Disease/Health

We should be racing for the cure… An Analysis of Parkinson's Disease

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Like most other degenerative diseases, Parkinson’s Disease (PD) is familiar to much of the population, however unless we know someone that is affected by the disease, this familiarity is only at face value.  Influential figures such as actor Michael J. Fox and boxer Mohammed Ali have brought this disease into the spotlight of our culture.  We always associate the symptoms of Parkinson’s Disease with the shaking that is observed when we see one of these influential figures walk up on a stage or give a talk.  We are starting to learn more about the disease, how it starts, and what is occurring, however there currently is no cure to the second most common neurodegenerative disorder.

Symptoms
Symptoms associated with impaired motor function are the most visible signs of Parkinson’s Disease.  Persistent tremors, delayed reflexes, rapid shuffling steps, and hunched over posture are all motor functions that are frequently observed, and serve as primary diagnosing tools for Parkinson’s Disease.  However recently, many non-motor symptoms such as depression, sleep disturbance, cognitive decline, and autonomic dysfunction have been linked with the disease.  In fact, many of these non-motor symptoms begin to occur earlier than their motor counterparts.  Therefore, understanding how these pathways is crucial for the diagnosis and treatment of the disease.

Cause
Neuronal loss, the subsequent loss of dopamine, and the presence of Lewy Bodies (structures containing the misfolded protein alpha-synuclein) are the primary causes of Parkinson’s disease, however there are several different pathways behind these losses.  Oxidative stress, mitochondrial disfunction, and inflammation have all been shown to be integrally linked with neurodegeneration and Parkinson’s disease.  Like many other neurological diseases, the primary cause of the progression of the disease is aging, early onset Parkinson’s disease is very rare.  Genetics also play a role in the development of Parkinson’s.  Several different genes (alpha-synuclein, parkin, UCH-L1, PINK1, LRRK2, and GBA), both autosomal dominant and recessive, have been liked to PD.  Lastly, head trauma has shown to increase the risk of developing Parkinson’s disease (evident in the case of Mohammed Ali).  Studies done on ex-NFL players has shown that repeated head trauma could significantly increase the risk of developing the disease.

Current Treatment Options
Over the past 30 years, the treatment of Parkinson’s Disease has not changed substantially.  Instead of treating the disease, many of the treatment options aim to combat the loss of production and function of the affected neurons.  Current therapies include administration of L-dopa, dopamine agonists, and enzyme inhibitors such as peripheral decarboxylase inhibitors,  catechol-O-methyl transferase inhibitors, and MAO-B inhibitors.  All of these treatments are directed toward treating motor symptoms, in fact very little is being done to address the non-motor symptoms.  Additionally, these treatments have not been shown to slow the progression of Parkinson’s disease.  A potential new treatment that is being looked into is the inhibition of glutamate, as glutamatergic function may influence disease progression.
 
While there are several developing treatments, targeting different areas associated with Parkinson’s disease, there is much more that must be done in order to discover a true cure to this debilitating disease.  It is here that Parkinson’s research could take a page from breast cancer research.  Increased funding towards Parkinson’s disease could provide us with the answers to these questions and save many individuals from developing many of the symptoms.  Therefore, we must race for the cure, so that those in the future will be spared from loosing the ability to do just that.

