Cobbers on the Brain

Alzheimer’s disease has affected over 4.5 million people within the United States, and the number is expected to grow to 13 million by the year 2050. Economically, this presents a huge problem. In 2009, $144 billion (per year) was spent on healthcare for patients with dementia. That turns out to be an average yearly cost of $33,000 per person. Obviously, this is less than manageable for many Alzheimer’s disease patients, which is why research into the disease is crucial for the advancement of treatment.
Alzheimer’s disease is a chronic, neurodegenerative disease of the brain that has been characterized by neuronal loss, b-amyloid plaque deposits, increased activity of catabolic genes and pathways, decreased energy production, mitochondrial activity, and free radical stress. Most importantly, it affects areas of the brain associated with learning and memory. However, it can also affect other areas of the brain. Two of the most common symptoms of Alzheimer’s disease are memory loss and dementia. By examining the MAPK signaling pathways, one can identify the mechanisms in which memory loss and dementia occur.
As stated before, b-amyloid plaque deposits are a major element in Alzheimer’s disease. Along with neurofibrillary tangles, b-amyloid plaques result in cognitive and memory dysfunction. Tau, a microtubule-associated protein, is known to be present in the neurofibrillary tangles. Since its phosphorylation is mediated by several kinases (JNK, p38, and ERK), it affects the MAPK pathways. Also, oxidative stress plays a key role in Alzheimer’s disease and is involved with the JNK and p38 pathways. An activated MAPK pathway is hypothesized to aid in the development of Alzheimer’s disease. The mechanisms in which it operates include induction of neuronal apoptosis, transcriptional and enzymatic activation of b- and g-secretases, and APP phosphorylation.
In recent years of research, scientists have made dramatic progress in understanding Alzheimer’s disease. Four genes have been linked to the disease. The mechanisms by which altered amyloid and tau protein metabolism, inflammation, oxidative stress, and hormonal changes may produce neuronal degeneration are being identified. This has led to the hypothesis that Alzheimer’s disease develops via MAPK signaling pathways.

Neurochemistry proved to be everything I have hoped I would experience throughout my educational experience at Concordia.  I believe that its function as a capstone course required that we students take it upon ourselves to learn the material and engage in discussion about relatively complex topics both for our educational gain and the education of our fellow neurochemistry classmates.  From a pedagogical standpoint I applaud the design of the course.  For the first time, we students have been given the vested responsibility to learn ourselves and help teach one another about topic covered in class as well as engage each other in discussion about the social, biological, and ethical implications of some the topics covered throughout the semester.  I guess I was pleasantly surprised to see the entire class step up to the plate and authentically care about the hand they had in progressing the class forward.
In addition to the discussion based aspects of the class I found that the exam formats were very effective in allowing the students to express what they had learned through both class based discussion and general problem-solving skills.  The format of the exams we took were of two parts, an in-class portion where the students were given a limited amount of information about a neurochemical problem and other factual information in addition to that problem, and secondly a take home portion of the exam in which the article the exam is based off of is given to the students and the students compose information regarding the cause of the problem as well as evaluate the accuracy of their in-class portion.  I found this to be an open-ended yet extremely effective method for students to apply the problem solving skills gained throughout the semester
Finally, the blog posts have been among the most rewarding experiences throughout the summer because it gives us students the opportunity to communicate science to the general public.  This scientific communication also happens to be the writing formats, which we would most like to read regarding neurochemistry and the social ramifications of particular problems in its realm.  I have been extremely fortunate to participate in this course at Concordia College and I will surely not forget the educational benefits of discussion based science courses in the future.

