Cobbers on the Brain – Page 138 – Student Commentary on the Neurological Sciences

Neurochemistry: reflections on a semester

Posted on December 16, 2015 by Joseph Kennedy / 0 Comment

While this year has been anything what I expected. I cannot say anything other than neurochemistry was an incredibly useful course to take that furthered my understanding of chemistry. At the beginning of the semester, I was somewhat hesitant to take the class simply due to my lack of a strong biology background. This feeling existed especially because I had to take the class in order to graduate with my degree. Despite my initial hesitation about the class, I was able to pick up enough of the biology and biochemistry to fill in the gaps in my knowledge. With my background as an inorganic/non-biological chemist learning how the neurons and the pathways worked was never easy. However, slowly, over the course of the semester I began to feel more comfortable with the cascades and the pathways.
By the end of the semester I, like much of the class, had found my niche: bio-inorganic chemistry. I was able to focus on how metals worked in the brain and how these metals were related to the various diseases. I had previously been aware of how metals had worked in the body, at least in a general sense. Too much metal means something bad happens, too little metal means something bad happens, and just the right amount meant that something not bad happens. With the diseases we looked at, I came to see that metal plays a much bigger role than I had realized. Zinc, something that had only been discussed as having some interesting chemical properties due to its full valence shell, is arguably the most important metal in the body other than maybe iron. Zinc is found in almost every enzyme that humans, and many mammals, need to survive even a short time. While iron is used to transport oxygen to various tissues to allow the Krebs cycle and generally help with the oxidation process.
Ultimately, I’m very glad that I took this class because I now feel confident on biochemistry, something I had been somewhat shaky on, and am significantly more confident on how metals react and work with nonmetals. Metals are a truly interesting topic for me, and seeing how metals play out across so many different systems was quite interesting and something I am very thankful for. Who knows, maybe one day I’ll find myself doing bio-inorganic chemistry and I’ll look back at this page in order to better understand some of the reactions I had previously looked out. Until then, happy holidays, and have a fantastic new year!

Health

Bulimia Nervosa: Not Just a Psychological Disorder

Posted on December 16, 2015 by / 0 Comment

According to the American Psychiatric Association, Bulimia Nervosa is characterized by “repeating episodes of of binge eating and compensatory behaviors, such as excessive
exercise, self-induced vomiting, diuretic or laxative abuse.” It, along with other eating disorders such as Anorexia Nervosa, is most notably a psychological disorder, and thus is typically treated through therapy.
What is to blame?
Most easily, we are able to cast blame on society and media. The use of photo-shop and alterations of the such lead to unattainable expectations for today’s youth (pre-teens, adolescents, early 20’s), while also having reports of eating disorders in older populations. Women AND men (affects both sexes) with the disease may never see themselves as having the “perfect” body, which adds to the psychological downfall leading into these dominating disorders. However, there is a certain pathophysiology revolving around Bulimia Nervosa, into which we studied.
The binge–purge cycle is introduced by first, overeating; which is perceived as ‘out of control.’ Purging acts to relieve or mitigate the distress of this state of being ‘out of control’ and provides an euphoric sense of increased control over food intake or weight. If this uncontrollable food consumption is so, well… uncontrollable.. why do it in the first place? As many people know eating releases endorphins and a lot of ‘feel good’ hormones, encouraging the person to seek out those foods he or she may like. In Bulimia, the act of overeating and compensatory behavior temporarily reduces the anxiety of feeling out of control. Thus this ‘out of control’ — ‘back in control’ cycle is reinforced through eating, and the process continues. The process of initiating binging and purging may be more than just through the media wanting us to look good, but may be because of our own susceptibility to external stressors and compulsive habits.
Compulsive traits of an individual have been found to be linked to serotonin dysfunction, notably through genetic polymorphisms within the serotonin system. With that being said, obsessive compulsive disorders share a common dysregulation in serotonin function, sharing some similar behaviors with bulimia. Thus, the serotonin system appears to be a unifying neurobiological system in which we need to understand more about its role in eating disorders such as bulimia.
One possible pathophysiology is of interest, and that is the vago-vagal reflex. This reflex is serotonergic in nature, and if serotonin dysfunction is present, this reflex may not function properly. This reflex is responsible for the ability to store food in your stomach. When food is consumed, the stomach muscles relax in order to provide more room, and reduce the pressure inside the lumen. When this reflex is dysfunctional, the food can still reach the stomach, but the walls are not relaxed, resulting in an increase of pressure. After many episodes of binging and purging, serotonin levels may become more and more irregular, thus reinforcing an improper reflex, resulting in pressure build-up, and then decreased ability to keep food down, resulting in a positive-feedback loop.
The dysfunction of the vago-vagal reflex is one of many physiological manifestations of bulimia. It’s a cycle of reinforcing the purging, thus leading back to seeking the necessity to over-eat. Although there are noted psychological anomalies associated with bulimia, we must first recognize that this disorder has to also be physiologically treated, and thus, the disease becomes even harder to cure than initially thought.