Disease/Health

The Many Pathways of Parkinson’s

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A friend of mine is quite fond of tattoos. She has several, and they all have their own special meaning. My favorite of hers, though, is the words “I love you” in her dad’s handwriting. This kind of tattoo would be special for anyone, but this particular one is even more special. My friend’s father has Parkinson’s disease (PD), so writing anything can be difficult for him. That “I love you” in his best handwriting is an accomplishment for him – one that my friend will take with her forever. But Parkinson’s is more than just a neurodegenerative disease that affects motor function. It also has many non-motor symptoms that are not as well-known or recognized.
Behind Alzheimer’s, Parkinson’s is the next most common neurodegenerative disorder. Average age of onset is 60 years old, and diagnosis between the ages of 20 and 50 is considered early/young-onset. The motor symptoms of Parkinson’s are the ones that are most commonly known and are obvious. These can include rigidity, tremors, gait and posture changes, difficulty speaking or swallowing, or little expression in the face. But PD is more than that; it also involves non-motor symptoms like depression, cognitive decline, rapid eye-movement sleep behavior disorder, and constipation, among others.
Important factors for diagnosis of PD include death of dopaminergic neurons and the presence of Lewy bodies. Lewy bodies are clusters of a particular protein called alpha-synuclein. When there is a mutation in any one of a number of particular genes, the alpha-synuclein protein can misfold. This means that it does not form into the correct shape and is then prone to cluster together and form the Lewy bodies. In addition, the enzymes used to clean up these unwanted aggregation of proteins do not work correctly so the Lewy bodies continue to accumulate. Eventually this leads to oxidative stress in the mitochondria and, finally, death of the neuron. PD is not as “simple” as that, however. There are multiple pathways that can cause the neurodegeneration, which is what makes PD so complicated and difficult to understand. Glutamate excitotoxicity is also thought to play a large role in PD. When there is too much glutamate in the body, it over-activates certain receptors that can lead to a huge influx of calcium into the cell. When there is too much calcium, the mitochondria again become stressed and cell death occurs. Inflammation in the brain has been linked to PD, as well. When there is inflammation, certain substances are produced, called cytokines. These cytokines then cause increased production of reactive oxygen species, which cause oxidative stress.
Because Parkinson’s follows so many pathways, it can be difficult to treat. Some research even suggests that PD is more of an umbrella, and full-blown PD is actually a syndrome encompassing several “diseases.” Risk factors for developing PD include age, genetics, and environmental factors. There is no cure for PD, and treatment can be difficult. Generally, MAO-B (monoamine oxidase B) inhibitors are used to prevent the breakdown of dopamine in the body. The two MAOIs used most commonly are selegiline and rasagiline. MAIOs are usually used alone in early PD and then used in combination with levodopa – another drug that helps increase dopamine levels – in later PD. Treatment usually helps with the motor symptoms of PD but has little effect on the non-motor symptoms.
Since Parkinson’s disease is one that is not completely understood, it is important that we continue research in finding what is causing this neurodegeneration to begin with and better ways to treat the disease.

Disease/Health

The many causes and symptoms of Parkinson's

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Most of us have heard about Parkinson’s disease and can visualize the symptoms of the disease.  You probably picture Muhammad Ali or Michael J. Fox exhibiting shakes or tremors.  What you don’t think of perhaps, is the mental aspects of this neurological disease.  Parkinson’s is a disease caused by neurodegeneration, neurons dying in excess, and this is brought about by a variety of different things.  Mutated or irregular genes is one possible way the neurodegeneration can come about.  Parkin, PINK1 and DJ-1 are a couple different genes that have been known to cause problems and lead to Parkinson’s.  Even though researchers have identified these genes and their link to Parkinson’s, little is known about the actual mechanism by which mutations in these genes can cause neurodegeneration.  Another big piece of the Parkinson’s disease story is inflammation.
Inflammation, for those of your neuronerds who follow this blog, has been talked about at length last week in relation to concussions.  Researhcers have found that inflammation may also be linked with Parkinson’s and this does not bode well for professional athletes in contact sports.  Inflammation being linked with Parkinson’s may seem like a no-brainer due to how fragile the brain and its structures are.  Inflammation causes harm to microglial cells, which help support neurons and keep them healthy, which can cause critical imbalances of chemicals needed for natural neuron function.  No matter what the cause, Parkinson’s is a disease that affects people in more ways than just the tremors.  A somewhat murky understanding of the mental problems associated with Parkinson’s is now being looked at more and more by researchers and might shed some light on the links between Parkinson’s and other neurodegenerative diseases.

