The Battle Against Drug Addiction

While we have amazing facilities in the US that aid in overcoming drug addiction, why are the chances of relapse are so high in drug addiction? The National Institute on Drug Abuse states that about 40-60% of people relapse. Relapse can be due to strong withdrawal symptoms and environmental triggers. Drug rehabilitation centers focus on cognitive behavior therapy to help change the thoughts associated with drug usage. These programs often last about three months or 90 days. While emersion in these programs often helps, there are still other factors at play.

In the case of drug addiction, we cannot forget biological processes as an opponent. With chronic drug use the cells change things that can be long lasting, and are a constant battle even after treatment.

Changes include increase receptors on the neurons which allow more binding of the drug and stronger effects of the drug. In the brain there is a region affected by drug use that contains spiny neurons which are true to their name, a neuron with spines coming off it. With chronic drug use, more spines develop on the neuron (long term potentiation) so it increases the receptors for drug interactions.

A common pathway associated with drug abuse is the dopamine or reward system. In the case of drug addiction, the brain system for reward is increased and punishment is decreased. Therefore, the good feelings associated with drug use are heightened and the feelings of punishment are lowered.

Some common words associated with drug use are sensitization and tolerance. In a biological sense sensitization means that with the increase of receptors, the brain is more sensitive or susceptible to drug use. With the same exposure a heightened or enhanced reaction happens. Tolerance means that although you may be sensitive to a small amount of drugs, it takes a longer time to satisfy the craving. This causes a user to need to increase the amount of drugs consumed to get the same effect.

Current treatments typically help with symptoms of drug addiction, withdrawal and aid in preventing relapse. However, we do not have drug that can target and stop these adverse pathways from happening. There are a few novel drug targets being researched. Until we are able to identify a viable, effective strategy, the battle continues.

Looking forward is important to continue researching and understanding the pathways involved in reward and drug-seeking behavior. Once we are able to couple therapy with an effective drug treatment can we begin to fight drug addiction on all fronts.

What Happens in Addiction??

It can probably said that everybody struggles with addiction. Not only the classic examples that often first come to mind of drugs and alcohol, but coffee, Netflix, sugar, exercising, chocolate, sex, pop, gambling, social media, etc. These are all things people may say they are “addicted” to. People become addicted to things because of the release of dopamine in their brain into their reward system. It makes them feel good and they want to do it more. They may even feel “withdrawal” symptoms if they don’t get their morning coffee or haven’t gotten to check Facebook in a while.
 
It can be hard to break old habits, but most people can survive and function if they don’t get their Pepsi for the day (even if they REALLY want some). The thing that people need to understand is that drugs of abuse and alcohol can actually cause structural and chemical changes in the brain, its neurons, and its signaling pathways. This makes it almost impossible for them to be able to stop using these substances without treatment or medication. They actually cannot help their behaviors even if they really want to stop, because their brain has changed and is controlling their actions in a different way.
 
The structural and chemical changes and pathways in the brain that may be affected are very intricate, but some basic changes from drugs of abuse and alcohol include the following:

  • Increased dopamine – this acts on medium spiny neurons in the striatum (associated with reward).
  • Synaptic plasticity – more medium spiny neurons grow as there is hyper-stimulation from the drugs, this means that they are even more susceptible to the dopamine being released. This can contribute to behaviors of drug users such as tolerance, sensitization, and dependence.
    • Tolerance – you need more of the drug to get the same “high”/effect/experience – receptors may be downregulated, so you need more of the substance to make up for that.
    • Sensitization – you need less of the substance to crave it more intensely.
    • Dependence – without the substance, you start to experience withdrawal symptoms.
    • This is essentially a downward spiral because you start to need more of the drug to feel the same effects, but you need less of the drug to want it more. Then if you don’t get the drug, you have withdrawal symptoms, which can be life-threatening in some cases. So not good….
  • Changes in signaling molecules – in the article we read, it mentions several signaling molecules, kinases, phosphatases, and transcription factors. Changes in these cause downstream effects that contribute to synaptic plasticity, drug behaviors, and long-term potentiation, which is further damaging to neurons.

