Disease/Health/Hot topics

MAPK pathway and the brain

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This week, the discussion topic was the MAPK pathway and its connection to Parkinson’s(PD), Alzheimer’s (AD), and Lou Gehrig’s (LGD) diseases.  One of the first things we discussed was whether we thought that there was a simple way to control or block the development of these diseases.  Unfortunately, we could not think of a way simply because the MAPK pathway is literally everywhere.  If we block any part of the pathway, it effects more than just the region we want it to, which is the biggest downfall in looking at such widespread pathways in the body with respect to disease.
Next we talked about insurance companies and being able to prescreen for risk factors for diseases.  We all know that certain insurance companies can deny you on pre-existing conditions and  we all thought that was ethically wrong but we all know it about money in this world and unfortunately that’s why insurance companies do that.  What we thought was that if people had to pay to get things treated that aren’t life-threatening, then insurance companies would be more apt to accepting everyone and then everyone could have it for when they need it.  One flaw that I saw from this was that some conditions aren’t life threatening in and of themselves but the fact that they lead people to have to miss work may end up threatening health, especially those people who need to work to provide for themselves and their families.
Next topic was the feasibility and morality of using stem cells to regenerate brain cells lost due to PD, AD and LGD.  What we found out was that brain cells regenerate when stem cells are injected into the area where the loss occurred.  However, because there are other factors that play into the development of the diseases, the stem cells are just a temporary cure and the neurodegeneration comes back and you would have to go through the process of re-injecting new stem cells into your brain.  You also run the risk of the stem cells not differentiating correctly and turning into some other cell in the brain which is not a good thing at all.  The morality issue has been around for a while in respect to stem cells because they come from fetuses.  This brings into the picture of when does life officially start and due to the extreme sensitivity of some people to this topic, I will not go any further than saying that it was brought up in our discussions.
All in all, there are many potential ways out there now that we could use to go about preventing or curing neurodegenerative diseases, some with moral side effects and some with physical side effects that need to be taken into account.  Who knows, maybe one day someone will stumble across the miracle drug that will cure all of these horrible, debilitating diseases.

Disease/Health/Uncategorized

Will the MAPK pathway lead scientists to a cure for many common neurodegenerative diseases?

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Neurodegenerative diseases such as Alzheimer’s disease (AD), Parkinson’s disease (PD) and Amyotrophic lateral sclerosis (ALS) are a scary thought for many people as they have either experienced one of these diseases personally or know someone that has been affected.  The thought of losing cognitive and memory function or having difficulties performing basic motor skills is absolutely horrifying, especially due to the fact that scientists are yet to develop a definite cure to these common neurodegenerative diseases that affect our society.  In the paper “Pathological roles of MAPK signaling pathways in human diseases”, that we read and analyzed this week in our neurochemistry class, scientists are looking at a possible cell-signaling pathway that could shed light on a possible cure to these devastating diseases.
 
The basis of these three common neurodegenerative diseases involves either cell death or loss of neurons that leads to the symptoms that are developed from these diseases.  Scientists have recently identified a few different cell-signaling pathways that could be involved in the development of these diseases.  The first pathway that was identified is known as the Mitogen-activated protein kinase, or MAPK pathway.  This pathway is associated with a number of different cellular activities that include cell proliferation, differentiation, survival, death and transformation.  Other pathways in the body that were explored in this paper include the p38, JNK and ERK pathways, all of which are responsible for different cellular responses in the body.
 
Alzheimer’s disease is the most common neurodegenerative disease seen in our society today.  In this disease, the MAPK pathway is triggered by oxidative stress and is responsible for neuronal apoptosis, ultimately causing AD.  Oxidative stress is simply an event that is triggered by certain reactive oxygen species such as the hydroxyl radical, superoxide anion or hydrogen peroxide.  Parkinson’s disease, the second most common neurodegenerative disease is also caused by oxidative stress.  In PD, oxidative stress activates the p38, ERK, and JNK pathways, ultimately activating the MAPK pathway causing an increase in neuronal apoptosis as well.  ALS is also caused by the activation of the p38 MAPK pathways resulting in a loss of motor neurons causing muscle atrophy.  The fact that all of these pathways are seen in the progression of these neurodegenerative diseases it is a very important that scientists target them when looking for a cure.
 
