Wow! I cannot believe I am doing this but I am writing my final blog for you guys. I hope that someone has actually been reading these blogs or it is going to be very awkward. Well, it’s that time of the year again when snow is falling, it’s -17 degrees out, and I am trying to cram everything in before finals week. I just want to say that this neurochemistry class has been one of my favorite classes that I have taken here at Concordia College. When I think chemistry class, I think chemicals and formulas until my head hurts but neurochemistry has been a pleasant surprise.
I think that this class fulfills every requirement that is needed to be considered a capstone course. It has been one of few courses that have been able to mesh everything that I have learned as a liberal arts student and have it make sense. If you have not noticed already, my blogs have been infused with chemistry, biology, psychology, and even a little sociology. I believe that the structure of this class played a crucial role in the overall quality of the class.
The first half of our semester consisted of learning everything that we needed to learn in order for us to even comprehend anything that the articles were talking about. This included learning about neurotransmitters, receptors, and other functions of the brain. But the fun came the second part the semester where we got to read and discuss articles like we have never done before. Typically, on Mondays we would go around and discuss what we did not understand about the articles and what we found interesting. This just got the juices flowing in our brain after a long weekend of fun and what not. I’m just kidding, I don’t do fun on weekends. They are saved for studying! DUH! On Wednesdays, we would teach our classmates on a topic that was not fully understood in the article. At first, I thought that Wednesdays were a dud because I was having a hard time paying attention to the twenty some topics that were being discussed but thankfully our professor changed up the format towards the middle of the discussions. We switched to a speed dating type of atmosphere where we could discuss topics to individuals rather than the entire class. This made it easier to pay attention to all the topics and made it more fun as well. Finally, on Friday mornings, after a long night at “the office,” we would come together and discuss the topic as groups. These discussions were not only about the article but the implications of the research along with more broad ideas. Since most of our class consisted of people that we have known for almost four years, discussions were free flowing and fun at times. The structure of the class really contributed to the experience that I had with my capstone course but I believe that I learned the most during our two “exams.”
Our exams were deconstructed versions of scientific papers and we were responsible for putting the ideas together to form ideas. This process required a lot of critical thinking along with utilization of previous knowledge. This is the part of the class that I was able to utilize everything that I learned as a chemistry and biology major. After piecing everything together in the in-class portion of the exam we took home a copy of our exam and a copy of the actual article. Our job was to evaluate our reconstruction of the concept. Our grade was not based on how well we put together the puzzle but it was based on how well we supported our thinking. This made me realize how much I had learned in such a short time here at Concordia College.
I could potentially argue that this was one of the best classes that I have taken in my college career. It was both fun and informative. I have learned more about the brain and its pathways than I have ever learned before. This class provided an environment where I was able to apply all my knowledge in a creative and scientific way. If you asked me on the first day of school, if I would have loved this class, I would have answered with a loud “probably not.” However, now that the semester is coming to an end, I believe that I will dearly miss this class.
Calcium and Its Connection to Amyotrophic Lateral Sclerosis (ALS)
Amyotrophic later sclerosis (ALS), also known as Lou Gehrig’s disease, is disease characterized by death of motor neurons leading to mobile impairment and eventually death. This disease affects approximately 30,000 people in the United States and is quickly gaining notoriety. The average lifespan after the diagnosis of ALS is between 3 and 5 years. In all honesty, I did not know that much about ALS going into this week and I learned a lot.
Our article discussed that fact that calcium homeostasis in crucial in the proper folding of proteins within the cell. Dysfunction of calcium regulation can lead to improperly folded proteins and neurodegradation. The UPR pathway is responsible for properly folding protein within a cell and is highly regulated by calcium levels. The current treatment for ALS is used to delay the symptoms by slowing down neuronal death.
The worst part about ALS is that it debilitates a person and it affects every person around them. Individuals with ALS require constant care and therapy. As a person who plans to dedicate the rest of my life serving the needs of people, I find this disease sad. I cannot image the pain it must cause to an individual’s family. I hope that new research is discovered in the near future to help combat this disease. Since this is the last blog that I will post about an article that we read, I just want to let everyone know that this stuff rocks and I will keep reading on.