 
Addiction to drugs of abuse and alcohol is scary as you hear stories of people dying from overdoses, hurting loved ones or causing car accidents, doing things they do not even know they are doing which can often result in injury, and having it consume their lives so much they lose their jobs, family, money, and that is all they can think about. The problem is there are so many things going on in the brain, it is hard to “treat” addiction. Rehab and treatment centers often incorporate therapy which is great, but it does not change the chemical and structural changes in the brain, which are essentially controlling the addicted person telling them to continue to use the drug. Medication can help with some withdrawal symptoms, but is it still not fully understood how restore receptors, neurons, and signaling to its normal baseline state, or how long that can take naturally. It also greatly increases the chance of relapse. You also have to take into account the psychological dependencies that can develop as well through drug and alcohol abuse.
 
Identifying signs of addiction is important as it may help save someone’s life if they get treatment. Especially as you hear of younger teenager becoming addicted to drugs, perhaps education may help reduce the risk of that. Remember how hard it feels for you to stop watching your favorite Netflix show sometimes, and remember that people who struggle with drug and alcohol addiction feel that much more strongly and all the time. Don’t look down on them, but let’s strive to give people they help that they need.

Addiction and the Brain

The biggest thing I have realized from our classes weekly focus on the topic of addiction is that addiction is a complicated, multifaceted behavioral disorder. The article we read for this week explained that addiction is influenced by genetic, environmental, and developmental factors. While there seem to be several receptors and molecule interactions that influence the pathophysiology of addiction, it is clear that the normal reward pathway is disrupted.

In addiction, intracellular dopamine, a key player in the reward pathway, is increased in the brain. Dopamine is the neurotransmitter that induces pleasurable effects in the brain and solidifies memories associated with the pleasurable effects. With this increase in dopamine, addiction signaling can be impacted through changes in tolerance, sensitization, and dependence on the pleasurable substance.
 
Interestingly, addiction can actually physically change the brain. An example of this is an increase in the connections made by the medium spiny neurons (MSN) of the dorsal and ventral striatum of the brain. With overstimulation by different neurotransmitters supplied by the pleasurable drug, neural plasticity can be induced.

After learning more about the neurochemistry and epigenetics of addiction this week, one of my main questions is how do we combat addiction as a genetic and behavioral problem? It seems like society treats addiction like a choice, with very little sympathy for the fact that the chemicals ingested can actually change the pathways in the brain, resulting in modified behavior. While the initial use of a drug is generally the choice of the person, two people could make the same pleasure seeking choice but only one person, who happens to be more susceptible succumbs to addiction, while the other person that made the same choice, does not.
 
It is however important to recognize that addiction is a behavior that seems to be correlated with irrational choices for pleasure seeking. Addiction is also interesting because people who are addicted are clearly able to make the choice to quit using a substance without professional help, since many have done it before. At the same time, people who quit using an addictive substance can also be influenced resort to pleasure seeking behaviors by different triggers, even years after they have been sober.

Another interesting thought is that pleasure seeking is not limited to addictive drugs. While pleasure-seeking behavior can be appeased through substances with negative connotations like cocaine or alcohol, more socially acceptable addictions can be induced by caffeinated coffee or an addiction to sugar.
 
So how do we combat addictions in their varying forms?

  • Specialized drug treatment facilities: provide counseling, behavioral therapy, medication, case management, and other types of services to persons with substance use disorders.
  • Behavioral Treatment: delivered in outpatient, inpatient, or residential settings by a variety of providers.
  • Limited pharmacological approaches:
  • Expanded Educational Programs: education to young people about the effects of drugs and addiction can be used to reduce the forefront of the problem. Apparently educational programs have been shown to postpone or prevent smoking onset in 20 to 40 percent of adolescents.

 
 
 

You’re Addicted to a Drug, and You Might Not Even Know It

It makes you happy. You get cranky when you don’t have enough of it. Once you’ve gotten used to a certain amount, you need more to sustain you.
It’s sugar.
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The way that sugar works on our brain chemistry is very similar to that of other drugs of abuse—it can cause one to become addicted to sugar . It affects our dopamine systems, flooding the brain with this feel good chemical and inducing a high. Picture the stereotypical child with an ice cream cone.