Uncategorized

The Role of Serotonin and Estrogens in Development of Bulimia nervosa

Posted on December 15, 2015 by / 0 Comment

Bulimia nervosa (BN):a disorder characterized by repetitive episodes of binge eating (consuming large amount of food at once and feeling unable to control) and purge behaviors (compensatory behaviors such as excessive exercise, self-induced vomiting, and ect.). https://moodle.cord.edu/pluginfile.php/495205/mod_resource/content/0/bulimia%20and%20serotonin.pdf
https://moodle.cord.edu/pluginfile.php/495206/mod_resource/content/0/wonderlich%202015%20review%20risk%20and%20maintenance%20model.pdf
Causes of BN:

serotonin dysregulation
disturbances in estrogen system

Low serotonin caused behavioral disturbances such as alcohol use disorder, binge eating, drug use and other risky behaviors. Estrogen is needed for prenatal brain development. After birth, serotonergic and estrogenic systems lead to overeating and fat deposits. As puberty emerges, the level of estrogen rises. Societal perceptions of “thin body” causes dissatisfaction of weight and height of individuals especially women. Changes in serotonin and estrogen systems at this period of life cause mood dysregulation as well.
An overvaluation of shape and weight influences self-evaluation; this leads to negative feelings, anxiety, anger, and depression. As a consequence, emotional eating occurs. This is binge eating and followed by purge behaviors, which either reduces the negative feelings at the end or distract and decrease self-awareness of the individual while conducting the behavior.
Culture of eating and development of BN:
As we discussed in our group, people tend to eat more than what they actually need. This can be due to the fact that there is too much food available. We tend to eat even if we are not hungry. The quality of food is not always the best. We mostly consume high fat and carbohydrate foods. It was mentioned in our group discussion that BN is not as common in developing countries. The main reason for that is not having access to food more than people actually can survive on.

What can parents do to help children?

One of the interesting questions we discussed was the role of parents in personality development of children. It is very critical and challenging for parents because of the huge role of media and social perceptions on the behavior of children. But, it is essential for parents to ensure to value their children and not criticizing them for how they look like. It is responsibility of parents to encourage a critical thinking habit in their kids. That is the secret of having them survive the poisonous thoughts and stimulations outside of home and even on the media.
Important lesson I learned by taking this course:
During the semester, we have gone over several diseases. Some of them are not well known to people. There is a significant need of raising awareness about diseases and causes of them. The education for the public can be in terms of slight changes they can make in their life styles. Diet and exercise are the main issues need to be changed. It is education and raising awareness that can help people with their decisions. Since we have access to lots of food, it is our responsibility to respect our bodies and our minds. We need to feed them and take care of them properly.

Disease/Health/Hot topics

A Vicious Cycle of Unattainable Ideals

Posted on December 15, 2015 by / 0 Comment

How do you empathize with an individual who seems to purposefully be doing harm to their body, as appears to be the case in eating disorders? Well first of all, people need to realize that eating disorders, such as anorexia nervosa (AN) and bulimia nervosa (BN), are disorders that are attributable to an imbalance of neurotransmitters in the brain, not just selfish acts of wanting to be thing. For many, this imbalance leads to a type of body dysmorphia disorder, as is showcased on the featured photo of this blog post. This harsh reality for those who suffer from AN or BN is a mystery many researchers continue to pursue everyday in order to one day fully understand the complexity behind these disorders.