I’m PUFA for Polyunsaturated Fatty Acids
Let me be clear, I am not clear to argue with anyone about autism, vaccines, or the content I feel for bad science (if you get what I am saying). I am just here to talk about what my classmates and I have talked about over the past week.
Autism spectrum disorders (ASDs) consists a multitude of varying disorders in which people have impairment in social and communication skills. Within the autism spectrum there is autism, Asperger’s syndrome, and pervasive developmental disorder. In the past two decades, the prevalence of autism spectrum disorders has increased drastically. It is difficult to pin point a single reason why this is occurring.
What our class focused on this week in our discussions was polyunsaturated fatty acids (PUFAs). PUFAs are fatty acids that are essential to proper brain function. What I have learned from class is that PUFAs help regulate processes that involve cell proliferation. In ASDs, PUFAs are either not metabolized properly or are not doing their jobs. This leads the problems seen in ASDs.
One thing that I found interesting from this article was the importance of prenatal care. Research has indicates that maternal infections leading to an inflammatory response may elicit altered gene expression lead to dysfunction of brain function as well as alterations in PUFA metabolism. This suggests that proper prenatal care is crucial in the combat against ASDs. One way noted in the paper was a diet rich in PUFAs. A diet high in PUFAs will provide the growing fetus with the necessary nutrients to maintain proper brain development.
That most interesting thing that I learned all week was that there is a potential cure of autism that has reached its clinical trials. This means that the study has moved past animal testing and plans to test the drug in humans. This drug is known as Suramin. Suramin is a drug that has been on the market for many years for the treatment of African Sleep Sickness but it has recently been seen to help alleviate some of the symptoms in autism. I am not going to go into the specifics of the science behind this new hope for autism but if you want to check out some information I advise you to look at the following articles.
“Purinergic signaling is involved in many biological processes linked to autism, such as the development of synapses, or junctions between neurons, as well as gut permeability, immune responses, brain inflammation, and the activation of microglia, the brain’s immune cells. “The cell danger response theory explains so much that was inexplicable before.”
“Antipurinergic Therapy Corrects the Autism-Like Features in the Poly(IC) Mouse Model”
Lithium, More than Just Your Average Alkali Metal
With the atomic number 3, lithium is widely known as an alkali metal in the scientific community. However, when you move into the medical world, lithium is known for its clinical treatment for bipolar disorder. Lithium helps to combat the manic phase in bipolar disorder but no one is sure about how this exactly works. To make this simple to understand, I will break it down for you. Lithium’s actions in the brain will lead to inhibition of apoptosis (cell death) or stimulation of cell proliferation. I do not want to bog you down with all the science but if you do want a more scientific look at it, here is an image.
You are probably wondering right now, “if lithium is such a good thing, why is it not used for more diseases.” Well…researchers have been looking into the potential of lithium as a treatment for a multitude of neurodegenerative disorders including Huntington’s disease, Alzheimer’s disease, Parkinson’s disease, etc. Researchers have found success in treating some of the diseases in animal models but success has not translated into human trials.
Although lithium seems like a good potential treatment for many neurodegenerative diseases, I believe that it comes with many consequences. Obviously, we have all learned too much of anything can turn into a bad thing but what do we do when we do not fully understand a good thing? Lithium has been used to treat bipolar disorder for the past 5 decades and we still cannot figure out how it does its job. Furthermore, if you look at the picture, you will notice that lithium can affect a whole bunch of other pathways. That is a lot of power for one simple alkali metal that I want no part of before I understand all of it. But as Uncle Ben said, “With great power, comes great responsibility.”
What a Hit! The True Story About Concussions
Concussions are possibly one of the most common injuries for contact sports like football, boxing, hockey, etc. Players get hit in the head all the time and injuries occur frequently. Although concussions are common, they are not fully understood by the general public. This week in our senior neurochemistry course, my classmates and I discussed the article The Molecular Pathophysiology of Concussive Brain Injury. The article does a good job of outlining what happens when a person is concussed.
When a player or person suffers a concussion, the brain becomes “leaky.” The brain begins to initiate random action potentials which then cause the release of excitatory neurotransmitters (glutamate). The brain then attempts to restore the balance. This will then cause the brain to go into hyperglycolysis, leaving behind an abundance of lactic acid. Next, there is a calcium influx which will lead to impairment of oxidative metabolism and eventually apoptosis. This is a very short version of the cellular events.