To compensate for this large amount of confusing dopamine, the overwhelmed brain will turn off its dopamine receptors. The only problem with this is that the brain doesn’t always realize to turn the dopamine receptors back on. This causes a withdrawal, because without the registration of dopamine, you feel unhappy—cranky even.
We can also develop a tolerance for sugar. The brain learns not to get too happy from this extra dopamine, and the dopamine receptors are regulated so that they need a higher concentration of dopamine in order to register. You know the experience where you try eating the bright blue frosting on a child’s birthday cake and can’t stomach it because of the sweetness? Yet most kids could eat three pieces without a problem. They have a higher tolerance.
Tatym, eating birthday cake.
Yet sugar is different from drugs of abuse. We let kids have it, and reward them with it. It’s socially acceptable to be addicted to sugar here.  Sugar is in almost all of our food, and it is perfectly fine to have three meals a day with snacks in between. Half of the time in America, we don’t even realize that we’re consuming so much sugar. It is hidden in ingredients lists, and corporations want to keep us in the dark. If we’re addicted to a substance, we are more likely to keep buying items that have that substance in it.
Like I said, you might be addicted to a drug, and you didn’t even know it. You didn’t even really have control of this addiction—especially if you didn’t know about its side effects, or that you could become addicted to it in the first place.
Sugar addiction isn’t a huge problem at first, but like most drugs of abuse, it can lead to some serious health problems down the road. For instance, high sugar intake can help lead to heart and liver disease, diabetes, and even cancer.
 
I don’t mean to guilt trip you because of your addiction, but maybe realizing how easy it was for you to become addicted to sugar will help give you some empathy for those addicted to drugs of abuse—people that need real help, and not dirty looks and an overabundance of acquisitions.

Brains of Abuse

The term “drugs of abuse” gets thrown around when trying to specify drugs that are detrimental in nature. This is opposed to the “drugs of use” that would include over-the-counter and prescription medication. It is far too often that these abusive drugs lead one into a path of addiction, and it is far too often that this path of addiction leads to death. So I must ask, why are “drugs of abuse” drugs of addiction?
Our remarkable human bodies have evolved in such fascinating ways. We, as a species, have honed in on the most practical ways to learn about the world, and remember what we learn, so that we might apply it in, ultimately, reproducing and raising our offspring. A result of this evolution is our ability to remember what gave us a “good” experience.
When I say “good”, I mean in the sense that the experience will increase one’s likelihood of creating and rearing successful offspring. This “good” experience can manifest itself in multiple ways: the awareness that comes along with a cup of morning coffee, the relaxation of a massage, the satisfaction in eating a pastry, or the intrinsic pleasure of sexual activity. It is such that all of these activities increase the odds of making successful children (some more directly than others).

Thanks to evolution, our brains devised incredible ways to “lock on to” these events, remembering exactly how they felt, and the specific steps taken to allow them to occur. Because of this, we get remarkably good at reproducing these feelings of pleasure, and most of the time, it is a very good thing.
The brain must transmit its signals somehow, and since the basic building blocks of life are chemicals, it chooses to transmit the signals as chemicals. Neurotransmitters, as they are called, are the chemicals released within the synapses of the brain, and they give us the ability to be humans. During the aforementioned “periods of pleasure”, many of these neurotransmitters are released, but the most important (and plentiful) of these is dopamine.

Dopamine is used colloquially as the “feel-good” hormone, and indeed it produces pleasurable effects. It is important in other aspects, however. As was mentioned, our brains are very good at remembering exactly how pleasurable events were created. It is dopamine that locks down these memories.
This is where drugs of abuse play such an important role. Nearly every abusive drug increases dopaminergic receptor agonism (“extra dopamine release”). This is either done in a direct (mescaline and amphetamine) or indirect (most other drugs of abuse) manner. Regardless of the process, the brain is receiving signals of pleasure from an unnatural source. Note, I use the term “unnatural” to mean that the brain is not triggering its own dopamine release, but rather substances from outside the body are.
Since these drugs can be administered in any dosage, it is quite common for internal dopamine levels to increase past the point of any natural setting. This incredibly high concentration of dopamine creates the “high” felt by abusers, as well as the second effect of dopamine: the formation of intense memories associated with obtaining the feeling of pleasure.
It is well-hypothesized that these “memory-forming” effects of dopamine play just as important of a role in addiction as the pleasurable effects do. While the pleasurable effects are likely more important in the development of withdrawal symptoms, the intense memories give addicts the urge that cannot be erased from their minds. When we look at the two together, we can see why the road to addiction is far too short.