Disease/Health

Parkinson's Disease: Another Neurological Mystery

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My previous knowledge on this week’s topic came from the movie “Love and Other Drugs.” In the movie, Anne Hathaway plays a woman in her early 20s living with the disease. I immediately think of the scenes where she is worn down physically and emotionally because she can’t do everyday things like drive to the pharmacy or simply to take care of herself. In this article, I got a deeper look into what happens in the brain of those with this PD.
First, the article talks about the need to look not only at the motor symptoms, but at the nonmotor symptoms (NMS) as well. In most cases, motor symptoms are expressed in the later stages of this neurodegenerative disease. These include difficulty speaking and swallowing, tremors, and an expressionless face. Specifically, damage to dopaminergic neurons in the substantia nigra leads to motor dysfunctions Some of the NMS include depression, sleeping issues, smelling impairment, rapid-eye movement, and cognitive issues. . By the time the physical symptoms occur, a lot of damage has already been done to the brain. If a method for NMS analysis can be fine-tuned, then current treatments, such as L-dopa and selegiline, may be more effective in slowing the progression of the disease.

PD is a complicated disease with a number of mechanisms for degeneration. The main categories are oxidative stress, mitochondrial stress, altered protein breakdown, excitotoxicity, and inflammation. The article states that inflammation is a general system reaction that may be the primary cause of dopaminergic loss. Inflammation is induced by the neurotoxins 6-hydroxydopamine (involved in the oxidative stress pathway) and MPTP (part of the mitochondrial stress pathway). All of these pathways seem to be in a complicated interplay. For example, oxidative stress may be induced by protein aggregation, specifically a-synuclein aggregation which are a component of Lewy bodies. Lewy bodies are a well-known marker of PD and are made up of unwanted proteins and cellular components which cluster together in the neurons. This oxidation may also lead to mitochondrial stress. However, mitochondrial stress increases reactive oxidative species (ROS), contributing to the oxidative stress. It is still unknown whether the pathways discussed are the initiators or downstream effects of some other cause of the disease. It may be that the specific mechanisms or combination of mechanisms are unique to each patient. Therefore, PD may never be reduced to one general cause.
Parkinson’s unlike other diseases we have looked at has more distinct environmental factors. The main environmental effectors are pesticides, exposure to metals, and solvents with the best evidence for pesticides. One herbicide, paraquat, mimics the neurotoxin precursor MPTP involved in mitochondrial stress. Paraquat is known to increase ROS which lead to oxidative stress. The mechanisms that the environmental effectors use highlight the combination of the pathways discussed. The environmental factors should not worry everyone. They are factors that require long-term exposure and are most commonly occupational risk factors. The combination of genetics and environment determine the expression of PD in each individual.  
In “Love and Other Drugs,” Hathaway’s character attends a conference for Parkinson’s patients. The room is full of people who suffer from the same disease, but who could be affected by any combination of the mechanisms discussed above. Some people may have had a weak sense of smell or depression long before they saw any motor loss. Some people may be early onset patients affected by the parkin gene while others could have been victims of old age. That room may represent the spectrum of cases seen in Parkinson’s disease. Unfortunately, all that can be done currently is to treat the motor symptoms. If the nonmotor symptoms can be used to diagnose the early stages of the disease, drug interventions may slow the progression so that young cases like Hathway’s character don’t have to succumb to the fate of PD patients.
Article discussed found at:
http://www.sciencedirect.com/science/article/pii/S0891584913000282
Image found at:
https://www.michaeljfox.org/page.html?what-is-parkinsons-infographic

