The past semester has gone crazy fast, and I ended up taking away a lot more from this class than I thought I would. Although there were a few topics in this course that were less exciting than others, I found myself drawn to a few key ideas. One topic I found very interesting, and relevant to many topics discussed, was our diet. I knew it was important to watch what I ate, but I was unaware of just how much my diet dictated my mental health. The physical outcomes of eating healthy are obvious, but the not so obvious benefit is our neurological health. I was unaware of how important our diet is in determining how our brain functions, and its ability to retain information. It made me reflect on what I was doing to my short and long term health; not only on being visibly healthy, but being healthy within too. Many of our discussions incorporated some sort of imbalance within the body, and came to the conclusion that if we have everything in moderation we should be able to keep ourselves mentally and physically healthy.
There were a lot of terms and pathways I was not familiar with, but after my classmates helped me through some of the ideas I was struggling with, I was able to take away a lot more from what we were reading. At first it was difficult to take away information that was presented, but after we found a technique that worked, it worked well. Not only was I learning information pertinent to neurochemistry, but I was able to take what others had told me and use them in conversations in other classes or with my peers. After reading many of these articles, I was able to discuss some aspects of them with my friend who is majored in dietetics. Granted we have oddly intense conversations occasionally, but it was fun to use something that I learned in a class in a casual conversation.
One great part of this class is that we were able to have these mini-learning sessions that classes that are large would not be able to do. It took a little while to warm up to each other, but eventually we were able to create an atmosphere where people could ask questions that would never be asked in a large lecture setting. On Fridays we were able to discuss ideas relevant to our week’s topic, but take those concepts and run with them. We often ended up going on tangents, and for me, lots of it came back to what we were putting into our bodies that dictated our mental health among many other things.
Another aspect of this class I greatly appreciated was our “exams.” They were more like puzzles we had to figure out using information given to us. I was forced to think critically and put together a collection of tidbits from a paper, which would (hopefully) represent the hypothesis from the research article. Along with this, we were given an out-of-class portion where we were given the research article. We had to evaluate what we had put together in-class, and discuss how we were either right or wrong. From this, I learned how to effectively read a research article and pull out important information.
The class setting was much more relaxed than other chemistry classes, but I found myself just as involved. It allowed me to see my science peers in a different light, and I enjoyed being able to do so. This class challenged me to think in a different way because I had to teach concepts instead of being taught them. This class incorporated many of central aspects of a liberal art learning, and I believe that by taking this capstone I can be more responsibly engaged in the world, especially with being more aware of how to try to prevent many of these diseases we studied and trying to inform others of what I learned. Over Thanksgiving, I tried to start with my family, and just as we assumed in class, you can give someone information, but it may take a while for them to actually believe you and take their health into more preventative measures. However, it is now my responsibility to tell those I love the information I know, and what they do with it is up to them (but my constant nagging may influence their response a little).
This class was both informational and fun. I learned a lot about the pathways within our brain, and how these pathways can be affected by what we do, or don’t do, by what we eat, and by what mothers do/eat while pregnant. Not only did I learn, but I had fun being able to see a completely different side of my classmates, and being able to use what I learned in conversations outside of class. This experience incorporated the goals of Concordia, and I believe that it allows me to be even more responsibly engaged in the world.
Obesity: A growing problem
“Welcome to McDonalds, what can I get for you?”
“Yeah I’ll get a number 1 with a large fry and a large Coke.”
“Alright, anything else for you today?”
“Yeah…can I get a medium Oreo McFlurry too?”
“Of course, we’ll have your total at the first window.”
Above is an occurrence that happens all too frequently everyday in the US, and at 1,970 calories, this meal is nearly enough for a whole day’s nutritional needs. This may seem obscene, but it’s what we have become accustomed to in recent years. This week in class we talked about obesity, and it’s effects on the brain and body of those individuals who have it. We have, however, begun to ask the question, “Is it their fault?” This week’s paper looked at the neurological pathways involved in the disease and discovered that, in fact, there are neurological ties to obesity, and it isn’t just overeating and laziness, as some people view it. In a sense, the article argues that we have no control over our natural inclination for a high fat diet or overeating. It turns out that when a baby is in the womb, their mother’s diet plays a huge role in the inherent disposition for the child’s eating habits. If the mother eats a high fat diet, the child will also be inclined to eat a high fat diet. This was tested and confirmed in a mouse model study. To get into the technical nitty gritty (for just a minute), there are two neuron types in the brain: the POMC and the NPY/AGRP. The POMC stimulates appetite and is overactive in obese people, and the NPY/AGRP suppresses appetite and is underactive in obese people. Other hormones and proteins play a part as well like grehlin (appetite stimulant), insulin (appetite suppressant), and leptin (appetite suppressant).