This may seem scary but modern medicine has allowed us to properly treat concussion and to limit the lasting effects. However, the worst part about concussions is that people sometimes do not know that they have a concussion or they just don’t care and want to continue to play. Symptoms of a concussion vary from person to person but common symptoms include behavioral changes, memory impairment, headaches, and cognitive impairment. The only thing a person can do to treat a concussion is to rest and allow the brain to heal itself. This may range from proper rest to eating a proper diet to watching your favorite shows. This seems simple enough but the case is that repeated concussions occur commonly. Repeated concussions have strong negative effects on a person’s cognitive ability and potentially lead to chronic traumatic encephalopathy which is a serious brain disorder that leads to death. This is why athletes must be continuously monitored. A person must let their brain fully recover before they can take another hit.
In my opinion, concussions in contact sports like football and boxing must be carefully monitored. Another way to combat the concussions is to educate the future athletes on preventing concussions. People may say that the evolution of football and the new rules that protect the players take away from the integrity of the game but the safety of the players is far more important than the game itself. I believe that more precautions can be made to ensure the safety and longevity of each player without distorting the integrity of the game.
Wait a minute, Doc. Ah… Are You Telling Me that You Built a Treatment for Parkinson’s….with Iron?
For all those not understanding my title, it is a rip-off of a quote from Marty McFly , portrayed by Michael J. Fox, from the 1985 classic Back to the Future. This past week my classmates and I discussed the article Targeting dyregulation of brain iron homeostasis in Parkinson’s disease by iron chelators. Honestly, I was blown away by the amount of information that I did not know about Parkinson’s disease (PD). What most people know about PD is that it is characterized by the loss of dopaminergic neurons and the formation of Lewy bodies which lead to tremors and muscle stiffness.
The article tries to discussion the role that iron may play in PD. Iron exists within the body in two forms: Fe2+ and Fe3+. It is essential for the body to have a homeostasis or proper balance of the two ionic forms. These two forms of iron are important to the redox reactions within the body. Dysfunction in this mechanism may have potential dangerous side effects. A dysregulation of the two forms of iron are seen in the brains of patients with PD. Elevated levels of iron may cause the formation and accumulation of reactive oxygen species (ROS) along with intracellular alpha-synuclein. Iron chelators help reduce the amount of iron in the brain and attempt to maintain homeostasis.
The most interesting part of this article, in my opinion was the discussion on how green tea can be beneficial to PD. I find this interesting, as I take a sip from my hot cup of green tea, because I come from a Chinese descent. Green tea, along with an oriental diet, has been shown to have many benefits. Green tea’s beneficial effects come from compounds known as catechins. The catechins have been shown to relieve oxidative stress by inhibiting the ROS-NO pathway and also chelate transitional metal ions. Green tea is such a “hot topic” that the Chinese Ministry of Health and the Michael J. Fox Foundation have been funding research to study the potential effects of green on PD. The potential of this research makes me hopeful for the future of those at risk for PD.
A Connection from Type 2 Diabetes to Alzheimer’s Disease
Alzheimer’s disease is well known neurodegenerative disorder that affects many people all over the world. Popular media and modern science has made it clear that there is a clear connection between type 2 diabetes and insulin resistance. Furthermore, new research presented in the article, Possible Implications of insulin resistance and glucose metabolism in Alzheimer’s disease pathogenesis has shed some light on the connection between diabetes and Alzheimer’s disease. In my personal experience, with most of the elder’s in my family having type 2 diabetes, I have learned that diabetes is a frightful monster than can lead to a plethora of health complications but I have never understood it well. Until this article, I was unaware of insulin’s essential roles in the brain. For example, insulin-like growth factor 1 (IGF-1) has been found to be essential in the proliferation of cells and the regulation of glucose metabolism. Right now, you might be thinking, “what in the world is this guy saying? I don’t get the connection.” My answer: stay calm you must my young padawan.