Disease/Health

A Look at Parkinson's Disease

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The first time I heard of Parkinson’s disease was when I watched an interview of Michael J. Fox. I was a huge Back to the Future trilogy fan. I remember seeing his tremors, and learning about the disease. It wasn’t until my great-uncle had been diagnosed did it become personal. It very difficult for people to see those you love suffer with something they can’t control. It’s important that we learn about this disease, so we can find a cure.
Parkinson’s disease is a neurodegenerative disorder. It is the second most common one behind Alzheimer’s disease. It is characterized by the loss of dopamine neurons in the substantia nigra, a specific area in the brain. The figure below highlights this area and compares a healthy brain and a brain with Parkinson’s disease. The disease has both motor and non-motor symptoms. The motor symptoms include rigidity, tremors, and posture change. I had known about these but was surprised about the non-motor symptoms. Some of those symptoms are olfactory deficits, constipation, rapid eye-movement, sleep behavior disorder, and depression. The medical field believes that if they could give an early diagnosis if they can recognize these symptoms as a part of Parkinson’s disease.
http://www.healthcentral.com/common/images/1/19515_9684_5.jpg
After some research, it seems like Parkinson’s is more like a combination of diseases under one name. I’ll highlight a couple of the important pathways that contribute to Parkinson’s disease. Glutamate excitotoxicity is one route. Glutamate is a neurotransmitter that allows calcium to enter. When there is too much glutamate, too much calcium enters. This leads to the mitochondria, the organelle that helps with energy production, becoming stressed (oxidation stress). This causes neurodegeneration. Another pathway includes the accumalation of proteins. Mutations can cause proteins to be folded incorrectly and enzymes not to work properly. This causes the proteins to tangle together and there isn’t anything to clean it up. This can cause oxidative stress just like the glutamate pathway, and leads to neurodegereation. The last pathway I’ll talk about is inflammation. When the brain experiences trauma, it becomes inflamed. The brain tries to fix itself, it can causes oxidative stress too.
To prevent Parkinson’s disease and treat the symptoms, research has gone into neuroprotection. These involve dopamine agonist, antioxidants, MAO inhibitors, and agents that affect mitochondrial function. They all try to prevent the initiation of the pathways that I previously highlighted. One interesting neuroprotector is estrogen. Men are more likely to have Parkinson’s than women, and this is due to estrogen. Estrogen has possible antioxidant effects and can inhibit glutamate receptors. While estrogen seems like a great treatment, it can increase the chance of breast cancer and coronary heart disease. Many people suffer from this disease, and we’re just beginning to understand it. We must continue this research and look for a solution for those who suffer with this disease.
Resources:
https://moodle.cord.edu/pluginfile.php/390935/mod_resource/content/2/bipolar.pdf
http://neurochemistry2014.pbworks.com/w/page/88087888/Parkinson%20disease%3A%20from%20pathology%20to%20molecular%20disease%20mechanisms
http://www.healthcentral.com/ency/408/guides/000051_1.html

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[Back To] The Future of Parkinson's Disease