So we know that it’s not our fault if we’re fat, but that doesn’t change the fact that there are a multitude of negative consequences. Take Type II Diabetes for instance, or heart disease. Those both suck. How about Alzheimer’s? Studies show that those who are obese are at higher risk for Alzheimer’s, as well as other neurological diseases. The real question that remains is what can we do about it? How can those who suffer from obesity fight the negative effects of obesity? Two different strategies were investigated in class, both of which seem to have beneficial effects towards fighting obesity, and both are simple to implement in everyday life. The first is eating the right kinds of foods. A diet composed of high fibrous food such as root vegetables (or really any fruit or veggie) has many advantages. These types of food fill you up faster and make you feel fuller for a longer period of time, because they slow down gastric emptying. Additionally these signal the upregulation of GPl1 and PYY, two hormones that curb appetite. The second strategy is to get more, a regular, sleep. Our society promotes the fast a frantic non-stop lifestyle that usually leads to unpredictable sleeping patterns. This has consequences on the circadian rhythms in cells. Ultimately, irregular sleep can lead to decreased metabolic function and weight gain.
I think that the most important thing is to be aware of what you are taking into your body. While there does seem to be a neurologic predisposition to obesity, if we as a society make smarter choices and regulate our consumption and sleep patterns (just to name two possible solutions), we can curb obesity and fight the growing epidemic.
The End is in Sight: My Capstone Experience
Concordia College is a liberal arts college that really helps students get a well rounded education during their time here. Not only do you take classes of interest to you (for your major) but you are also required to take classes outside of that. For most that includes one final capstone course in the last year you are a studen here. It is a senior course that requires a lot of writing and is often discussion based with heavy reading involved. For me however I am required becuase of my major and minor to take two capstone courses before graduation. Neurochemistry was my first capstone experience.
This semester I took my first of two capstone courses I am required to take before graduating in the spring. To be honest I never thought I would like a chemistry or biology course because they have always been very intimidating to me. Taking neurochemestry though was a great choice. I have learned so many things throughout the duration of this course and am so thankful I got to experience it. I am a psychology major with a neuroscience minor, so to me signing up for this class was a bit of a scare, but once we got going with the curriculm it was fantastic and a lot different then I had immagined it to be. This was not an ordinary class where you got a lecture, took notes, and handed in assignments. No, this class was mainly discussion based making the class and professor interact as if we are all equals learning together. We would all come to class Monday’s having read and prepared questions for an assigned article (these articles were not easy to read and were very difficult to understand with all of the scientific jargon thrown into them). But then every Monday we would discuss what questions and concerns we had about the article and would all get assigned a topic within the article to prepare for Wendsday’s class. Then on Wendsday we would all get together and “teach” every other person about the topic we had been assigned. This helped many of us answer questions to what we did not understand while reading the article. On Friday’s we would hold discussion about everything we had learned about the topic that week (anything we found surprising or intriging about the article and would discuss from there). Everyone got two chances to lead discussion throughout the semester and that not only helped us build confidence in our leadership skills but also gave us an opportunity to speak out if we had not had chances to in the last week. Friday’s were by far my favorite days in this class because I felt like I had actually learned something at the end of the week (as opposed to just memorizing for a test, not hearing anything in lecture, etc.). We also took two exams that were more like in class assignments with a take home portion attatched. They were tough enough but they did not feel like you were taking a test at all. It was applying what you have learned in class to an article that was given and explaing what you thought was going on in that article. Then for the take home part you got to look at the entire article to see if your hypothesis was correct. If it wasn’t then you got to justify why you were wrong. It was all essay and really made you think about everything we had talked about in class. Over all I really enjoyed this class and my capstone experience it was great!
What is ALS?
Amyotrophic lateral sclerosis (or ALS) is a progressive neurodegenerative disease that affects nerve cells in the brain and spinal cord. The motor neuronal death within the brain reaches the spinal cord and then from there reaches the muscles throughout the body. Through the progression of this disease, patients inevitably lose their ability to initiate and control their own muscles. People in the late stages of ALS often become completely paralyzed. ALS is not reversable and there is no cure as of yet. Once a person is diagnosed with this disease they basically use a lot of medications and resources to make themselves as comfortable as possible before they inevitably die as a result of their inability to control their muscle movement.
