Cobbers on the Brain

Liberal arts education provides a wide-breadth of knowledge for students to deal with the ever changing and complex problems facing our world today. This is the foundation that Concordia’s educational mission statement is based upon.
“The purpose of Concordia College is to influence the affairs of the world by sending into society thoughtful and informed men and women dedicated to the Christian life.”
As students at Concordia, we complete a core curriculum that provides educational experience in areas outside of our primary focus. This includes language, science, religion, arts, and history.
If you happen to ask any student about what this means for them, you will most likely have the term “BREW’ing” yelled at you. This term is frequently used on campus and stands for Becoming Responsibly Engaged in the World.
It is the idea that behind learning connections between diverse areas of study and how that can be used to make positive impacts locally and globally.
Personally, at the begging of my education I did not fully grasp what BREW really means. My ‘aha-moment’ came during a religion class where I made connections between the importance of understanding the issues facing societies across the world through different perspectives. For example, how religion can act as a source of empowerment for marginalized groups that can bridge gaps in literacy, healthcare, and more.
A recent psychology course I took also brought my attention to an issue of the career path that I am currently on. This is the gender disparity that exists in science, technology, engineering, and math (STEM). A metaphorical leaky pipeline exists that describes the loss of women at all stages along the STEM pipeline.
I was inspired to BREW and do something about it. I participated in an outreach program that encourages young women onto the STEM pathway. The experience inspired me to continue efforts after my time at Concordia and into my own science career.
The neurochemistry course I took this semester was the culmination of my global liberal arts education. Through this class, we learned how neurometabolic pathways are impacted by environmental and biological factors associated with disease pathology. Topics included stress, obesity, neurodegenerative disorders, and more. We also had the opportunity to engaged the community regarding these issues. Communication of current science with the public is important for improving outcomes of these diseases. My group focused on raising awareness for the critical need for Amyotrophic Lateral Sclerosis (ALS) research and support.
If you have been on social media recently, you may be aware of the current fight for science regarding issues facing the scientific community. A major disconnect exists between the scientific community and public. Part of the blame falls to scientists that for too long have neglected this relationship. Members of the scientific community need to more effectively communicate to separate facts from misconceptions. This will demonstrate the importance of science with improving many aspects of society.
BREW’ing during my time at Concordia has helped me identify, and creatively help solve issues such as this. I plan on using the skills gained during my time here to do my part as a engaged citizen. As a young hopeful scientist, I have a passion for issues in regarding STEM. I now have the tools and drive to make lifelong positive impacts and I have my liberal arts education to thank for that.

I forgot that my research group was meeting in our classroom instead of the professors office? Does that mean I have Alzheimer’s disease?
To answer my own question, no that does not mean that I have Alzheimer’s. One of the common misconceptions by the general population (myself initially included in this group) is that anyone having memory problems, particularly older individuals, has Alzheimer’s. In actuality, Alzheimer’s is a sub category of a neurodegenerative disease called dementia. Although Alzheimer’s makes up the majority of dementia cases (roughly 50-60%) it has specific criteria that separates it from other forms of dementia.
 
Alzheimer’s is usually noticed by people’s family members and friends first. However, it can be tricky to spot because some of the early symptoms are easily brushed off, such as forgetting newly learned information and confusion. It seems like this happens to most of us on a regular basis, but with Alzheimer’s  people continually are in states of confusion and have difficulty performing every day tasks. More advanced Alzheimer’s is easily identified.
I was at a rotary club meeting for lunch while I was shadowing a physician, and the local Alzheimer’s chapter was giving a talk on when you should see a doctor about dementia. The example was that the speaker’s grandmother made chocolate chip cookies every week her whole life. As she was getting older, the grandmother had trouble remember the recipe that she normally would never have to look up. It is instances like these where you should see a physician soon.
 
What’s happening to my brain if I have Alzheimer’s?
The Alzheimer’s Association does a fantastic job of helping people visualize what’s happening on a cellular level with Alzheimer’s ( Here’s a link to their website http://www.alz.org/alzheimers_disease_what_is_alzheimers.asp )
 What physicians and scientists are seeing on a molecular level is that the brain’s cells (fancy people call them neurons) are dying from an aggregation of proteins. These proteins form a plaque, and they prevent the neurons from functioning normally. Wondering how and why these plaques are forming? I was too! So my neurochemistry class decided to read a paper on what might be going wrong in Alzheimer’s.
 
Two main points can be taken away from our group’s discussion on Alzheimer’s.

1. There is an involvement with the PI3k/Akt pathway
2. Insulin resistance is occurring

PI3K/Akt pathway
The findings from our paper rather surprised me. From the other neurodegenerative disease we’ve read about, usually the PI3K/Akt pathway is suppressed. This makes sense to me, because this pathway is involved in cell proliferation and survival. I.e this pathway keeps brain cells alive. In Alzheimer’s however, this pathway is overactive, which results in several negative effects, and it could be contributing to the overall demise of brain cells.
 
Insulin Resistance
I was rather skeptical about the involvement of insulin in Alzheimer’s until I spoke with one of my peers. As he described what is occurring to me it made sense. Some scientists who are researching Alzheimer’s are actually describing it as Type 3 diabetes. Click on this link if you’d like to read their review article https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2769828/
Once the PI3K/Akt pathway is initiated, the downstream signaling proteins block the insulin receptor by internalizing it into the cell, and the cells become resistance to insulin. This occurs in type two diabetes in the pancreas and fat tissue, and it’s happening in the brain tissue of people with Alzheimer’s. Thus supporting the assertion that Alzheimer’s may be another form of diabetes, it’s simply happening in the brain instead of the pancreas this time. Mind=Blown.