You might be wondering, if scientists know what pathways are present in the development of these neurodegenerative disorders, why haven’t they already developed a cure?  Although there are different inhibitors to these pathways that can be used to slow the progression of these diseases, it is very difficult to inhibit a certain pathway without it having many other effects in the body, as these pathways are responsible for so many other cell responses in the body and it’s almost certain that by inhibiting these pathways, many negative side-effects will also be present.
 
Now that scientists have been able to determine that these complicated cell-signaling pathways are involved in the pathogenesis of these neurodegenerative diseases, they have a very promising target when trying to develop a cure for these diseases.  It will be very interesting to watch the progression as scientists attempt to find a cure for these very scary neurodegenerative diseases.

Disease/Health

The Complexity of the MAPK Pathway

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Our article this week talks about how the MAPK pathway is highly linked with several neurological diseases including Alzheimer’s Disease, Parkinson’s Disease, ALS – Almytotropic lateral sclerosis (or Lou Gehrig’s Disease), and cancer. A single pathway that is connected with so many influential diseases is exciting in that it offers a great deal of potential and a great challenge.
The MAPK Pathway
At the most basic level, the MAPK (Mitogen-Activated Protein Kinase) pathway is a set of proteins that activate one another by setting off and activating a kinase chain eventually leading to transcription factors in the nucleus being activated and the expression and coding of genes. More specifically, while not the only factor, it controls cell life and death.

This flow chart from this weeks article shows the three different MAPK protein pathways: ERK, p38, and JNK. In general, ERK can be associated with cell life or proliferation, while p38 and JNK can be associated with cell death or apoptosis. In Alzheimer’s Disease the ERK transcription is blocked and the p38/JNK pathway activated, which leads to cell degradation and apoptosis. In Parkinson’s Disease the activation of the p38/JNK pathway leads to the death of dopaminergic cells which lead to the symptoms associated with the disease. In ALS activation of the p38/JNK pathway leads to death of motor neurons. In Cancer, patients experience the over proliferation of cancer cells. In all of these cases there is malfunction of the MAPK pathway.
Research Possibilities
The link between all of these diseases and the MAPK pathway could be a great research opportunity because any new information that is acquired on the subject has the possibility of being applied to one or more of these diseases. This gives the prospect of moving forward in understanding of several diseases at the same time.
Using treatments of the MAPK pathway to find and treat the cause of the disease instead of treating symptoms . Since the MAPK pathway is highly linked to so many different diseases as well as cell life and death within the brain, selectivity of treatment would pose a dilemma. It would be unfortunate to find a way to treat one disease only to find that the treatment is leading to the cause of another disease or malfunction of the MAPK pathway in other parts of the brain.
The link between Alzheimer’s Disease, Parkinson’s Disease, ALS – Almytotropic lateral sclerosis (or Lou Gehrig’s Disease), and cancer through the MAPK pathway gives insight into how the brain works, and how these diseases effect the brain. It could in the future offers opportunities to find ways to treat the cause of the diseases, not only the symptoms. Other options such as gene therapy pose similar problems in that changing certain genes associated with the disease may help with the disease but cause unknown other problems in the future. There are still so many things we do now know or understand about how the brain works.