Obesity in America has come to be known worldwide as the epidemic of the western world.  Though the fast food industry has been the patsy of many lawsuits regarding uncontrollable weight gain, the culprit may actually be the 32 oz cola rather than the burger and fries.  The most common sweetener used in soft drinks and other non-diet beverages is high fructose corn syrup (HFCS) a mixture of glucose and fructose.  HFCS has taken the place of sweeteners such as glucose, for two reasons: fructose is more readily supplied by corn, America’s most prevalent crop, and pound for pound HFCS tastes sweeter than glucose.  Sounds great right?  A smaller amount of HFCS provides the same sweet sensation that we get from an equal amount of pure glucose, thus HFCS provides more sweetness for less calories.  This is true but fructose doesn’t play the same ballgame that glucose does in the body.
The Concordia Neurochemistry class focused on the role leptin and insulin play in obesity, and the results were concerning to say the least.  The article under investigation clarified HFCS’s potential role in increased weight gain through an improper biological response to the sugar.  Even though they both taste sweet, fructose and glucose are fundamentally different.  Glucose is extremely important to our natural energy production.  Glucose is transported into the cells of our body as a result of elevated insulin levels.  Cellular glucose intake means increased energy production.
Fructose does not play the same role as glucose.  Fructose actually bypasses the transport into the cells and goes straight to the liver, where the liver then transforms the fructose into a precursor to triglycerides (fatty molecules).
So regarding obesity in America, much of it can likely be attributed to our excessive intake of HFCS through soft drinks and processed foods.  In addition to the fat producing effects of HFCS, it does not merit the same spike in insulin levels that glucose does, so we don’t realize that we are full.  The absence of insulin levels while consuming food that is high in HFCS can lead to overeating which lends itself to an energy surplus, thus we gain weight.  The positive correlation between fructose and weight gain is impressively strong.
In conclusion, all sugars are not equally processed.  Indeed overconsumption of any calories will lead to weight gain, however, considering that HFCS is immediately converted into a fat precursor, it is advisable to opt for foods that are primarily sweetened with glucose.

Brain plasticity, what does it mean?  Usually we associate brain plasticity with the ability to readily learn new tasks and recover from potential damage, however recent research regarding concussions show that not only do periods of heightened plasticity not protect subjects from mechanical brain trauma but it makes them more vulnerable.  Indeed the most common period for us to experience brain trauma is when our brains are not fully developed, specifically our frontal lobes, which continue to develop throughout the age of 25.  The reason behind the long-term brain trauma vulnerability, is that the myelination, a cholesterol-like protective tissue, of our frontal lobes has not entirely taken place.  So unlike brain trauma experienced by their elders, young adults exhibit a susceptibility to slower recovery and worse overall long-term cognitive outcomes in the wake of brain trauma such as a concussion.
This brings to light a serious question regarding the ethics of athletic performance throughout early adulthood especially regarding whether or not a previously concussed participant are ready to reenter the athletic field.  Looking back on my high school athletic experiences what was most obvious was the potentially self-destructive notion of more pain, more gain.  Keeping this in mind, and considering the glory of athletic success throughout those years, it was blatantly obvious that people, who have suffered from a concussion, were eager to “recover” so they could quickly return to the field and support their team.
Our neurochemistry class talked extensively about the potential long-term damage an athlete could subject themselves to because of premature reentry.  The primary reason that premature reentry is so dangerous for concussed subjects is that the brain’s natural defense system against trauma has been drastically weakened.  This defense system incorporates your brain’s ability to repair mildly damaged neurons and to re-equilibrate the chemical levels of those neurons.  If a second traumatic event occurs while the brain is fervently working to repair the first concussion, the brain goes into a significant state of decreased repair, which often leads to irreparable damage.
Furthermore, in order to properly recover from a concussion it is advisable for the subject to take a break from the functions of a normal day. In fact concussion victims that immediately engage in normal tasks such as schoolwork, normal motor function, and coordinated motor function show a marked decrease in cognitive recovery rate.  If such therapy required for a concussion victim to recover fully, are we ultimately jeopardizing students’ academic and cognitive future by allowing them to participate in concussion related athletics and return to the field without knowing indefinitely if they have fully recovered?  While concussion related stories about professional athletes and permanent damage increases to become more prevalent in the media I believe there will be a movement toward improving concussion recovery diagnostics and much controversy surrounding the potential dangers surrounding school athletics.

This morning I did something I don’t normally do, I stopped eating. I still had food on my plate, I just didn’t feel hungry anymore. Even though it seemed like the right choice I still got scoffed at from my girlfriend for not finishing my plate, I almost felt peer pressured to eat more then I wanted to! This isn’t just my girlfriend either, it can be seen with others like from parents telling their child to finish his/her plate. Along with pressure, boredom or procrastination on homework are other pitfalls for eating.In fact in a effort to procrastinate another 5 minutes on writing this blog post I finished off the role from this morning. So with procrastination and peer pressure it would seem that our body figures are doomed. But wait, something is amiss, there must be something stopping us from eating all of the time, and as with everything else the answer lies in chemistry.