Since extra dopamine is flooding the synapses, the brain thinks something is wrong, and down-regulates its dopamine receptors. This is, again, a result of evolution as it is meant to “reset” the brain to a normal state. But once the drug wears off, and dopamine levels return to normal, the brain cannot activate as many receptors as it normally would have. The result of this is initially depression, but follows with all sorts of horrendous symptoms which the reader may look up for themselves. This process is characterized as withdrawal.
The sad case of the matter is that eventually addicts do not seek the drug to experience a high, but rather to avoid a low.
The memory-effects of dopamine also come into play here, for just as the drug wears off, an abuser will remember the “good ol’ times” vividly. It will cease to matter whether the process of getting the drug is detrimental (expensive or dangerous); the addict will seek out a repeat experience nonetheless. And of course, each time the process “works”, the abuser will have strengthened the memory further. It is through this process that the “cravings” of addiction are created.
And so, terrible withdrawal symptoms, coupled with cravings, arises from repeated abuse of drugs. The well-known saying that drugs “hijack the body’s reward mechanism” are completely true. There is little escape from the self-administration of “dopamine” because of its grip on creating habits, and when administered in high concentrations, our bodies cannot prepare. What was meant to reinforce habits capable of creating life, in the end creates habits capable of destroying it.

ALS and the Contributions of Oxidative Stress

In the life disrupting disease known as amyotrophic lateral sclerosis (ALS), degeneration of upper and lower motor neurons eventually causes disability through the inability to control locomotion, speaking, eating and breathing. The most unfortunate parts of this disease are that the cause of ALS is not completely understood, treatments are limited with no cure, and ALS tends to progressively worsen over time even with treatment and therapy.

According to the ALS association, approximately 6,000 people in the U.S. are newly diagnosed with ALS each year. The average length of survival after diagnosis is three years, but there is much variability in length of survival as 5% of those diagnosed with ALS will live 20 years or more, like the famous physicist, Steven Hawking. Since ALS is such a debilitating disease, understanding of mechanisms of ALS and coming up with novel treatments will be essential to making a difference in the lives of those diagnosed with ALS.

This week we focused our learning on the paper: Oxidative stress and mitochondrial damage in the pathogenesis of ALS. This review identified 4 important possible contributors to ALS:
 

  • Oxidative stress: occurs when a cell is unable to detoxify reactive intermediates, resulting in cellular damage. ALS tissues were found to have an accumulation of oxidative damage to proteins, lipids and DNA. This could be caused by a mutation in the SOD1 gene (superoxide dismutase), which normally acts as an antioxidant enzyme.
  • Mitochondrial damage: oxidative stress can cause mitochondrial damage, creating energy deficits, calcium mishandling, and altering of RNA metabolism. Mitochondrial damage is especially important in motor neurons, which are known to have a large number of mitochondria.
  • Altered RNA metabolism: Oxidative stress also causes the aggregation of RNA binding proteins (like TDP43 and FUS) into stress granules, which disrupt RNA metabolism. When RNA metabolism is disrupted, the overall health of the cell is compromised through the loss of functional proteins. Another important fact is that stress granule accumulation is common in patients with ALS.
  • Unfolded protein aggregates: improper protein folding is a common to ALS pathogenesis. Stress granules may be trapping chaperones, proteins that assist in proper protein folding, having a widespread effect on cell physiology. In this situation, the protein degradation pathway is imbalanced, leading to the accumulation of misfolded proteins in ALS tissues. Improper folding of mitochondrial proteins will also affect mitochondria function!

 

These four cellular malfunctions found in ALS could all be impacting each other, resulting in a vicious cycle of damage to the important cellular organelles and processes that maintain a functioning motor neuron. While more research needs to be done in order to understand the complex pathways that contribute to ALS, the seeming overlap of oxidative stress and mitochondrial damage in ALS could be a potential target for future therapies to reduce the damage caused to motor neurons during the progression of ALS.

The Mystery of ALS: Motor Neurons

Amyotrophic lateral sclerosis (ALS) is a disease surrounded by a lot of mystery and frustration as the mechanisms of the disease are not fully understood, and there is no current way to cure, or even truly successfully treat the disease. ALS is a fatal disease characterized by degeneration of upper and lower motor neurons. Most patients with ALS end up dying of respiratory failure as their diaphragm is no longer able to function to help them breathe. Once patients are diagnosed, they are usually given a life expectancy of around two years. There is some hope though, as there have been certain people, like Stephen Hawking, who live for decades with the disease, we just have to figure out what to treat.
There are a couple main target points in the body that researchers have found to be associated with ALS. One is mutation of the SOD1 gene, which normally functions to protect the body from metabolic waste. ALS has been found to be associated with high oxidative stress in the body as well. This may be partly due to dysfunction of the SOD1 gene. It also appears to affect two RNA binding proteins, FUS and TDP43, not allowing them to properly function in RNA metabolism, affecting the functionality of other proteins in the body. The decreased function of these proteins may also lower the body’s ability to protect it from oxidative stress. Oxidative stress is also hurting mitochondrial function by affecting its proteins and metabolism. Thus, these two possible mechanisms seem to cross-over with each other.
 