How do you encourage someone to change their eating style and life habits if what they see in the mirror is not reality?

Educate. Educate. Educate.

It all starts with education, and debunking the stigma and negative assumptions often associated with those who are so unfortunate to go through an eating disorder.

The reality of eating disorders is they are in fact mental disorders. And if it takes decades longer to understand that mental disorders do exist, even though they cannot be “physically” seen, fine. We have made strides, but in the meantime, these conversations must happen and frequently, for they are what will bring about a changed societal mindset.

So let’s get started!

Focusing specifically on BN, serotonin, a main inhibitory neurotransmitter, has been discovered to be attributable to the disruption within the brains of those with BN. Serotonin plays a role in the activation of emotions, sex, eating and sleep within the basal forebrain, frontal cortex, limbic cortex and hypothalamus (as can be seen in the picture below).

However, in BN patients, there appears to be less serotonin. There also appears to be less serotonin transporters, which can lead to too much or too little brain arousal. Research has discovered that the transporters and receptors of serotonin appear to not be functioning properly. This is often seen at the behavioral level, as symptoms of BN can often be associated with anxiety and mood disturbances.

The binge-purge cycle characterized in BN has been thought to be either positively reinforcing for the individual or negatively reinforcing, dependent on the individual’s personality. If their personality is more anxious and/or obsessive, overeating (binging) gives them a sense of comfort, but then their realization of their binge episode causes anxiety again, forcing them to compensate for their binging by purging.

It is almost as though these behaviors start out as impulsive, but then BECOME impulsive…

But why is it then that eating disorders, such as bulimia nervosa, are three times more likely to affect women than men? There are many factors that probably attribute to this known fact, but let’s focus on two.

Estrogens

and

Societal Expectations

Estrogens
Estrogen is involved in the neuronal systems related to feeding, as well as impulsivity and compulsivity, a reason why many researchers are assuming its involvement with eating disorders is so prevalent in women. Estrogen has shown to interact with serotonin, influencing serotonergic neuronal firing. This may relate to BN, as there appears to be an increased serotonin system activation, which may lead to heightened anxiety and fear conditions in individuals with BN.

But even with all of this information, I think there is still one LARGE piece of the puzzle we have not discussed yet…

Societal Expectations
The standards that society has set for women are quite literally unattainable. Many advertisement companies, such as Dove, are now promoting beauty for all women, showing how our perceptions in the media are simply computer generated. As can be seen below, the woman they have model doesn’t even look like the final product…

But what is to be done about this? I think Dove has the right idea…

Continue To Educate!

Our society must be educated on the realities of eating disorders, both at the physiological level, as well as the national social media level. Doing so will decrease the likelihood of a “perfect storm” to occur, where those who are more susceptible to an eating disorder won’t feel the societal pressure to change. By doing so, these unattainable ideals society holds for all people, not just women, will become a thing of the past.

Community

Neurochemistry Capstone Overview

Posted on December 15, 2015 by / 0 Comment

That’s me at a neuroscience conference reporting on a year + of undergraduate research under Dr. Askvig at Concordia College. My fiance, Mitchell, is next to me. My college experience was a lot of long nights studying and doing homework, conducting research, and a couple of fun moments spending time with my peers and Mitchell.
But wow, how do you summarize your whole college experience in one post? Trying to pick a picture to summarize it made me want to make a never ending collage encompassing almost 4 years of my time. (Don’t worry, I didn’t actually do it- I realize it would only be my nostalgia clogging up the post then…)
I graduate college in less than a week and it honestly hasn’t hit me yet. That was a lot of work packed into less than 4 years.
I’ve spent my whole life that I can remember in school – and even though I am not done with my degrees yet, this will mark the end of another chapter. I can’t believe I won’t be living in Moorhead anymore either!
I can’t help but look around at all of the faces of my classmates and realize that I may never see them again after spending so much time staying up all night studying with them or seeing them in class every day.
That’s a weird feeling.
When I look back at all of my classes in my college career, (although I had a lot of issues trying to post blogs on here) my neurochemistry capstone course makes my top 5 list for classes I will be able to use outside of college.
This class took all of my science courses in biology, chemistry, and neuroscience and made me think critically about each field together. It was also a welcome break from the lecture, lab, and exam format we are so used to.
We read scientific papers and had to engage our classmates from different fields of study on how to critically analyze each article. We started by telling each other what we didn’t understand, then we each tackled one of those topics to report to the class the next day, and finally we learned how to talk about these subjects in a way that is useful for the public.
Before this class, I’d never learned how to explain scientific papers to people outside of the scientific community. I’d tried to explain some things of course, but it didn’t always come out as well as I had planned.
Now I can say that I know how to relate these topics to more people, so when I am not in an academic environment all of the time (in less than a week!), I’ll be able to speak about these things in a much better manner.
Overall, this class helped me to make connections between all of the fields of study I have been researching in the last years. It blew my mind to see how one pathway can actually relate to almost all of the neurodegenerative diseases we have seen.
The class has shown me how many things I do not understand and given me a hunger for more.