Fat is deposited into adipose tissue, so it would seem that this adipose tissue would have to communicate with the brain in some way to control how much we eat. It was proposed that there exists molecular signal that acts in the central nervous system that is proportional to body fat. So the more fat we obtain the stronger these signals are, and these signals would stop us from eating. A pretty nifty checks and balance if I do say so myself. But obviously with the level of obesity we have something must go wrong.
At the moment there are two signaling molecules that have been determined to be part of this signaling cascade. Insulin and Leptin. The paper we looked at for this week tried to tie together the different signaling pathways of the two molecules, in a effort to paint a more holistic shot of the chemistry of obesity. Our authors were able to conclude that “[both insulin and leptin] may share both intracellular signaling properties and mechanisms by which these pathways become disrupted leading to resistance to their actions.” What I would take from this message (just like my other blog posts) is that scientists are still working to get a true understanding of the body. Everybody wants the body to be simple, it would be much easier if just one chemical was responsible for obesity, and it would be great if that was the only molecule in the body. Then researchers would be able to just target that molecule and eradicate it, and obesity would be a thing of the past. Sadly this is not the case all of these molecular systems are intertwined everything seems to be dependent on everything else. There are so many factors that go into obesity, especially at the mental level. We are wired to love fatty foods, we would much rather eat a meal then write a paper, there is eating when your board, or eating when your depressed. Meaning all of these different pathways that are created by our different states of mind are connected. And it will be a long time till we are able to untangle this mess.

With the semester officially over, I am left to consider what gains have been made in the past few months. Usually it’s a little challenging to identify how my knowledge has changed and grown, and what new information or skills will be immediately useful to me in the future. However, this year it’s easy. Neurochemistry has been extremely helpful in taking my knowledge of neuroscience further and integrating my understanding of the nervous systems with areas of science I am not as familiar with. This includes upper level chemistry, biology, and genetics–classes that are difficult for me to access as a psychology major unless I tack on a few extra majors or minors. Neurochemistry, however, demonstrated that this isn’t necessary, and that careful analysis of the literature and extra readings and research in areas I’m not familiar in can provide a great foundational understanding of neurochemistry.
The interdisciplinary nature of neuroscience is what drew me to the discipline in the first place. As a psychology major and neuroscience minor, I am interested in how the brain creates thought and behavior at the cellular, molecular, and systems levels. Generally, I hover somewhere in between the areas of psychology, biology, and chemistry–farther enough on the physiological end of psychology to dread the familiar, “Oh so you’re a psychology major? What are you going to be, a shrink or something?” No. No, actually, I’m not. Yet I’m not a chemist or biologist either. Neuroscience is the perfect place to blend all of these interests. Not only does it allow a multidisciplinary approach to studying the science of the brain, but I think it also fosters cooperation between scientists and fields that may contribute to better research and progress. As the scientific field becomes progressively more and more specialized and reductionistic, neuroscience remains a bastion of cooperation and integration between multiple fields. Where else can computer scientists, mathematicians, cognitive scientists, linguists, psychologists, doctors, chemists, biologists, and even philosophers meet at a common interest? Exactly.
How did neurochemistry impact my learning this semester? I feel that it has enabled me to more fully appreciate and join the multidisciplinary area of neuroscience. Before, I leaned heavily on the psychology end of things and had limited knowledge of chemistry and molecular biology. Throughout the course, however, I learned through personal research and additional reading that these concepts greatly augment my understanding of brain function. Through in class lectures and discussions of papers, I became more and more familiar with chemistry and biology concepts. There were many “aha!” moments when I realized a signalling pathway, gene, or chemical responsible for a phenomenon in psychology. I truly came to understand much more about the biochemical signalling in the brain, and to integrate that with what I already knew about behavior and the mind. I was also able to share with others my knowledge and experience with psychology and mental illness. Coming away from this class, I feel that I have much more mature understanding of brain function as well as an appreciation for the diverse perspectives that converge in the field of neuroscience.
It was also enormously effective to include a writing and communicating focus in this class. I’ve observed that many science majors, including myself, can be deficient when it comes to communicating about science to the public. This can be disastrous, as the public frequently and severely misunderstands scientific research and issues. Good communication skills will be vitally important among scientists as research progresses. I feel that this class pushed us to be better communicators–not just in reporting scientific knowledge to others in the field (i.e. us) but also to the general public. These are two quite different skills. Learning how to write in a blog format about big issues in neuroscience research was a challenge but also a lot of fun. I feel that I grew just as much as our intended audience may have as well.
As I consider a career in neuroscience myself, I’m excited about all the different directions, perspectives, and areas of expertise included in this field. Neurochemistry has taken me one step closer to joining this diverse community.