current accepted rate of ASD ∼1% worldwide, placing this disorder as one of the most common developmental disorders in the world.
The mechanisms and pathways going wrong in Autism are extremely complex and still under debate, however, it is interesting to find how some may effect individuals in different ways than others.
One particular area found to be important is the role of neurexin proteins. Neurexins are synaptic adhesion proteins that are known to play a key role in synaptic formation and maintenance. The functional significance is poorly understood, however, mice with a deletion of these proteins show symptoms of ASD. Disruption of a synaptic protein like this would lead to defects in transmission at excitatory and inhibitory synapses, disrupting the E-I balance in post-synaptic neurons which is a key mechanism in ASD.
Many mutations in genes encoding neurexins have been associated with ASD. A 2008 study compared symptoms of people with the same chromosomal abnormality with a dysfunctioning neurexin and found the Father didn’t have signs of ASD while the child did showing that the neurexin is not fully causing autism, but must interact with many other factors. However, subtle changes in certain others can contribute to the susceptibility of ASD in others.
There are several different kinds of neurexins (ex. 1α, 2α, 3α, 1β, 2β, 3β). Alpha neurexins are found to be essential for survival. Neurexin-1α is also required for calcium triggered neurotransmitter release and the function of cortical voltage-gated calcium channels. Deletion of α-neurexin genes in mice impaired both excitatory and inhibitory neurotransmitter release, which was attributed to calcium channel disruption, despite normal numbers of cell-surface channels. Despite the reduction in calcium neurotransmitter release and severe impairment in synapse function in α-neurexin knock-out mice, synapse numbers and their ultrastructure are nearly normal, implying that α-neurexins are essential for the proper assembly of synapses into a fully functional unit but not for the initial formation of synapses.
Neurexin proteins are one of possibly thousands of different areas that may be going wrong in the autistic brain and it is important to know the different roles so maybe one day we can find new treatments for this increasingly prevalent problem.
Image citations:
https://www.google.com/search?q=neurexin+proteins&safe=active&espv=2&biw=1215&bih=679&site=webhp&source=lnms&tbm=isch&sa=X&ved=0ahUKEwijnMzWp7rMAhWIWSYKHTMnBEUQ_AUIBigB#imgrc=1wah03MAl3yTqM%3A
https://en.wikipedia.org/wiki/Pervasive_developmental_disorder_not_otherwise_specified

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Neurochemistry – The Epitome of the Capstone Experience

Posted on April 30, 2016 by / 0 Comment

I’ll start by saying that I’ve never taken a class like Neurochem. But that shouldn’t be a surprise – it’s the only capstone course I’ve taken, so it should be different than the others. But the reasons why it was different are important to understand. Coming into the class, I expected more of a discussion based day to day experience, but beyond that, I was in the dark. Now leaving the class, I can say that Neurochem absolutely fulfilled its requirements as a capstone.
Firstly, this class was definitely based on discussion. If the people in the class weren’t able to contribute to the topic at hand, they basically didn’t contribute to much at all. Luckily, this semester’s class was full of some awesome and capable students that were seemingly all passionate to learn about the brain and its abnormalities.
Secondly, the class was challenging. This is important to understand because, according to some of my other peers, not all capstone classes are challenging in the slightest. This class not only required discussion and participation, but everyone had to come prepared having read the material, the class wiki had to be posted to, and the exams we had required a significant amount of thinking as well. Additionally, the second part of each exam – the oral exam – was not only enjoyable but was also challenging.
Lastly, this class was a group effort. No doubt about it. We all were learning together and problem solving together, including Dr. Mach. Having the opportunity to learn alongside the instructor is undoubtedly unique as well as beneficial in my opinion. I think that this component especially epitomized the capstone experience. No matter how discussion based or BREW-oriented a class is, if the instructor is there just to test the students on how well they know the material, it’s too similar to a standard class. Neurochem was very different in that sense.
Overall, this was one of the most enjoyable classes I’ve taken during my time at Concordia. I wholeheartedly enjoyed discussion each day, and felt that I learned a ton regarding the brain, the chemistry behind it, and the numerous abnormalities and disorders associated with it. In addition, I felt I will be better prepared in my future studies as a medical student because of the many discussions I had with my peers and Dr. Mach regarding the material we learned about. Without hesitation, I would recommend any student taking Neurochem as their capstone.

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Neuronal Networking – A Connection Between Autism and Concussions?