Before this class I had not thought a lot about ALS, I had heard of it but did not really know what it was or how it effected the brain. The article we read this week during neurochemistry was very insightful and helped me to see what actually goes on in a persons body when they have this disease. Though there is little we can do to prevent or reverse this disease some things have been found to be slightly helpful. For one there is one treatment medication that is well known for this disease. It is called Riluzole and it was first approved in 1995 as a treatment for ALS. The way it works is that it decreases glutimate release in the brain thus reducing the motor neuron death. It extends the life of the motor neurons which temporarily improves the quality of life for the patient. Another way to prolong the life of the patient is to accumulate a lot of fat on the body. It is not very sientific, but it has been suggested that people with higher body fat live longer with this disease than people that have little body fat.
This disease is aweful and takes it’s toll on an individual; not only does it effect the entire rest of their life, but they also need to be cared for by numerous people. As the disease progresses the patient becomes weak and cannot do a lot for themselves. Family and friends can be very helpful, but once the disease reaches a certain point many other professionals need to be brought in. These specialists include doctors, pharmacists, OTs, PTs, social workers, nutritionists, nurses, hospice care, and therapists. It takes a lot just to keep this person as comfortable and stable as they can make them while facing the end of their life. Personally I think making a person feel better while they are suffering from ALS would be beneficial but at the same time it would make their life worse bcause they know the outcome no matter how long they can prolong it. A lot is still not understood about this disease or the brain in general for that matter, so there is hope that one day we will find a cure for this disease so that people do not need to suffer this kind of tradgety any longer. One last “fun fact” that I learned about this disease is that to many people it is known as Lou Gehrig’s disease and recent research has discovered that Lou Gehrig may not actually have had this disease. They think that he possibly suffered concussions that led to CET. CET is a disease that happens in people who suffer many concussions or blows to the head and shows very similar symptoms as a person suffering from ALS.
Back to the Future: a look at Parkinson's Disease
When I think about Parkinson’s Disease, the first thing that comes to my mind is Back to the Future. Weird, I know–but Michael J. Fox is one of the most visible people with Parkinson’s and a huge advocate for the cause. This past week we investigated an article regarding PD called Targeting dysregulation of brain iron homeostasis in Parkinson’s disease by iron chelators. Not only reading this article, but all of the research that went along with understanding it, gave me a far greater understanding of Parkinson’s Disease and it’s pathology.
As the article’s title suggests, there is a connection between PD and iron. This was new information for me, and struck me as quite interesting. Iron levels in a person with Parkinson’s differ quite a lot compared to someone without Parkinson’s. Those with Parkinson’s have much higher levels of iron. In addition to iron levels, PD staples include loss of dopaminergic neurons, the aggregation of -synuclein to create lewy bodies, and neurofibrillary tangles.
I thought the article was really awesome because it added to the current research being done on Parkinson’s, but the thing I found most interesting was the parts about iron homeostasis in the brain. I was responsible for researching the mechanism for regulating iron in cells and found some pretty awesome stuff. Iron is bound in the cell by two different receptors: IRP1 and IRP2. The IRPs serve as a dual mechanism in which iron can be regulated. A quick and dirty explanation is as follows: if iron levels are adequate in the cell, it is sequestered and stored for later use; if iron level are too low, the IRP binds to ferritin (this binding inhibits iron sequestering), that way there is more iron available inside the cell. Iron has many properties, one of which is it’s ability to oxidize/reduce molecules in the cell. If the regulation of iron is out of whack, then the oxidation/reduction within the cell will cause problems. This brings us back to -synuclein aggregation and lewy bodies, which are caused by oxidative stress. In other words, this new-found information about Parkinson’s helps explain the things that were already known about the disease. Nifty!
So the question remains: what do we do about all of this iron dysregulation? The answer is in the title of the paper, iron chelators. Iron-chelators bind iron in the cell and help reduce the high levels in individuals with Parkinson’s. This remedy to iron dysregulation is a great option because it will reduce oxidative stress on the cells and lower the amount of -synuclein aggregation and lewy bodies.
This article was really informative and made new connections in the big picture of Parkinson’s research. I think it’s safe to say that next time someone brings up Parkinson’s Disease I won’t immediately think of Back to the Future.
Concussion: More than just a bump on the head
This weeks topic was concussions, which turned out to be really cool and applicable to a lot of people in the class. Before this week I really was not sure what a concussion entailed, having never had one before, all I knew was that it involved getting hit in the head. It turns out there’s more to it than just that…who knew?!