Thanks for reading my posts (if anyone actually has). 😉

Community/Disease/Health/Hot topics

The Role of Synaptic Pruning in Autism

Posted on December 15, 2015 by / 0 Comment

What is Autism?
Autism is a neurodevelopmental disorder characterized by impaired social interaction, verbal and non-verbal communication, and restricted and repetitive behavior. Parents usually notice signs in the first two years of their child’s life.
The causes of autism are attributed to genetics and environmental cues, but the exact causes are being investigated by researchers right now. Because autism is a spectrum disorder with many varying degrees of severity, there might be a slightly different cause for each person.
One symptom found in almost all cases of autism spectrum disorder is too many synapses in the brain.
Synaptic Pruning and Autism
During childhood and adolescence, the brain needs to prune many synapses so other areas of the brain can develop more specific functions and not be overloaded with stimuli.
Biologically, in autistic patients there is an oversupply of synapses in some parts of the brain. This means that there is something happening in their brains that is not allowing them to prune the neurons.
The increase in synapses can explain common symptoms like oversensitivity to noise and social experiences in addition to the epileptic seizures as there are more electrical signals being transmitted in the brain.
SIDENOTE: This biological problem seen in autistic patients is caused by interactions between their genes and the environment, NOT vaccines.

Some research studies have now shown the increase in dendritic spines in autistic adults in comparison to a normal adult brain.

They have found that in people with autism, their brains have a dysfunction in how they get rid of those extra synapses. Researchers have shown this in pictures looking at autophagy markers. Autophagy is a term for the process of getting rid of the extra synapses or unused cells in the brain.
Future medicinal options
Researchers have made rats that have autism to study different potential drugs for the disorder. One drug they looked at, rapamycin, was able to prune the brain of these extra synapses in the adult autistic rats. This drug would be too harsh to use on humans though.
These results give researchers hope that finding a drug that could help the pruning process in humans could make those with autism have less severe symptoms.

Community/Disease/Health/Hot topics

How Stress Can Lead to Obesity

Posted on December 15, 2015 by / 0 Comment

We’ve all heard that stress can lead to weight gain, but how does it really do that?
Chronic stress causes many harmful cycles that can lead to this excess weight and here are the top four ways this happens:
1 – Hormones:

When our brain feels threatened whether it is from a bull running at us or studying for an exam, our body releases adrenaline, CRH, and cortisol. In the short term, this makes us less hungry and feel alert and ready to “fight” or run away, “flight.”
Unfortunately, once the adrenaline wears off, cortisol stays in the body and signals us to replenish our food supply that we burned up in the fight or flight response.
Cortisol does this by controlling blood pressure, insulin release, and carbohydrate or fat metabolism. Since we are not running away from a bull and we are sitting at our desks working on homework, the eat more signal is NOT working in our favor.
The stress is also causing decreased blood sugar and fatigue, leading to more food. Moreover, our bodies are designed to store visceral fat deep in our bellies to use in times of need. It is difficult to get rid of and it releases cytokines that trigger inflammation. The chemicals released from these fat stores are linked to the development of heart disease and diabetes.
2 – Anxiety:

The adrenaline makes us alert and wired up, but it is also shown to trigger emotional eating.
The American Psychological Association conducted a survey that found that 40% of Americans deal with stress by eating. Many of the respondents also reported that they like to watch TV or do other inactive activities to destress.
Memories from childhood can also lead people to associate sweet foods with comfort. Eating for comfort and not being active lead to weight gain – and the cycle continues.
3 – Fast Food and Cravings:

Chronically stressed individuals report craving comfort foods that are easy to get, high in fat, sugar, and salt.
This concoction of food causes chemical changes in our brains that rewire the body (and stomach bacteria) to crave more of the unhealthy food. Cortisol plays into this role as well as the rewired reward system in the brain.
Stressed people are more likely to eat unhealthy food with easy access rather than use energy to plan and cook a healthy meal after a long day at work.
4 – Less Sleep:

With long days at class and then at work coupled with the hours of homework after, there is little room left for sleep.
Research also shows that chronic stress is a leading cause of insomnia or trouble sleeping.
Less sleep = more stress = less sleep.
With less sleep, people compensate with coffee or caffeine pills which further disrupts sleep. Lack of sleep disrupts ghrelin and leptin levels which control appetite.
In studies on weight loss – even with a fixed calorie diet, those with more sleep lost more weight.
How do we fix this?
Overall, our bodies just aren’t made to live under the chronic stress that is our everyday lives. This is why exercise and other stress relieving activities are so important to add to our schedule.
Those activities as well as sleep should be moved up into our priority list as a society if we want to see massive weight loss and healthier people.

Disease/Health/Hot topics

The Role of Nitric Oxide in Alzheimer's Disease

Posted on December 15, 2015 by / 3 Comments

To be honest, I did not know much about Nitric Oxide (NO) before reading the scientific paper on the topic for our neurochemistry class. All I could have told someone is that it is important for vasodilation and that body builders take it as a workout supplement to get more blood pumping (supposedly to help them build muscles faster).
This week though, I got to make some pretty cool connections between this toxic NO buildup from microglial cells and Alzheimer’s disease. I’ll go over some basics and then reveal the connections.
The Basics
Alzheimer’s disease:

This is the most common form of dementia and is characterized by progressive mental deterioration as people age. One main issue in Alzheimer’s disease is the aggregation of amyloid plaques between nerve cells in the brain.
This makes it hard for the cells to communicate properly and puts them under a lot of stress.
Nitric Oxide:

In people and other animals, NO is an important cellular signaling molecule in the right amounts. It is a powerful vasodilator and keeps the blood vessels open and lowers the amount of plaque in them.
Too much however, can damage brain cells and help to increase inflammation in the brain. This is seen in many neurodegenerative diseases such as Parkinson’s disease, Huntington disease, ALS, and Alzheimer’s disease.
Microglia:
This type of cell makes up the brain’s immune response and accounts for 10-15% of the cells in the brain. They respond to neuronal damage and remove the damaged cells by phagocytosis.
When they are activated however, they cause an inflammatory response which can lead to a cascade of damaging events in the brain.
Putting It All Together
Through this paper we read on NO and inflammation, I found out that microglia actually MAKE amyloid precursor protein in response to injury from too much neuronal excitation. Remember that buildup of amyloid beta is what causes the plaques seen in Alzheimer’s disease.
When the amyloid precursor protein is abnormally cut, it makes the amyloid plaques.
This process stimulates inflammation, toxins, and nitric oxide production which damages and kills the brain cells even more.
The extra damaged cells make more microglia activate to get rid of the damaged cells – which creates more nitric oxide, more inflammation, and more amyloid beta plaques as seen in Alzheimer’s disease.
The image below is an overview on the never ending cycle I just described.

It’s terrifying to think that our own body’s reaction to cell damage can cause even more damage. Most of the time microglia are helpful and don’t harm other neurons, but when we age – this is a cascade that is happening to many adults when they get Alzheimer’s disease.
More research needs to be done and is being done on how to stop this process from starting in the first place.