Disease/Health/Uncategorized

Rethinking reasons for weight loss: Alzheimer’s and type II diabetes

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I don’t mean to harp on body image and societal pressures too much. I know that this was my topic last week, but our article this week begs me to write a second post about the topic. I am one of the two thirds of Americans who are overweight or obese and like so many Americans I am trying to lose weight. I have many reasons and motivations for my journey. I can’t lie; body image is one of them. What woman doesn’t want to look good in that pair of skinny jeans or the classic little black dress? I have other reasons too, though. I love being outdoors and adventuring in the wilderness, state parks, and national forest reserves. I plan on spending the summer after I graduate guiding canoe trips in the Boundary Waters Canoe Area in northern Minnesota. I want to be able to climb mountains and go spelunking, lead an active lifestyle. There are also the health risks that are associated with being overweight. Most often I think about cardiovascular problems like heart disease, diabetes, increased wear on joints, sleep apnea, each of which should be good enough motivation to lose weight in and of itself. All together… Ufda.  So let’s add one more to the list of health problems that can have overweight and obesity associated risk factors: Alzheimer’s. I know what you’re thinking, ‘it makes sense that obesity would lead to the breaking down of your body, but your brain too?’ Connections have been made between obesity, type II diabetes, and the neurodegenerative Alzheimer’s disease.
Type II Diabetes

Type II Diabetes is an epidemic in the United States. It is caused by high blood glucose which leads to the body rejecting the insulin that it is making along with overall lower insulin levels. One main cause of Type II Diabetes is linked to obesity and one of the treatments for it is diet and exercise. Insulin shots are also prescribed to help lower blood sugar.
A bit about Alzheimer’s Disease (AD)
Alzheimer’s Disease is as mentioned above a neurodegenerative disease. It breaks down the brain giving patients symptoms such as loss of memory, difficulty with speech, and motor impairment. The degradation of of the brain of an advanced alzheimer’s disease patient is shown below.

There are two main reasons for this deterioration: plaques and tangles. The build up of beta-amyloid forms plaques and creates pressure on surrounding neurons. It also leaves the brain cells more susceptible to oxidative stress which leads to apoptosis, or cell death.
The Link
So how are these two things linked? Insulin has a key role in the neurons ability to survive and low levels of insulin can be indirectly related to the build up of plaques in and tangles in the brain. The lowering of insulin levels in the brain created by type II diabetes decreases activity in certain parts of the brain including parts that help to break down plaques and tangle build ups leading to over production of beta-amyloid and cell death.
The links between type II diabetes and insulin are clear and the link between Alzheimer’s Disease and insulin are becoming more clear. This leads into some interesting thoughts about how the two are linked. People have plenty of reasons already as to how obesity is adversely affecting their health including heart disease. If they were aware of the mental degradation and link to Alzheimer’s could that information help to motivate more Americans into a healthier lifestyle? It’s obviously never quite as cut and dry as this though. Factor such as the pricing of fresh versus processed foods, the amount of time to make dinner versus going out to eat, the time it takes to lead a more active lifestyle all contribute to America’s obesity problem and are difficult problems.
It’s hard to think that the addition of Alzheimer’s to an already long list of reasons to lose weight will change anything, but the more that people know about the adverse effects of obesity and type II diabetes, the better. If anything, it can’t hurt.

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Diseases Inhibited by Pharmaceutical Inhibitors