One of many key links between these two diseases is INFLAMMATION. If you have too little insulin, this will cause an increase in an inflammatory response and an increase in oxidative stress. This will lead to apoptosis and the destruction of the synapses in the brain. Furthermore, decreased insulin will lead to decreased norepinephrine and eventually, decreased cognitive function. Insulin’s ability to regulate inflammatory responses in the brain is critical in the development of Alzheimer’s disease.
As time has passed in our nation, processed foods and high fat diets are more and more common. Type 2 diabetes has quickly become one of the most concerning diseases in the young American public. If this connection between diabetes and Alzheimer’s becomes a legitimate concept, we could potentially see a spike in Alzheimer’s disease occurrences along with early onset of the disease.
This is some scary stuff, right? I find that new research like this is terrifying but I realize that not that many people actually care. People have known that diabetes comes with a cornucopia of health complications but the American public has failed to do anything about it. Diet plays a large role in the development of diabetes and I believe that is where we start our assault on diabetes and ultimately Alzheimer’s disease. Prevention of diabetes has never been more important than now. With more and more research being published about this connection, we risk the health of many Americans if nothing is done to correct the diets of our society. Obviously, Alzheimer’s disease is a multifaceted disorder but people can learn to minimize their risk by properly regulating their diets.
When In Doubt, Sit It Out
What exactly happens when you get a concussion? Are there any long-term repercussions of getting one? Previous to reading this weeks article, I figured that getting a concussion or multiple concussions was detrimental, what I didn’t know were the serious, long-term negative effects that multiple concussions can have. Repeated concussions can lead to a disease called CTE (chronic traumatic encephalopathy), which leads to many dementia-like symptoms. Clinical symptoms include changes in mood, behavior, cognition, and in some cases motor disturbance. This disease is often found in athletes, many times in contact sports such as football, boxing, or ice hockey. Most often these symptoms do not appear until many years after trauma, and to make matters more complicated, as of right now the disease can only be diagnosed postmortem. Many have died not from the disease itself, but from disease related behaviors such as suicide. It is a serious disease that does not seem to get much attention. So, back to my first question, what exactly happens when you get a concussion?
Right after trauma to the brain a complex cascade of neurochemical and nuerometabolic events occur. The flux of ions gets thrown off, leading to physical membrane defects. Due to this, neurotransmitters are release and this results in further ion flux. Energy is used up by the brain attempting to keep ionic balance. When these events occur just once and the brain has time to heal, not much damage is done, but when repeated injuries occur this may result in permanent damage and conditions such as CTE. All this science mumbo jumbo may not mean much; what should we do about this issue?
An easy solution would be to simply stop playing sports after a certain number of concussions, or to take a very safe amount of time off after suffering from a concussion. Unfortunately, the solution is not this simple. Many athletes who get a concussion wish to keep playing regardless, especially when it has been a while since the concussion occurred. Many do not take serious enough how long it takes to fully recover from a concussion. Athletes may feel completely fine after a concussion, even if the brain is not fully recovered. It is important to note that there are various levels of severity when it comes to concussions. Depending on this severity and the number of concussions someone has suffered in the past, athletes may be out for up to a month or should stop playing for the rest of the season. The fact is, that this is not always what is really happening. Many athletes go back to playing or even just practicing before they should, resulting in more concussions and thus major brain injuries later in life. By reading this article, I have come to realize the severity of multiple concussions. This problem may be larger than we realize and many athletes may suffer later in life from something they don’t even know is currently happening in their brain. We need to start taking concussions more seriously and hopefully more research will aid us in understanding diseases such as CTE before death so we can do something to prevent or treat them.
Autism: Genetics or Diet?
It seems that every year more and more children are being diagnosed with a cognitive disorder called autism. Over the past 32 years the number has risen from 1 in 5000 people having this disorder to 1 in 150 having this disorder. There are several different reasons that this could be occurring. One reason that this could be occurring is that there is a broad spectrum of symptoms that are related to autism. When diagnosing autism there are three different broad categories to look for in the child. They are social skills, communication skills, and behavioral skills. If a child has autism they might be more inclined to be an introvert, shy, appear unaware of others feeling and poor social behavior. The communication skills that may be lacking in an autistic kid is that they don’t speak very often, can’t keep a conversation going, and they may repeat phrases exactly as someone else has said them. The behaviors that may develop are a desire for an inanimate object, repetitive movement, or become disturbed at the slightest change in routine. All of these could be confused for a personality disorder or simply the unique personality of the child.