Posted on April 30, 2016 by / 0 Comment

What does that even mean – “A connection between autism and concussions?” Well, recently I’ve learned about the neurochemistry behind what occurs in the brains of autistic patients and found that the root of the problem is simply too many networks, signals, or connections in the brain, which leads to overstimulation of the brain. Obviously that’s very simplified, but at the root that is the problem.
In the case of a concussion, the root cause is a little broader. The trauma the brain experiences leads to many things going wrong. These include oxidative stress and anatomical deficiencies in the structure of the neurons. Specifically, the axons of the neuron are literally “broken,” which leads to a lack of networking in the brain and, subsequently, things going wrong in the longterm if the concussive patient isn’t given adequate rehabilitation time.
There’s the connection – the brains of patients with autism and those experiencing concussions are basically the opposite, in terms of axonal connections. Interesting, right? Well, recently, I’ve done research in the area of axonal sprouting and targeting the neurochemical pathway – PI3K-AKT – that is involved in autism. If this pathway is “turned on” too often, or not inhibited enough, autistic behaviors are observed in test subjects. However, a molecule responsible for inhibiting this pathway – phosphate and tensin homolog (PTEN) – is also an interest of mine in potentially treating brain injuries like concussions. If PTEN can be inhibited, the negative outcomes of a concussion can be better controlled. Below is a simplified schematic outlining this idea.

Following binding of a ligand to the tyrosine kinase receptor on the membrane of the cell, PTEN inhibits PI3K signaling by dephosphorylating the lipid signaling intermediate PIP(3), which is a necessary factor in the communication between PI3K and AKT. This dephosphorylation prevents the pathway from promoting cell survival and inhibiting apoptosis, or programmed cell death.
However, if PTEN is inhibited, PI3K-AKT is turned on even more, which will lead to more axonal sprouting and more networking. So, would this PTEN inhibition lead to autistic behaviors, then? Or would a potential treatment for concussion lead to promising results with little drawbacks? That’s a question that has yet to be answered. But, like many areas of neuroscience, it interests me significantly. Obviously this idea that autism and concussions are somehow related is very broad and not understood well, but nonetheless, I believe it deserves some attention.

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Thoughtful and Informed Citizens

Posted on April 30, 2016 by / 0 Comment

“The purpose of Concordia College is to influence the affairs of the world by sending into society thoughtful and informed men and women dedicated to the Christian life.”
Engraved in the stone at the center of campus, these words could not be more true of Concordia College. The overly theme of my Concordia experience has always been service and contribution to the larger society. While at times campus has felt small, since the day I stepped on campus, it has been the goal of my professors, coaches, and mentors that when I step off of this campus I am equipped with the necessary tools to positively influence the world around me. This goal is carried out and proven by courses such as Neurochemistry.
Rather than sitting in a classroom listening to a professor describe, in detail, the neurological pathways of various diseases, this class challenged me to read, research, comprehend, and communicate the finding of empirical articles. Because of this, I was more invested in my own learning. It also taught me how to be engaged in a scientific society outside of the classroom. As an undergraduate, it can be difficult sometimes to remember science is an ever changing field with new discoveries occurring everyday. Because of this, I came to realize that the field of science is much more than just facts and information, but rather it is a field of discovery and curiosity.
In order to be an effective and and successful learner the most important trait to possess is curiosity. Curiosity is what sparks the human interest to discover. This is what has driven the field of study in neuroscience and it is what has driven our educational system. Neurochemistry has taught me how to harness my inquisitiveness and dig deeper into the available resources to find answers or find the real question I am asking.
The other essential aspect of learning that neurochemistry has taught me is that learning can be about formulating questions rather than finding answers. Throughout school, the goal of classes has been to find the correct answers to questions. However, this semester it was our job to ask questions. I found this to actually be more challenging for the same reasons as described above. We were responsible for figuring out what we wanted to learn rather than being told what we were supposed to learn. This is the cornerstone of being social active in society.
Individuals that greatly impact the world in a positive light do not sit around waiting for someone else to make a change. Instead, they are at the head of the pack leading the charge. They have the ability to formulate their own ideas and opinions and communicate them in an affective manner. This is what it means to be a Cobber.
As I leave this place for the last time, I take with me countless memories, friends, and life lessons. Why most students discuss the former, I believe that it is the later that will propel my career and life to a vocational calling. Throughout my Concordia College career and especially during my final semester, I have learned to learn, how to be responsibly engaged in the world around me, how to effectively communicate my thoughts and opinions in a professional manner, how to be curious, and how to see the bigger picture. Education is the culmination of all of the topics and experiences one has throughout school, not just the individual tests and classes one takes. This semester of Neurochemistry has taught me to think in a way that draws upon all of my knowledge rather than isolated topics.