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We live in a society where drugs (pharmaceuticals) dominate the medical world. Are you clinically depressed? Try Lexapro or Cymbalta. Is your cholesterol too high? Maybe Lipitor or Zocor will work for you. But don’t forget that drugs rarely work in the body without unwanted side effects! Why is this? How do pharmaceuticals work?
The majority of pharmaceuticals work by acting on receptors that are found on the surface of cells or enzymes (which regulate the rate of chemical reactions). The receptors have a high specificity for a particular substance, similar to a lock and key. If a molecule (the key) does not fit the receptor (the lock), it will not bind to the receptor. When a drug mimics the action of an endogenous compound, it is called an agonist. Essentially, the drug is encouraging a certain physiological response to transpire. For example, when Drug A binds a receptor, it may initiate a cascade of events to occur (called a signaling pathway) that leads to the synthesis Protein A. On the contrary, when a drug blocks a physiological response from occurring, it is called an antagonist or an inhibitor. By binding a receptor, it blocks an agonist of the receptor from binding and prevents that response from occurring. Continuing with the previous example: when Drug B binds the receptor, it prevents Drug A from binding and Protein A is not synthesized within the cell. The number of ways pharmaceuticals are used in the body is extraordinary and continues to grow each day.
The MAPK, or mitogen-activated protein kinase, pathway is recognized for its role in certain neurodegenerative diseases as well as certain cancers. Specifically, MAPK is identified for its role in Alzheimer’s disease (AD), Parkinson’s disease (PD), and amyotrophic lateral sclerosis (ALS).
Scientists have determined that the MAPK pathway can induce neuronal apoptosis, or neuronal suicide. In Alzheimer’s disease, these pathways are upregulated and cause increased phosphorylation of certain proteins and increased expression of specific secretases that are known to induce AD. Similarly, these pathways are also affected in Parkinson’s disease. The activation of the MAPK, p38 and JNK pathways leads to the death of dopaminergic neurons in the brain, which characterizes the symptoms seen in patients with PD. Furthermore, the activation of the same pathways listed above may also prompt motor neuron death. As these motor neurons die, patients with ALS experience muscle atrophy, paralysis, and eventually die from the symptoms of the disease.
Unrelated to neurodegenerative diseases, but altogether related to diseases associated with the MAPK (and other listed) pathways are certain cancers, such as colon cancer. Scientists have focused on the ERK pathway in the cancer story. As certain proteins in the ERK pathway are phosphorylated, they encourage cell proliferation and growth as well as cancer cell migration.
You might be wondering why these pathways exist in the body if they can lead to such diseases, but as with most things, the danger comes in too MUCH activation of the pathway and not the existence of the pathway itself. In fact, the body NEEDS mechanisms that lead to the death of neurons. Similarly, it is vital that the body is able to grow and divide its cells to replenish dying ones.
However, as patients with these diseases do have pathways that function properly in a variety of ways, scientists are left to find ways to counter-act the problems specific to the disease. In the cases of AD, PD, ALS, and cancers, scientists look to inhibitors (or antagonists), drugs that suppress the physiological responses that are activated more often than they should be and cause excessive cell death or excessive cell growth. Ultimately, the goal of the research is to understand the mechanisms associated with the diseases and then to find ways to inhibit these mechanisms with accurate specificity. As always, negative side effects exist. Influencing a pathway, whether by activating or suppressing it, almost always leads to unwanted side effects. Nonetheless, at some point the symptoms of the disease override the unwanted side effects and this is when we rely on pharmaceuticals to “solve” all of our problems.

Health

Isolating Cell Signalling

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Our topic this week was the MAPK pathways. Quite simply, the MAPK pathways are a series of signalling molecules that carry messages from outside sources into the cell’s nucleus. This signal is carried from a receptor on the surface of the cell activating a signalling molecule. After that signalling molecule is activated, a signal cascade occurs. That is to say that a series  of molecules whose purpose is to activate the next molecule in a chain of events are all activated. This carries the signal to the nucleus where it can have diverse effects from killing the cell to making the cell divide.
One apparent problem with these pathways is that the same molecule can occur in several pathways that  lead to very dissimilar results. One can only imagine how disastrous it would be to promote cell death whenever the cell was supposed to divide and vice versa. Within our cells, however, there is little to no crosstalk between the pathways in spite of the same molecules being used. The reason for this is that in many cases, the signalling molecules are bound to scaffold proteins that keep them localized in one area and direct their signal to specific other molecules.
Although scaffold proteins do not play an active role in carrying the cell signal, by coordinating which molecules receive it next and where in the cell that signal goes next, they are one of the most important parts. They are analogous to the designer who decides how an assembly line is to be set up: although the designer doesn’t actually put any of the pieces together, they in effect decide what is going to be made through their organization.