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Everyone (undoubtedly) remembers Michael J. Fox for his work in the Back to the Future movies.  However I don’t believe his acting career will be what people remember.  His career in acting has been very successful by any standards, especially considering his early retirement due to Parkinson’s Disease.  Mr. Fox’s career could have seen even more great films and awards had he not been sidelined early with a neurodegenerative disease that stripped him of his ability to focus on his work.
Parkinson’s disease isn’t like every other neurodegenerative disease although it does share some similarities.  Parkinson’s does see neurodegeneration leading to non-motor symptoms like cognitive decline, similar to what is seen in Alzheimer’s.  However, what sets Parkinson’s a part, is its combination of motor, and non-motor symptoms that afflict those suffering from the condition.  Another unique aspect of this disease is that it appears to spread throughout the CNS, starting in the lower brain stem and eventually spreading to the midbrain and cortical regions.
Many patients tend to suffer from the non-motor symptoms (depression, sleep disturbance, sensory abnormalities, autonomic dysfunction, and cognitive decline) first, with the motor-symptoms (bradykinesia, rigidity, tremor, and postural instability) having a later onset.  Right now there is a good understanding of what is causing the motor symptoms involved in PD however the non-motor symptom pathology is still not understood at this point in time.  As you can imagine, this makes treating PD a very difficult task.
The pathology causing PD is currently being understood as cellular degeneration resulting from oxidative stress and accumulation of lewy bodies (aggregates of misfolded proteins [primarily α-synuclein]).  Cellular degeneration occurs when misfolded proteins accumulate in the cell, forming large lewy bodies that displace other cellular components and put stress on normal cellular function.  Oxidative stress occurs in cells and causes but also results in misfolded protein aggregation.  This causes a bit of a “chicken and the egg” argument as to what causes initial cellular stress leading to degeneration.  When oxidative stress occurs in cells, mitochondrial function is stressed and less ATP can be produced to support cellular functions.  This leads to cellular degeneration.
Protein misfolding in cells isn’t uncommon however there are “clean-up” services that remove these proteins before they aggregate and cause cell damage.  These “clean-up” components of cells are known as lysosomes and proteasomes.  They clean up damaged and harmful molecules found in cells when tagged by a marker known as ubiquitin.  In PD, a gene known as Parkin (which codes for the production of ubiquitin) is mutated and thus proper tagging of harmful molecules in the cell is inhibited, leading to improper aggregation of misfolded proteins.  The proteins that are misfolded in PD is commonly α-synuclein.  Once a cell dies, α-synuclein can be taken up by neighboring neurons and thus can act as a “seed” for further misfolding and protein aggregation leading to neuronal death.  This process is what sets PD apart from other neurodegenerative diseases because of its ability to spread.
Current research is focusing on a “cocktail” of drugs with the ability to treat PD in patients.  One drug isn’t really able to do the trick because of how multifaceted PD is.  There is hope however for PD because of the new findings and amount of research that is currently occurring thanks to generous donors like the Michael J. Fox Foundation.
The future of PD research appears to be bright and though this disease has caused pain in so many peoples’ lives, there is hope it will come to an end.  Michael J. Fox may never appear in another blockbuster hit again; however his work after his acting career may end up being what people most remember him for in the future.  His foundation has shed light on a deadly disease as well as fund research so that the future can be bright for those with this disease.
Until next time,
Sebastian
 
 

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The Parkinson's in Me

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The Parkinson’s in Me
I was sitting in my college dorm room during my sophomore year at Concordia. My desk was cluttered as usual with the week’s homework. My phone began to ring; it was my mother. Cheerily, I answered with, “Hello!” expecting her happy response in return. But the happiness was not to be heard, and she solemnly asked how I was doing. I could immediately tell that something was wrong, and over the next few minutes, she informed me that my beloved uncle had been diagnosed with Parkinson’s disease.
That evening I cried, wondering how his life would change over the coming years. I wondered how I could support him, but vowed that we would not treat him differently simply because his developing condition had been given a name by a physician. In the back of my mind, I could not help but think of how similar I am to my uncle, bearing more of a resemblance to him than most of my family members. As a scientist myself, I know that external looks certainly do not have to be genetically linked to a disease such as this, but I could not avoid pondering the thought that our family medical history now included Parkinson’s disease.
I have heard that there comes a time in medical school in which too much knowledge is dangerous. After learning about a plethora of diseases, each medical student will introspectively become more aware of the body and will realize that he or she has all of them! This is exactly how I felt. Suddenly, my morning hand shakiness during class (from lack of protein and energy because breakfast had not fully digested) and an occasional drool during the night were not natural occurrences, but instead were pre-emptive indicators for Parkinson’s disease.
While it is silly to think this, especially in my young age because Parkinson’s disease is almost entirely seen later in life, these are the types of conclusions that make medical education so important in the general public. I cannot say that I really ever knew more than a trivial fact or two, and even after my uncle had been diagnosed, I hardly knew enough to begin judging my personal dispositions toward the disease.
But this week during my neurochemistry class, we delved into what is currently known about Parkinson’s disease in relation to what is actually occurring in the body. Overall, we learned that it is incredibly complex, and there are many avenues and factors that seem to contribute. I will try to focus on a couple that seemed to be front and center. The first is a little protein called Parkin. This busy protein is like a handyman in the neurons of your brain. Parkin’s job is to travel around the cell and physically mark things that don’t appear to be functioning properly or that should be cleaned up. This process is called ubiquitination, and it is Parkin’s way of telling your cell, “Hey, take out the trash!” = (Get rid of those toxins!) or “This needs fixing.” = (Patch up this cellular machine!) In one of the genetic forms of Parkinson’s disease, Parkin ends up being inactivated, so these cellular toxins accumulate, and the cell has trouble recycling some of its damaged organelles. This causes the eventual death of the neuron, and I’m sure you can imagine that the death of neurons in your brain would not be ideal.
A second aspect that seemed to be particularly important was another protein called alpha-synuclein which I will refer to from now on as AS. Normally, AS is found at the connections between neurons and helps to mediate the use of neurotransmitters, which are signaling molecules that your nerves use to communicate information. Anyway, for a variety of reasons (eg. mutation, damage, oxidative stress), in Parkinson’s patients, AS proteins tend to stick to each other in clumps which we have called Lewy bodies. Because they are large and “in the way” of your normal cell processes, they get transported outside of the cell where they are thought to accumulate and play a role in causing the death of the neurons.
As I mentioned before, Parkinson’s disease is incredibly complex, and scientists are still working vigorously to unearth its secrets. In the meantime, I am investing myself in a medical research career, and perhaps I too will one day work in this fight against Parkinson’s disease. I already was motivated by my own ambitions, but my uncle’s diagnosis two years ago has made this into a personal battle. Perhaps his condition developed naturally over time, or maybe he was pre-disposed by the genes in his DNA. In either case, I approach the situation with maturity, as it is simply another obstacle in the game of life with which to deal. If Parkinson’s disease is meant to appear in my future, then I will treat it with the respect it deserves. But to live life thinking about the obstacles that may happen is to live in fear─ I choose to live in control with the courage to overcome. Will you take a leap of faith to tackle the unknown, or do nothing and become an old man filled with regrets?
Final thoughts on Parkinson’s disease written by Steven Dotzler