A concussion, aside from being painful, is a very complex reaction to force exerted on the head. This force causes an initial mechanical trauma causes a whole cascade of things to happen, ultimately leading to a flux of ions through many channels in the brain. This rapid depolarization to the brain has many consequences and can lead to permanent damage if not cared for and healed properly. Effects can be memory impairment, behavior changes, headache, inability to concentrate, and in severe cases permanent brain injury. What is worse than one concussion is repeated concussions, especially if the first one hasn’t had time to heal properly. This is seen a lot in high contact sports such as football and boxing. Repeated concussion can lead to long term damage and CTE (Chronic traumatic encephalopathy), which is large-scale neuronal degradation and tau protein build up.
The topic of concussions is one that is actually really applicable to people in our class, as concussions tend to be common in younger people, especially athletes. As we learned in class, a concussion is a time consuming injury, and can be extremely detrimental to physical, and mental function for about four weeks after the fact. Being that proper care for concussion is extremely minimal physical and mental stress, it can be hard to cope with as as a student. This was one of the main points we talked about during our weekly discussion. How should students (whether they be elementary, middle school, high school, or college) go about dealing with a concussion as well as keeping up with classes, and if the concussion was sports related, whether or not to continue with that sport. This topic brought about a lot of good discussion and perspective from students, teachers, and athletes alike. As a group we determined that it would be nearly impossible to keep up with college coursework if you got a concussion, because let’s be real, four weeks of no class isn’t exactly ideal. We came up with the semi-solution of perhaps being able to continue taking classes as independent studies and finish at your own pace. This is a great idea, but would take a lot of logistical work to be able to be implemented.
Green with envy
Flick the lighter. Burn. Inhale. Ahh…that’s the good stuff.
It appears that this routine is becoming more and more common in the daily lives of many Americans. Medical marijuana is on the rise, and multiple states have now legalized it. A lot of people criticize this new trend, while many others are green with envy of the availability of medical marijuana. Why such a discrepancy in opinion? When most people think of weed, the only thing that comes to mind is burnt out hippies and junkies. Weed has a bad rap, and carries a stigma with it. But why?
This week’s article, Endogenous cannabinoids revisited: A biochemistry perspective, introduced us to a pretty fascinating system within the body. The endocannabinoid signaling system is a family of receptors in the brain that bind the endogenous cannabinoids, 2-AG and AEA, that our body makes naturally. These endocannabinoids (eCBs) play a role in pain relief, appetite stimulation, and motor control. It also just so happens that these eCBs are extremely similar to THC, the active ingredient in marijuana (incredulous gasp!). This means that there are actually specialized receptors in our brains that are made to bind things like THC. This brings me back to the above question: Why does medical marijuana get such a bad rap? Ignorance, mainly.
It has been supported by scientific studies, like the paper we read this week, that THC as a cannibanoid binds the eCB receptors in the brain and has beneficial therapeutic effects. So why not make medical marijuana legal everywhere? One of the biggest arguments against the use of medical marijuana is it’s addictive qualities. Now yes, marijuana might be addictive, but what isn’t? It isn’t any more addictive that the pain meds that people take everyday. It seems silly to me that people would rather keep using chemically synthesized pills that have who knows what side effects, over this natural alternative. One of the coolest things about medical marijuana (besides the pain relief, and other awesome benefits) is that there are essentially no negative side effects (with proper use of course).
I think that steps need to be taken towards universal legalization of medical marijuana. The biggest thing that needs to be done is raising awareness of the benefits. People opposed most likely don’t know that medical marijuana actually does have positive effects on the user. Maybe if everyone knew that THC is basically the same as the endocannabinoids already found in the body they would be less opposed to using it as a therapeutic drug. This would be a huge step in medicine, and would help countless individuals suffering from chronic pain, eating disorders and many other diseases.
Dopa what?
Typical conversation before reading the proceeding blog post:
Average Joe: “What’s dopamine?”
Neurochem student: “Well, it’s one of the most common neurotransmitters in the human brain.”
Joe: “Isn’t that some drug that athletes use?”
N.S. : “Not exactly, that’s just called “doping,” and isn’t actually related to dopamine.”
Joe: “Dopamine..like, cocaine, right?”
N.S. : “No, no, Dopamine itself isn’t an illegal drug. It does, however, play a role in drug addiction.”
Joe: “So basically Breaking Bad then..yeah?”