Disease/Health/Spirituality

Quality of Life and End of Life Decisions

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In a discussion of neurodegenerative diseases, especially those that appear as late-onset varieties, a question arises about prolonging life and improving quality of life.   Amyotrophic Lateral Sclerosis (ALS), or Lou Gehrig’s disease, is a neurodegenerative disease involving the loss of motor neurons to the point of muscle atrophy.  This results in weakness and an eventual loss of mobility in the extremities and the rest of the body.  In advanced and severe cases, loss of these neurons in the chest region can cause difficulties in breathing well on one’s own, if at all (See the ALS Association website for more information about ALS: http://www.alsa.org).  Medical technology of the last century has enabled our society to sustain the life of individuals long past what would have been their natural time of death.  While less invasive methods can drastically improve quality of life and mobility by artificially taking on the body’s natural capacity to sustain life, more invasive methods require patients to become dependent and much less in control of their own life.  At this point, life support merely delays the inevitable and may draw out the most physically and emotionally painful part of a person’s life.  How long should life support be used and when is it acceptable to end another person’s life by terminating life support?
The issue of implementation and removal of life sustaining measures has and will continue to be a source of conflict in our society.  The legal, medical definition of death in all fifty states includes the loss of cardiopulmonary functioning and/or the irreversible end of all brain functioning, including the brain stem; others may personally see death when there is the loss of higher brain functioning, such as those in a permanent vegetative state, or a loss of personhood (Munson 2012).  Let us examine again the case of a patient with ALS whose chest muscles no longer function in breathing.  If this patient is put on a ventilator, modern medicine has effectively circumvented medical definition of death number one: the loss of cardiopulmonary functioning.  Once this happens, we may no longer rely on the cut and dry, legal, biological definition of death.  Intervening in this way has propelled us to a much more ethically problematic situation.
I would like to avoid the ethics question altogether by posing a different question entirely: What is the purpose of implementing life-sustaining measures?  I see these measures as a means of buying time when there normally would be none.  They allow the time needed to repair injury or to alleviate the body from the strain of sustaining itself when weak, such as when a patient with ALS develops pneumonia.  Often, these measures may result in a loss of dignity, may lead to a permanent need for medical care, drain the emotional stamina of friends and family as well as financial resources, and prolong life at the expense of quality of life.  When damage is irreparable, these measures can be wasteful, unnecessary, and not being used for the purposes which they were intended.   Of course, many people will disagree with me.  I, myself, may disagree should I find myself faced with a loved one at a turning point between natural death and medically sustained life.
When making decisions regarding the end of life, keeping the lines of communication open becomes extremely important.  While variable, the average life span after diagnosis of ALS is two to five years (http://www.alsa.org/about-als/facts-you-should-know.html).  With this in mind, any treatment for advanced cases of ALS could and should be viewed as end of life decisions.  Beliefs and wishes regarding medical treatment should not only be made clear to loved ones, but be recorded in a living will or durable power of attorney for health care.  This will ensure that in the event of an imminent medical emergency, one’s wishes will be followed.

Disease/Health

MAPK: the Wrong Way?

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The more I read about neurochemical systems and associated diseases and disorders, the more I get a sense for how vast the problems and intricacies for treatment are and how much work there is to be done. Signaling systems are intertwined with other processes, proteins have multiple functions, and often there are multiple contributing factors to a disease, making targeting for disease treatment extremely difficult. As with any problem, there are many possible routes to solve these health problems, and one of the first steps is determining which routes are most effective and feasible.
Fairly recently, studies have determined the mitogen-activated protein kinase (MAPK) system as an integral contributor to neurodegenerative diseases such as Alzheimer’s (AD), Parkinson’s (PD), and Amyotrophic lateral sclerosis (ALS). The general layout of the MAPK has several steps: typically, stimuli activates a MAP4 kinase enzyme, the MAP4 kinase phosphorylates a MAP3 kinase, which in turn phosphorylates a MAP2 kinase, which in turn phosphorylates a MAP kinase, resulting in phosphorylation of various proteins including transcription factors, all ending in a cellular response. In short, there is a phosphorylation cascade with at least three enzyme intermediates before a protein is affected that induces a cellular response. The three most common MAPK pathways are called ERK, p38, and JNK.