 
 
One big question about the disease is why it only seems to cause degeneration of the motor neurons specifically?
I have come up with 5 possible reasons from looking at some research done by the ALS association:
1.     Axon structure and proteins – motor neuron axons are around a meter long. This is a long way to transport messages, it would have high metabolic demands, and there is a lot of room for proteins associated with it to be affected making it harder to protect.
2.     Too much cell apoptosis – even cell death that is programmed by the body can be harmful if it is happening too much. Possible halting some of the apoptotic events is being studied by scientists to possibly help the neurodegeneration.
3.     Mitochondria – the motor neuron is huge and requires a lot of energy to stay functional. The mitochondria provides energy to its neuron, and as the mitochondria becomes dysregulated or dysfunctional, the motor neuron will lose its ability to function.
4.     Glutamate – this is the main excitatory neurotransmitter of the body. Too much excitatory activity of a cell can lead to cell death, and in ALS there may be too much glutamate around and acting on the motor neurons.
5.     Inflammation – this immune system process often happens as a result of cell death. If there is too much apoptosis going on or motor neurons or their surrounding cells dying from excitotoxicity, inflammation may be upregulated further damaging and killing more motor neurons.
 
Obviously there is no solid answer right now of the ALS disease mechanism. Maybe solving the “motor neuron mystery” will be key in treating ALS. It will be important to keep people aware of this disease, and keep research moving forward.

Quick Overview of ALS

Amyotropic Lateral Sclerosis (Lou Gehrig’s Disease) just might be one of the most terrifying conditions out there. For starters, at this point in research, 95% of cases are defined as sporadic. That essentially means that there is no known cause or biomarker that can determine one’s susceptibility of having ALS in the future.
 
Oxidative Stress and ALS
Image result for oxidative stress and ALS
Motor neurons become bombarded with oxidative stress from substances such as radical oxygen species which leads to multiple different responses from the cell. SOD1 which is an enzyme that captures these radical oxygen species and converts them into a manageable molecule that can be destroyed within the cell. In some cases of ALS, SOD1 enzymes are not properly formed, allowing the radical oxygen species roam within the cell causing oxidative damage.
Stress Granules
Image result for stress granules electron microscopy
When certain cells are exposed to oxidative stress they begin to form complexes of proteins and untranslated mRNA to become what is called a stress granule. These granules can perform several different tasks such as signaling, the decay of RNA, and apoptosis (cell death). Stress granules may seem like they could be a problem because they can lead to cell death, but they are a designed protective measure by the cell that helps protect the cell while it is experiencing oxidative stressors. The problem comes from the overabundance of stress granules due to prolonged oxidative stress. This leads to a build-up of granules blocking other cellular processes leading to further dysfunction within the cell.
 
Big Picture?
Image result for ALS
So, what does all this oxidative damage do? Over time these motor neurons are killed by the prolonged damage leading to a lack of signal from the brain to various muscles. The slow deterioration of motor neurons leads to muscle weakness and slowly ends up in paralysis of muscles. The scary part is that there isn’t necessarily a defined path that ALS follows in which muscle usage deteriorates. Furthermore, many may not realize that they have ALS symptoms because the age of onset doesn’t come until people are in their 50s (average) so they may view these symptoms as a normal process of aging.
Prevention and Treatment
This is the more disheartening aspect of ALS because there is no surefire treatment that has extended the patient’s life significantly. There is some recent research into using antioxidants to help slow down the progression of ALS but they are too recent to find out the results of the study. This seems to pose the question, “What do I do to prevent myself from getting ALS?” Some may say that there is no way to prevent ALS from happening, but I would venture to assert that antioxidants wouldn’t hurt. Clearly, we are missing a piece that might help us figure out the cure but that might be further down the road so at this point the best bet is to live life to the fullest until the inevitable comes.

Does ALS Stand for All Is Lost Suddenly?

Does ALS Stand for All is Lost Suddenly?