You’ve likely heard about the neurotransmitter called dopamine. The first time I heard about it was in 7th grade health class when we were talking about illegal drug effects on the brain. I was surprised to learn that both stimulants (things like meth) and depressants (stuff like heroin) both cause a rush of dopamine in your brain. This creates the feeling of intense pleasure and even euphoria. However, dopamine also has a job you probably haven’t heard of…

 
To understand dopamine’s other job, we have to talk about what it actually does to your brain cells. Dopamine can be both excitatory and inhibitory. That is to say that it can make it easier for brain cells to signal other cells, or it can make it harder. There are two main receptors for dopamine (Receptors are small proteins usually on the surface of a cell that capture signaling molecules and relay their specific signal). The first is D1, which is an excitatory receptor. The other is D2, which is an inhibitory receptor.

The part of the brain that is shaded in red is one of the main hubs of dopamine in the brain. It’s called the substantia nigra because in a healthy brain the brain cells are actually black in color! This part of the brain plays a huge roll in regulating both desired and undesired movements. Brain cells from the substantia nigra have long projections that travel to the switchboard of the brain called the Thalamus, and to the reward center of the brain called the Striatum. These brain cells release dopamine, which bind to the D1 and D2 receptors I previously wrote about.
Desired Movement:
For desired movement, the substantia nigra releases dopamine into the striatum, which in turn does not signal the thalamus. This allows for an overall excitatory effect, which makes sense because rewarding the movement we just performed will make it happen again, thus creating desired movement.
 
Undesired Movement
Undesired movements, such as shakes and tremors, are inhibited by the substantia nigra. It does this by releasing a different neurotransmitter called GABA, which has an inhibitory effect. By inhibiting certain movements, we end up with an overall smooth stabilized movement. This is vital for simple tasks like picking up a class of water, or bringing a spoon to your mouth.
 
 
Parkinson’s: When the Substantia Nigra has a problem
A neurodegenerative disorder you’ve likely heard of is Parkinson’s disease. Simply put, Parkinson’s is the death of the substantia nigra. With the death of the substantia nigra, motor problems arise. There is no inhibitory effect on the thalamus, and tremors result. Additionally, dizziness, trouble sleeping, speech trouble, and loss of smell may also be present. On a cellular level, a type of plaque called Lewy bodies (composed of a protein called alpha synuclein) accumulates around the dead cells. Treatment for Parkinson’s involves replacing the lost dopamine with a precursor of the neurotransmitter called L-DOPA.
 
Current Research:
The paper we discussed for Parkinson’s highlighted the importance of a subset of signaling proteins called kinases. Kinases are activator molecules that relay tons of different signals in the cell. Scientists are beginning to investigate the role between kinases and the accumulation of the Lewy bodies. The kinases perform many different functions within the cells, but they mainly involve recycling mitochondria, oxidative stress, and inflammation. These kinases offer a chance to combat Parkinson’s and may be a stepping stone to curing this neurodegenerative disorder.
 
 

One word that parents always dread hearing is coming up more and more in elementary schools. Autism. For some it’s a debilitating disorder that impairs basic function. For others, it can be a minor hinderance, but one that can be coped with. Regardless of the severity, autism can offer several challenges for individuals who have been inflicted by the disease. With the rising amount of diagnosed cases of autism comes increased research on the disorder. In our Concordia College neurochemistry class, we discussed a paper on the environmental effects of autism, and I’m here to dispel several myths (and add a few truths) about what we currently know about autism.
 

1. There is no (zip, nada, zilch,) correlation between vaccines and autism, but there is a correlation with maternal viral infections.

That’s right. Vaccinating your children won’t give them autism, but some data has indicated that if the mother’s immune system could be playing a role in autism. The mother’s antibodies may be interfering with the development of the baby’s nervous system. 
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4776649/ ▲
2. Autism is not a disease that’s all or nothing, instead it’s a spectrum.
One thing that I’ve found rather interesting with the diagnosis of autism being redefined is that it’s a spectrum now. Now, some diseases that were once their own separate illnesses have been put under the umbrella of autism. In middle school I knew an individual who had some classical symptoms of Asperger’s syndrome and as such he was diagnosed with said syndrome. In high school, the idea of autism being a spectrum disorder received traction, and he explained to me and the rest of our class that his diagnosis had technically changed even though his symptoms had remained consistent.
 
3. Autism could all be caused by a zinc deficiency
Wait what?? A zinc deficiency? That’s it? Those were my thoughts as well. Interestingly, zinc is needed for proper neurological function as well as stabilization of some protein domains and proper immune function. It’s also a trace element, meaning we don’t need a whole lot of it. Women who become pregnant often do not know until many weeks after conception, and then begin taking their prenatal vitamins. Although zinc is unlikely to be the only culprit, it could be playing a significant role in autism’s development.
 
4. It’s a developmental disorder
One of the concepts that our neurochemistry class grappled with after reading the literature on autism is the actual onset of the disease. It still remains unclear, and there is added difficulty to understanding this problem since autism has a wide array of manifestations. One possibility is that the damage from autism has already occurred when the baby is born. This is one of the hardest things for people to wrap their head around, especially since we don’t typically see symptoms until the baby is a couple of years old already. https://www.autismspeaks.org
 
Although much remains unclear about autism, one thing is for certain. Scientist, psychologists, and parents are all hard at work trying to understand this disease and how we can deal most effectively with it. Moving forward, it is likely that more research on neural development under stressful conditions will be needed to fully comprehend this disorder.