Six steps? Really?? Just cut to the chase and make it one, already.

Alzheimer’s disease is characterized by β-amyloid plaques in the brain and neurofibrillary tangles leading to neuronal apoptosis (cell death). The MAPK system plays a role in AD in a few different ways. Oxidative stress provides conditions for JNK and p38 to be activated, which then directly or indirectly activate the β- and γ-secretases, leading to β-amyloid plaques and neuronal apoptosis. Also, kinases such as JNK, p38, and ERK mediate the phosphorylation of the protein tau, which results in neurofibrillary tangles and apoptosis. Lastly, the JNK and p38 pathways have been shown to directly induce neuronal apoptosis, contributing to AD pathogenesis.
The main characteristic of Parkinson’s disease is a loss of dopaminergic neurons. As opposed to that in AD, the role of MAPK in PD is seemingly a secondary factor for its pathogenesis. The primary factors in the development of PD involve a defective gene encoding a defective protein which then activates MAPK signaling. One mechanism starts with a defective α-synuclein protein which aggregates, activating MAPK signaling, resulting in inflammation and dopamine neuron death. Another mechanism involves the p38 pathway inducing the expression of the protein Bax which, along with α-synuclein aggregates, decreases mitochondrial viability and leads to dopaminergic apoptosis. Still another mechanism involves the JNK and p38 pathways; the defective, mutant proteins parkin and DJ-1 can activate the JNK and p38 pathways leading to dopaminergic apoptosis.
Amyotrophic lateral sclerosis is characterized by a selective loss of motor neurons. The primary cause for this is thought to be a mutation in the SOD1 gene and protein, causing activation of the JNK and p38 signaling pathways. Overactivation of p38 has been shown to correlate with motor neuron degeneration, directly relating the p38 pathway with ALS development.
In describing the roles of MAPK pathways in these neurodegenerative disorders, I glossed over a fair number of intermediate steps. Many intermediate steps do exist with these mechanisms, however, which generally means that altering one component may result in many unwanted side effects down the cascade; a bigger system means it’s more complex and a bigger pain in the neck, unfortunately. This makes me skeptical as to whether the MAPK system would really be effective as a target for treatment; it is involved in so many different processes and often can lead to both positive and negative cell responses, including cell growth as well as death. Instead of MAPK inhibitors, I would suggest gene therapy for some of the mutations involved in these diseases, or perhaps an increase in mitochondrial protection. Forgive me for the football reference, but if a team is doing poorly, they either have to beef up the offense to attack the opponent more effectively or strengthen their defense to deter the opponent’s advances. In this case, I’m wary of going on the offensive to destroy the MAPK system, so better protection may be a safer and more effective route since a lack of protection from oxidative stress is a widespread factor in neuronal cell death. As always, more time and research will tell!
A Jared for the mitochondria would cure EVERYTHING.

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A Hopeful Future for Alzheimer's Patients?