N.S. : …….Oy vey
So what exactly is dopamine, you ask? This is a relatively new area of study for me, but I’ll do my best to get across the important stuff…without putting you to sleep. Let’s start with the basics: first and foremost, dopamine is a neurotransmitter. That is, a chemical compound in the brain that sends a signal from one neuron to another. Neurotransmitters are key players in neural pathways and are essential for executing all of our basic actions and functions. This week in class we looked at a more specific facet of dopamine: the Akt/GSK-3 pathway. I know what you’re thinking, probably something along the lines of “Ak-wha? I’m over this blog.” Don’t let it scare you! The Akt/GSK pathway is actually really nifty and is prevalent in many common neurological disorders. The bare bones explanation of the pathway is as follows:
1. Dopamine binds to the D2 receptor
2. Binding causes the -arrestin complex to form
3. arr deactivates Akt
4. Deactivated Akt allows GSK to remain active
5. GSK gets to do all sorts of fun things in the cell!
Now you’re probably thinking “Why should I care about any of this?” The simple answer is that, whether you realize it or not, your life is filled with topics revolving around this pathway. This is the mechanism of many antipsychotics, is directly related with the treatment of bipolar disorder, and plays a huge role in addiction and substance abuse. Pretty neat, right? While learning about the nitty gritty details of the dopamine pathway or the Akt/GSK cascade may not be as entertaining as watching the latest episode of Breaking Bad, it is far more relevant to our everyday lives. Don’t worry if you don’t understand everything about it–I don’t either!
Living with ALS
I was not very familiar with ALS before this week. I had an idea of what it was, but I was not aware of how a person got it, or what was done after they were diagnosed. That being said, I feel that I have learned a lot this past week. I was informed that it is hard to determine when someone has ALS, and when a person in diagnosed, there is very little that can be done to help. There are a few medicines that help prolong the disease, and I also found that by having a larger fat reserve, people with ALS live longer. However, people who are diagnosed with this awful disease will live a very difficult life that will end too quickly.
Not only does this disease take over the individual’s life, but it also requires help from others. Many patients depend on their families or care givers to help them with simple tasks, and hopefully they have a strong support system to help the patient feel as comfortable as possible while facing this devastating illness. I believe that an individual’s attitude towards life, whether he/she is sick or healthy, depends on the people that surround them; this is true for ALS patients as well. The main thing that can really be done for ALS patients is to make their life as comfortable as possible. It would be the hardest thing in the world to watch someone I love lose a battle with a disease after fighting so hard, but I would do everything in my power to help.
There are still a lot of questions I have about this disease like: how can we improve the lives of these patient and make their time on this earth better? There is so much unknown about the brain and why things happen the ways they do, and how can we fix one problem without creating another one? Scientists in this field have a lot of work ahead of them, but I feel we are headed in some sort of direction; whether or not it is the right one will be discovered soon enough, but for now I am thankful that there is research being done to understand the basics of many diseases that have ruined the lives of many.
A Glass of Milk A Day Keeps ALS Away?
Amyotrophic lateral sclerosis, better known as ALS or Lou Gehrig’s Disease, is a rapidly progressing neurodegenerative disorder. The symptoms of the disease usually start between 40-60 years of age. Initial symptoms include mild muscle weakness, cramps, muscle spasms, or muscle stiffness. Although the symptoms are often overlooked at first, symptoms progress until a patient is no longer able to care for himself, eat unassisted, or breathe unassisted. The symptoms of ALS can be attributed to loss of motor neurons; however, like many neurodegenerative disorders, the cause of the degeneration of motor neurons is still unclear.
One possible cause of motor neuron loss is protein misfolding and cellular response to misfolded proteins. The article “Calcium-dependent protein folding in amyotrophic lateral sclerosis,” suggests that changes in the normal calcium levels or signaling causes stress in the cell, which causes the cell to not function properly. The first issue is protein folding. Basically, the cell requires proteins for transport, structure, enzymes to assist reactions in the cell and many other functions. Not only must the building blocks (amino acids) be strung in the right order, but the proteins must also be folded into the correct three-dimensional structure in order for it to function properly. This is where the endoplasmic reticulum (ER) comes into play. When proteins are made, they travel through the ER and are folded along the way. Chaperone proteins, found in the ER, are responsible for folding other proteins into the right shapes. Ca2+ levels in the ER regulate the chaperone proteins’ activity.
When calcium levels in ER deviate from homeostasis, the cell attempts to continue folding proteins correctly. One way to do this is to activate the unfolded protein response (UPR). The UPR tags a protein to tell the ER not to allow the protein to leave until it is properly folded. Without the proper UPR, the cell will experience ER stress for accumulation of proteins, which ultimately results in cell death. Both ER stress and UPR are thought be implicated in ALS pathogenesis. Further research is needed to develop treatments that target the ER and UPR to improve ALS symptoms and survival time. Currently, the average survival time for ALS patients is 3-5 years. By better understanding the progression of this disease, advances could be made in treatment to slow the progression or even cure ALS. Investigating calcium and calcium-dependent folding proteins appears to be a promising direction for ALS research.