Amyotrophic lateral sclerosis, better known as ALS or Lou Gehrig’s disease, is a central nervous system disease where motor neurons are targeted. The motor neurons send signals to your muscles all over your body, even ones used to speak, swallow, and breathe. According to the Mayo Clinic website, ALS symptoms begin with muscle weakness in your hands, feet, and limbs, and continues to spread over time. As the disease progresses, the more vital processes such as breathing and speaking make living with the disease very difficult. Individuals that are diagnosed with ALS typically are told they have only a couple years left. However, this does not mean that it will always be the case. Genius Stephen Hawking has lived 50 years with ALS. So what causes this awful disease? What hope is there for those who are unfortunately diagnosed?
As of today, there is no certain answer as to what is the official cause of ALS. However, researchers have determined a few processes that are present in ALS patients. These processes are as follows:
Oxidative Stress and Mitochondrial Damage
Oxidative stress comes from a high amount of free radicals and not enough response to break down these free radicals. The body naturally has antioxidants and enzymes to regulate these free radicals, however, in ALS patients, the enzyme SOD1 typically used to relieve oxidative stress is mutated and cannot function properly. This oxidative stress causes the mitochondria to become damaged and RNA to be incorrectly spliced/metabolized. Below is an image of a motor neuron. The mitochondrion can be seen labeled toward the bottom (the little tan bean shaped organelles).

RNA Dysmetabolism
There are two RNA binding proteins called FUS and TDP43. Both of these proteins are supposed to be in the nucleus of a cell and interact with RNA to help in making more proteins properly. However, in ALS patients, FUS and TDP43 are removed from the nucleus and accumulate in the cytoplasm. Since they are no longer in their proper location, the proteins that they would have helped produce would no longer be made correctly, causing mayhem in the mitochondria. Since oxidative stress is highly localized in the mitochondria, the relocation of FUS and TDP43 can be linked to the cause of oxidative stress and mitochondrial damage.
Protein Folding and RNA Binding Proteins
FUS and TDP43 also have an effect on protein folding. There are certain chaperone proteins that allow other proteins to be imported into the mitochondria and allow the proteins to fold correctly. However, FUS and TDP43 can actually trap the necessary chaperones which does not allow the proteins to get where they need to be and are not folded correctly. If proteins are not folded correctly, they are unable to do their jobs and must be broken down by the cell. If there are too many misfolded proteins in the mitochondria, oxidative stress builds and the mitochondria is damaged, and RNA is not metabolized correctly.
 
As we can see, it seems that each of these causes discussed stems from and causes the others. Unfortunately because of this, no one knows where ALS truly originates, and it is almost impossible to know what exactly to target to treat this disease. One drug does exist that only extends life for 2-3 months, but this drug also costs $14,000.
It is never easy to hear a loved one has been diagnosed with an illness that has no known cause or cure. Coping can be difficult and your life is forever changed. I am confident, however, that our modern medicine and advancing research will, one day, find a way to treat or even cure this most unfortunate disease. For now, all we can do is hope. All is not lost suddenly.

What Science Doesn’t Know – ALS

Amyotrophic Lateral Sclerosis (ALS) – also commonly known as Lou Gehrig’s Disease – is a degenerative disease that can effect motor neurons in the central or peripheral nervous system. This leads to a steady loss in motor skills -including coordination and movement of skeletal muscles. Sometimes dementia can form even if it isn’t a common symptom. Eventually, death will occur when the degeneration of motor neurons begins to affect basic functions such as breathing, swallowing, and heart rate (1). Unfortunately ALS is an incurable disease with no known cause or treatment at this point in time.Furthermore, there are currently no known indicators for ALS onset. In fact, diagnosis of ALS often is the result of ticking off what other diseases it could be.
Which brings up the point: why is so little known about ALS?
This question is especially frustrating considering the harsh reality of the disease. And like with most diseases the answer is complex and multifaceted. The matter of the underlying causes of ALS isn’t necessarily just about what can lead to ALS – but what doesn’t contribute to ALS. Numerous studies have linked glutaminergic excitoxicity, genetics, immune dysfunction, misfolding of proteins, environmental toxins, and even military service to the development of ALS (2). The disease is also known to occur more frequently in men. So it’s quite difficult to pinpoint any given cause to the development of ALS let alone find an effective treatment. However, that doesn’t mean that a cure or treatment for ALS can’t be achieved.
If you wish to donate to ALS research you can give any amount to the ALS Association (no Ice Bucket Challenge required).
Sources:

  1. http://www.webmd.com/brain/tc/amyotrophic-lateral-sclerosis-als-topic-overview#1
  2. http://www.mayoclinic.org/diseases-conditions/amyotrophic-lateral-sclerosis/symptoms-causes/dxc-20247211

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