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This week, I would like to talk to you about Alzheimer’s disease, a serious disease that has been brought up on this blog before just a couple weeks ago. When we talked about it before, we brought up the topic of diabetes and how the malfunctions of insulin in a diabetic patient could lead to Alzheimer’s disease. This week I will talk about another pathway scientists believe may be a factor in the development of Alzheimer’s disease.
This week, we focus in on the MAPK pathway. This pathway is responsible for several operations within our extremely complex bodies, but we will be concerned with its effects on cell proliferation, growth, and death. The pathway works through a series of activating different proteins within the cell and when each protein is activated, it can go off onto its own path and either promote cell growth or cell death.
As you know already, Alzheimer’s is signified by a buildup of Aβ plaques and neurofibrillary tangles within the brain. But what is believed to be the cause of these buildups? Well, scientists believe that activation of these MAPK pathways through oxidative stress (a risk factor for Alzheimer’s) eventually lead to a certain protein or enzyme which promotes neuron destruction which will lead to Alzheimer’s. As you can imagine, the actual process is a lot more complex, but we’ll keep it simple here.
When we compare the two paths for Alzheimer’s we have covered thus far, we must ask ourselves, “Is one of these a better option than the others when looking into curing this disease? And if so, where would our money be better spent?” Personally, I think the MAPK pathway is a more important area of research than the diabetes. To me, the rate of diabetes in the country can be significantly lowered just by changing your lifestyle, which really isn’t too hard. It just involves eating a little healthier and going outside a little more. If everyone in the nation did this alone, I feel it would cut our diabetes in half and thus lower their risk for developing Alzheimer’s disease, therefore not worth our time to research. The MAPK pathway, however, is not something we can change as easily. The oxidative stress comes from our lifestyle and how stressful it is, but it is not as easy to change that as it is in the diabetes case. The MAPK pathway also has implications in many other diseases such as Parkinson’s disease, ALS, or even cancer, so research in that area could also prove to be crucial in several other diseases. The only problem with working on the MAPK pathways brings up is the fact that they DO control so much in our body, it is not a single pathway we can just stop. It is a nasty maze that hurts your eyes looking at the entire pathway (see image), but perhaps more research in the area would help overcome that obstacle.

As you can see, the MAPK pathway proves to be crucial in the development of Alzheimer’s disease and personally, I think money should be invested into researching this area more in hopes of a brighter future.

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Lou Gehrig’s Disease: How close to a cure are we?

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1

              Prior to 1939, Lou Gehrig was on top of the world. He was coming off several great seasons leading the New York Yankees to World Series titles in 1936, 1937, and 1938. He was so good Time magazine wrote an article in 1936 described Lou Gehrig as “the games number 1 batsman” and someone who “takes boyish pride in banging a baseball as far and running around the bases as quickly, as possible”. However, Lou Gehrig’s career came to an abrupt end by the end of the 1939 season due to a sudden decrease in motor function. Lou Gehrig went to the Mayo Clinic in 1939 where he was diagnosed with amyotrophic lateral sclerosis (ALS), commonly called “Lou Gehrig’s disease” today.2
Today, 73 years after Lou Gehrig was diagnosed, the cause of ALS is still not completely understood. However, some progress is being made. In the research paper our class examined, scientists have identified a mutated gene encoding for an enzyme called SOD1. SOD1 is an enzyme responsible for stopping highly reactive molecules called free radicals from damaging important components in cells. However, in ALS this defective SOD1 enzyme doesn’t stop the free radicals. As a result the body initiates a biological pathway called the p38/MAPK pathway to kill the cell. This leads to the death of many types of cells such as the motor neurons causing ALS.
To better understand the effect of free radicals and the SOD1 enzymes in cells I have thought up a metaphor which may help. Imagine bringing your kids to a toy store. Now imagine your kids had the worst sugar and caffeine rush you have ever seen while you were in the toy store. They would probably be running all over the store, trying to play with every toy in sight and it is up to you to stop them from damaging anything. In essence, this is what is happening in our bodies. The SOD1 enzyme (you) are trying to control the free radicals (kids) from making a mess. Now imagine letting your sugar and caffeine crazed kids, and all other sugar and caffeine crazed kids in the store, wander around unsupervised. This would probably result in a scene similar to one found in the movie Cheaper by the Dozen and if it got too bad the store might have to close down to clean up. This is like what happens in the motor neurons in some ALS patients.
So what can be done to stop ALS? Is stopping the SOD1 gene from mutating the key to stopping motor neuron death in ALS? Unfortunately, it does not seem SOD1 is the key to stopping ALS. Mutation of the SOD1 gene is only responsible for approximately 10% of the ALS cases. The cause of ALS in the other 90% of cases is still unknown. Therefore, to successfully cure ALS additionally research is needed. This means for people like Lou Gehrig there is hope that one day we will cure amyotrophic lateral sclerosis, but it appears that this day may still be in the distant future.
Sources:
1) bleacherreport.com
2) http://en.wikipedia.org/wiki/Lou_Gehrig
 

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