One idea that has come about when talking about autism is that there needs to be genetic screening to see if there is a way to diagnose the disease. The problem with that is there are so many mutations that are prevalent in autistic children is that it is hard to narrow it down to a few that may cause autism. One study showed that there are 130-234 mutation points that may be linked to autism. One of the more interesting mutations that occur happens on chromosome seven. If there is a deletion on chromosome seven in a specific region a child is more likely to develop Williams’s disease. This is a disease that children to me overly friendly to strangers and to be very social. If there is a duplication that occurs in this region, there is a tendency for the child to develop autism. This is interesting because one point in a child’s genome may determine a major characteristic of their personality. Another idea that was tested during study was that the researchers wanted to see why males are more likely to have autism than females. They determined that this is because females are more resistant to these genetic mutations. It takes larger changes in the genome for them to be affected. An importance to figuring out the genetics behind autism is that proper diagnosing can occur. Physicians will be able to figure out whether the child has autism or the have a personality disorder. This would change the treatment process of the neurological disease.
Another cause of autism is the diet that the person has. The diet can affect the molecules that are in the brain and how the brain develops. If someone has a diet that is high in linoleic acid (LA), it will be beneficial to the brain. This is because this acid promotes arachidonic acid (AA) and eicosapentaenoic acid (EPA). Both of these acids will cause brain growth and development. This will cause the correct neurotransmitters to be released in the brain. If the neurotransmitters, such as acetylcholine and serotonin, are not released correctly, the brain will not have correct neuron function and neuronal preservation. This can then lead to autism spectrum disorders.
Can genetics affect obesity and the brain?
There are many negative side effects of being obese. Some of the effects that are not looked at though, are the effects that obesity has on the brain. There are many problems that can occur within neurotransmitters because of high fat diets and obesity. One of the main systems that is affected by a high fat diet is that leptin activity is inhibited. This causes many downstream effects to occur. One of these is that Erk is inhibited and this causes the up regulation of the Gsk-3 pathway. This is detrimental because less BDNF is produce. BDNF is a transcription factor that helps protect the cells and prevent apoptosis. A high fat diet will also increase the chances of having type II diabetes. With type II diabetes there will be insulin resistance within the cell. From one of my previous blogs, it can be seen that insulin resistance will lead to decreased cognitive function. This insulin resistance will also cause the inhibition of leptin activity. Then the cycle that was described earlier will occur in the neurons. Another result from a high fat diet is lipid peroxidation. This causes oxidative stress to occur within the cell. This oxidative stress will disrupt the unfolded protein response (UPR). If the UPR is not correctly working, the cell will end up dying because of apoptosis. This apoptosis will cause a decrease in cognitive function. Another problem that can result from this diet type is disruption in the blood brain barrier. The blood brain barrier is disrupted because of the down regulating the mRNA expression of Claudin-5 and -12. The reason that this is a problem is that harmful chemicals can enter into the brain if the blood brain barrier is not working correctly. It also disrupts the ability of the brain to flush molecules out of the system.
One important idea that is associated with the problem is that some people may have a gene that may incline them to be more obese. This gene is known as the fat mass and obesity associated gene (FTO). The gene is for a enzyme that catalyzes the demethylation of 3-methylthymine. This gene has been shown to be upregulated after food deprivation and negatively correlated with the food stimulation of food intake. This gene has been shown to have a greater effect on the person if they have both alleles for it. This means that if both of the chromosomes have the FTO gene, the person has a higher chance of being obese. The problem with this though is that people may try to use this as an excuse on why they are obese. This gene may cause this but it can have no effect if someone diets and exercises properly. Another problem with this gene is that people with it tend to have a tendency to show more symptoms that are commonly associated with metabolic syndrome. These symptoms include higher fasting insulin, glucose, and triglycerides, and lower HDL cholesterol. This may be caused though by the weight gain rather than the gene itself. A final problem that may occur because of this gene is that there is a decrease in the frontal lobe in the brain and an impaired verbal fluency performance. Like I stated earlier, a person may have this gene but it can be a non-factor if some has the proper diet and exercise regimen.