Cobbers on the Brain

Autism is a disease that has affected families around the world and has become an ever-growing problem in the United States. Autism is known as a complex, developmental disability linked to abnormal biology and chemistry in the brain. Experts believe that Autism presents itself during the first three years of a person’s life. The condition is the result of a neurological disorder that has an effect on normal brain function, affecting development of the person’s communication and social interaction skills. However, the exact mechanisms in which the disease functions remains unknown. In the United States, autism has been on an unusually steep rise since 1970. It is the goal of researchers to determine what has caused this sharp increase. In order to explain this, researchers have turned to examining the disease mechanistically.
Researchers have learned from twin and sibling studies that genetic factors play a role in autism. However, the genetic factors cannot be the sole reason autism develops in young children. Thus, experimental factors are proposed to be the cause for the increase in autistic individuals. These factors can include diet, exercise, vaccine sensitivity, or anything outside the body that could alter the interior. Being that this brings about a broad category of factors that could lead to autism, researchers have hypothesized a “redox/methylation” hypothesis.
In this hypothesis, researchers have noted that environmental factors lead to oxidative stress. Because neuronal cells exhibit the most sensitivity to oxidative stress, the brain is affected the most with autism. Given the correct risk genes, a number of adaptive responses involving sulfur metabolism are initiated once oxidative stress has taken its course. This leads to an inhibition of methionine synthase, which greatly reduces methylation activity. Most importantly, this affects DNA methylation and dopamine-stimulated phospholipid methylation. This decrease in DNA methylation disrupts epigenetic events that are characteristic of normal development. The decrease in dopamine-stimulated phospholipid methylation restricts the frequency-dependent synchronization of neuronal networks. Thus, communication between neurons is altered. This is linked to the lack of attention and cognition.
Although the “redox/methylation” hypothesis is purely speculation, the research has led to areas of interest involved with autism. The hypothesis has found a general explanation for autism but does lack in areas regarding specific cases of autism. However, the “redox/methylation” hypothesis does provide a starting point at which researchers can hope to build upon. In order to validate the hypothesis, the specific causes of autism need to be identified.

Prior to walking into the Neurochemistry 475 classroom for the first time, I merely thought of the class as just a capstone required for graduation. However lazy this may seem, I think it is safe to say that several of my classmates had similar notions. Despite my lack of enthusiasm, I would later find out that the next three to four months of my life in Neurochemistry 475 would provide discussion into many controversial topics involved with neurodenerative disorders, behavioral disorders, and many other mechanisms involved with the brain. This may seem like pure science malarkey, but it actually turned out to be a combination of viewpoints blended into one mass discussion. This was not a simple coincidence, though. It was the underlying agenda of Professor Mach that brought the cornucopia of student masterminds to the discussion table. Students’ majors included biology, chemistry, and psychology. This provided for a conversation displaying a wide range of the opinionated spectrum.
The first few weeks of class were spent investigating background information relevant to the articles we would eventually discuss. This seemed to be what we college students refer to as “busy work,” but it was much more than that. We studied topics ranging from amino acids and nitric oxide to the endocannabinoid system (the system through which marijuana acts). Contrary to my prior belief, neurochemistry was starting to spark my interest. I found myself having conversations involving the class material outside the classroom. Being a chemistry major, it is rare to find a connection between science talk (molecules, mechanisms, etc.) and what is considered to be normal/social conversation. Not saying that I am completely antisocial, but it was nice to be able to bring something from the classroom into everyday life.
Since the ultimate goal of every college student is to get hired at that perfect job and become successful, it is only right that students apply what they learned in college to their occupation. This class has given me a brief insight into that sort of application. More importantly, I feel that the last four years of my life, particularly referring to chemistry, have combined to make this class more of a discussion on what I have learned than a traditional lecture-based class. I thoroughly enjoyed the group discussions for the mere fact that everyone in the classroom brought their own opinions to light. There is a time for talking, and there is a time for listening. By hearing the opinions of my peers, I was able to formulate my own ideas with their influences. I guess I found it really interesting how the different majors made for such diverse responses to the articles we read.

            Overall, I really enjoyed this class. It allowed me to reflect my own thoughts into areas concerning my major and listen to others’ insights. The controversial topics we covered definitely grabbed my attention and made the assignments much more enjoyable. I was actually intrigued by the information we were researching. If I can leave any advice to Concordia students (particularly chemistry, biology, and psychology majors) aspiring to take this class, then I would have no problem in saying that Neurochemistry 475 is great for bringing together what you have learned over the past four years of your life.

Alcohol abuse is an issue of both old and new generations. Leaving not one continent untouched, alcohol raises economic and health issues around the world. Alcohol abuse is a disease that is characterized by a pattern of excessive drinking despite the negative effects of alcohol on the individual’s work, health, legal, educational, and/or social life. Alcohol abuse affects approximately 10% of women and 20% of men within the United States. Given this information, a search for a pharmacological treatment seems necessary in an age where alcohol is an everyday commodity. In order to make that a reality, scientists have researched the mechanisms in which alcohol (ethanol) alters the nervous system.
The studies have revealed that ethanol has been found to modulate signal transduction through cascades that involve PKA and PKC pathways. Also, ethanol’s effect on the brain (via the previously mentioned cascades) has been observed on genetically engineered mice. This has led to the discovery that specific regions of the brain are involved with ethanol’s effects depending on the presence of signaling molecules. An example of this can be seen by examining the NMDA receptor and its sensitive response to ethanol. DARRP-32 and Fyn kinase regulate the NMDA receptor in the hippocampus. The PKC pathway also plays a role in which isozymes on GABA_A receptors are the area of interest. PKCg has been shown to support ethanol enhancement of GABA_A receptors and PKCe is an inhibitor.
This research has led to a greater understanding of how ethanol’s mechanism works within the brain, but the specific molecular mechanisms remain uncertain. If scientists are able to identify the specific genes that act in the brain in the presence of ethanol, then the targeted gene can be modulated to alter behavioral responses to ethanol. In the best possible scenario, this would lead to potential drug targets for treatment of alcohol abusers. This would be beneficial to some, but to others, just an escape from the alcohol’s grip. If a drug were to succeed in a fight against alcoholism, certain moral factors need to be implemented in the sale of it. Only those that really need it (alcoholics) ought to be the only ones prescribed. However the drug is used, it is still an area of great interest in a world that struggles with alcohol abuse.

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.