Disease/Health

A Promising Outlook to a Devastating Disease: Lewy Body Dementia

Posted on December 15, 2015 by / 2 Comments

What is Lewy Body Dementia?
Lewy body dementia is characterized by abnormal protein deposits that aggregate in the brain. When Lewy body proteins aggregate, they cause issues that deplete the body of the neurotransmitter dopamine, which leads to the Parkinson’s disease like motor issues.
In Lewy body dementia however, these abnormal proteins travel to other areas of the brain including the cerebral cortex. This means that cognition is affected earlier in Lewy body dementia than in Parkinson’s disease because the Lewy bodies affect those areas of the brain sooner than the motor regions.
Also in Lewy body dementia, another neurotransmitter acetylcholine is depleted which causes the problems around perception, thinking, and behavior for these patients. Hallucinations and delusions are common early on in this disease.
Lewy bodies have been seen in Alzheimer’s disease and in later stages of Parkinson’s disease – leading to Parkinson’s disease dementia (PDD).
If motor symptoms occur before cognitive problems, they diagnose the dementia as PDD. If the cognitive symptoms occur first, then it is diagnosed as Lewy body dementia.
Additionally, later stages of both of these diseases can lead to the A-beta plaques and tau tangles seen in Alzheimer’s disease patients.
The Potential New Drug
A drug, nilotinib, which is used to treat leukemia, is being tested on patients with Lewy body dementia and Parkinson’s disease.
In high doses, the drug forces the cancer cells into autophagy and they go through apoptosis. In lower doses, the drug starts the process of autophagy for just long enough for the neurons to clear the toxic proteins out of their cells without causing cell death.
The drug would have to be taken daily, but each of the people in the trial saw cognitive and motor improvements and not just a slower progression of disease. One man actually started the trials in a wheelchair and was able to walk after the trial was over. The drug company donated a life time supply to the trial patients who wanted to continue using it.
The drug is going to go through the next stages of clinical trials in 2016 and was discussed at a large annual neuroscience convention in Chicago this year.

Uncategorized

Capstone Experience: Bringing it All Together

Posted on December 15, 2015 by / 0 Comment

(click on image for motion)

ZOOOOOOM!

‘Woah! Did you see that?!’

‘I’m not really sure!’

‘Wait, what the hell are you talking about…?’

At this point in time, that is what my college experience feels like. At this point in time, that is what my… Um, well, this is embarrassing. What am I supposed to be talking about again?
*** outside voice, “Your Capstone experience.”…
Oh yeah that’s right! Well, if anything that further exemplifies one of my points. To start off, I will begin to illustrate some of my personal convictions as to where the required Capstone course fits into the core curriculum at Concordia College. One of the primary objectives at any liberal arts institution is to achieve a high quality education by incorporating all kinds of disciplines in their students. By imploring an entire “disciplinary spectrum” Concordia College arms its students with an education that allows them to critically analyze any obstacle whilst they continue on with the rest of their lives, and in turn, will become responsibly engaged in the world. As a senior, Concordia’s Capstone course submerses students in a course that captures a collaboration effort of all the views of critical thinking they have obtained in their first three years at the college.
In my case in particular, my Neurochemistry Capstone deviated away from a traditional scientific format. It encompassed an array of “hot topics” in the neurochemical world. Upon reading literature, engaging in discussions amongst my peers, and finally addressing what needs to be known about the topic to the public, the course offered a welcomed break from traditional lecture/testing chemistry coursework. Neurochemistry honed in my ability to converse about difficult issues amongst other academics, address a solution, and relay messages on to the public. Personally, this framework completely encompasses what a capstone course should be at Concordia College. Not all of us, in fact very few, students will go on to create a revolutionary drug, re-define the way business is conducted, create a revolutionary social movement, or whatever it may be that has a major impact on the world. Although, a well-purposed capstone course that captures the goal of a liberal arts education summarizes the diverse critical thinking goals of a liberal arts education and that is exactly what Neurochemistry did for myself.

All-in-all, my time at Concordia has flown by in an instant. It doesn’t seem very long ago when I thought I didn’t need to study for my first chemistry exam or I didn’t think I could get hungover or I was the greatest thing since sliced bread. I can only hope that I have grown up since them even with the appearance of such a minimal time gap. Even at this point in my education I am not exactly sure where I am gonna be in 10 years, and as I have grown here at Concordia, it seems as if there is some intention there. That fact may have worried me two years ago, but now it doesn’t seem near as threatening. My time at Concordia through the lens of my Capstone course seems promising, and that is all that I can hope for.