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The Protein Behind Parkinson’s: Alpha-Synuclein

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Alpha-synuclein is a protein that is abundant in the brain and its dysfunction is known to be a key player in the pathway that leads to the neuro-degenerative disease of Parkinson’s. This protein becomes a problem in the neurons of the brain and can lead to Parkinson’s when it is either created with improper structure due to a mistake in the DNA or the protein’s is altered once it is created from the DNA sequence by another intracellular compound.  Alpha-synuclein, as the name implies, is normally in the form of an alpha helix which is essentially a long thin strand of twisting amino acids put together in a similar fashion to the classic image of DNA we all think of.  If the DNA sequence that codes for the alpha-synuclein protein is even slightly out of order you can get a mutation that causes the protein to take a completely different shape known as the beta-sheet.  This shape of a protein is very different than an alpha-helix, as the name implies it is when the amino acids of the protein come together in a sheet like formation, similar to a piece of paper.  In the case of Parkinson’s this becomes a problem because in this beta sheet formation the proteins are able pack closely together, like a ream of paper, and create these protein aggregates that cause the neurological problems that we see in Parkinson’s.  Another way that the alpha-synuclein protein could be modified to be formed in beta sheets instead of an alpha-helix would be through direct modification by another cellular component.  One type of compound that could cause this would be peroxynitrite, which is an oxidizing compound, meaning that an oxygen type of molecule will react chemically with another compound and change it usually for the worse.  This is why we here so many things about food products with antioxidants being so good, because the idea is that they will prevent this oxidation of important components of your cells.  Back to the protein, if the protein is oxidized and the structure of it changes it too can also end up in a beta-sheet formation which like I have previously mentioned would lead to the aggregation of these proteins into large masses that eventually become Lewy Bodies and cause a lot of problems in the neurons of the brain.

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Let 'Em Play Ref

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In neurochemistry we recently discussed an article written about concussion and traumatic brain injury.  This is a very relevant topic and I’m sure we have all heard much about it in recent news, especially in regards to the best sport on the face of the planet, football.   Reports of previous NFL players coming out with confessions of repeated concussions and the terrible side effects that developed out of them have spurred officials to take drastic measures in concussion treatment and prevention.  As seen in the video link that is embedded, the NFL and its players are by and large positively receptive to the changes taking place within the NFL.
Video: http://www.vikings.com/media-vault/videos/Vikings-Helping-To-Raise-Concussion-Awareness/e94acbfd-0d6c-4b54-8dea-811b53a6c480
The video mentioned ways of testing for concussion on the sideline.  What our article talked about was the neuroscience behind concussions.  Things like blood-brain barrier shearing, axonal retraction balls, and widespread neuronal depolarization are products of the physical injury caused by the biophysical acceleration of a concussive injury.
What makes me sad about concussion is that although it is a serious issue and does need to be watched carefully, many parents forbid their children from playing based on the risks of concussion.  Concussions can be devastating, especially if there is a repeat injury before the body can heal the initial damage. However, individual concussions are not nearly as damaging as chronic repetitive concussions as long as adequate time is given for recovery. Meaning, in short, that if adequate measures are taken children and teenagers should be allowed and encouraged to play sports.

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To Play or Not To Play?

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Concussions are a tricky subject in sports. On the one hand, there are risks in just about anything one does: a car accident is possible when making a short trip to the grocery store, being hit by the mailman is possible when getting the mail, getting a concussion is possible when playing a contact sport. On the other hand, concussions are a pretty serious form of injury that maybe is not taken seriously enough. This week in my Neurochemistry class, we read a paper about what happens in the brain with a concussion. This led me to take the opinion that the public and even sports players and coaches do not know enough about concussions and their long term effects and should thus be more educated before pushing themselves or their players.
With any concussion, traumatic brain injury may occur, but a concussion is marked by no gross pathology such as internal bleeding of the brain or brain structure defects. Mild concussions do not cause a loss of consciousness while severe concussions cause a loss of consciousness (i.e. knockouts in boxing). Repeated concussions over time can lead to a chronic condition called chronic traumatic encephalopathy, or CTE. CTE is extremely similar to Alzheimer’s disease in how it affects the brain and in its symptoms.
So what exactly occurs in the brain during a concussion? As the head is impacted hard whether by the ground, fist, or person, the head accelerates then decelerates quickly. This causes the brain to do the same and the accelerating and decelerating forces stretch the neurons in the brain. The stretch of the neurons causes ions like potassium and calcium to enter into the cells at a higher than normal rate.
One effect of these ions is to cause excitation of the neurons which eventually leads to an increase in excitatory neurotransmitter release (namely glutamate). Increased release of glutamate is characteristic in many neurodegenerative diseases (i.e. ALS). Glutamate can excite other neurons causing numerous effects like hyper -metabolism, over activation of cellular pathways, and can eventually lead to cell death.
Another damaging effect of the initial calcium coming into the neurons is that microtubules in the neuron can become damaged. The microtubules act as a transportation system (kind of like a railway) for the neuron. As the microtubules get damaged, the neuron axon swells up and the proteins that should be transported accumulate in the neuron axon. Some of these proteins are the infamous tau and amyloid beta proteins that cause a problem in Alzheimer’s disease. As these problematic proteins build up, they can turn into the neurofibrillary tangles and amyloid beta plaques that stop signaling in the brain.
All this from a few concussions?!? Yes, that was my response! So, get a few concussions while playing football, suck it up, continue playing, and have a possibility of getting CTE, which is basically like giving yourself early-onset Alzheimer’s. This knowledge may not prevent most athletes from playing contact sports or even getting back in the game after a blow to a head, but it is important to know as a parent of an athlete, coach of a sport in which concussions are common, or an athlete of such a sport.
Because concussions are not a visible injury and we must only rely on responses from the athletes, concussions don’t often get taken as seriously as other visible injuries. However, we should take concussions seriously because they have serious effects (especially long-term), and we should educate ourselves on what is actually happening in our brains due to the mysterious injury called a concussion.
Article Referenced:
http://www.sciencedirect.com/science/article/pii/S0896627312010367
Picture From:

Brain Concussion. What You Need To Know.

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