During the week of October 7 in my neurochemistry class, we explored and discussed the most commonly used illegal drug in Western societies, marijuana. Throughout the week, we discussed many different aspects of the drug, such as the endocannabinoid system, its process of binding within the body, the release and uptake, and any beneficial aspects that marijuana may have for a person. Personally, I found this article to be very interesting and informative because marijuana and endocannabinoids are two things that I know very little about, and I’m sure this is true for the majority of the general public. Even after reading the paper and discussing it for a week, there is a lot that I don’t completely understand, but I hope to convey the information as accurately as possible.
In order to understand the endocannabinoid system and how marijuana is interrelated, it is important to first understand the basics of marijuana. The genus species name of the marijuana plant is Cannabis sativa. For hundreds of years, it has been used for medical and recreational purposes, and is the most widely used drugs in various countries throughout the world. Cannabis sativa contains at least 400 chemical components, in which 60 of them belong to the cannabinoid class. Tetrahydrocannabinol (THC) is the main psychoactive component of cannabis, and is responsible for giving people the feeling of being “high.” Marijuana, as well as other cannabinoids may be therapeutically useful, but this is greatly hampered by their psychotropic effects and by their potential for abuse. Research is currently being carried out to find new approaches to harness the therapeutic properties of marijuana without causing unwanted effects.
Important to the function of endocannibinoids is their binding to G-protein coupled receptors (GPCRs) on the cell surface. GPCRs work by binding a G-protein, which activates the complex by producing GTP from GDP. This complex then goes on to activate the enzyme, adenylyl cyclase, which produces the second messenger, cyclic AMP. Lastly, cyclic AMP carries out many different functions in the cell. Endocannibinoids bind to two different types of GPCRs: the CB1 receptor and CB2 receptor. The CB1 receptor is present throughout the central nervous system and is highly expressed in the cortex, hippocampus, basal ganglia, and cerebellum. They have effects on memory, movement, and nociception. Unlike CB1, the CB2 receptor in primarily expressed in the immune cells and carries out important functions in the immune system.
After their biosynthesis, endocannabinoids are released to extracellular space and activate the receptors by membrane diffusion or by a transporter. Due to their lipophilic nature, endocannabinoids can diffuse through the plasma membrane and bind to the appropriate GPCR. In addition to the psychotropic effects that marijuana has after it binds to a receptor, marijuana can also have helpful therapeutic effects for a person. Marijuana can help treat an eye disorder called, glaucoma. During our discussions during the week, we talked a lot about other therapeutic effects that marijuana can have. One student in our class mentioned that his relative is prescribed medical marijuana to help ease chronic pain back pain. He said the marijuana has a significant impact on the reduction of his pain. We also watched a video in which a patient uses medical marijuana to reduce the symptoms of Parkinson’s disease. In the video, you could definitely observe the fact that the marijuana helped reduce the symptoms. As you can see, marijuana doesn’t only have negative effects, but it can also have helpful therapeutic effects.
http://www.youtube.com/watch?v=KdvprGD5TXU
Connection Between Diabetes and Alzheimer's Disease?
Over the past week in my neurochemistry class, we explored and discussed a very interesting new discovery in the pathogenesis of Alzheimer’s disease. It has been discovered that type 2 diabetes mellitus is a significant risk factor for Alzheimer’s disease. Insulin resistance and glucose metabolism of patients with diabetes mellitus are the two main implications for developing this neurodegenerative disease. Personally, I found the article that we read to be very interesting and was amazed by the fact that two unrelated diseases in terms of pathogenesis can actually be interrelated and have connections with one another. Even after reading the article and discussing the topic for a week, I still don’t quite understand everything, so I will stick to the basics when describing this topic to you.
In order to understand the connection between type 2 diabetes mellitus and Alzheimer’s disease, it is first important to know the characteristics of each disease. Alzheimer’s disease is a neurological disorder characterized by profound memory loss and dementia. The pathological hallmarks of Alzheimer’s disease include a few obscure scientific terms such as, amyloid plaques, neurofibrillary tangles, and amyloidal angiopathy. Loss of neurons and synapses in the central nervous system is also observed in patients with this disease. Types 2 diabetes mellitus is characterized by excessive amounts of glucose in the blood primarily because they are insulin resistant or are insulin deficient.
Like I mentioned earlier, type 2 diabetes mellitus is a significant risk factor for developing Alzheimer’s disease. It has been determined that insulin has important outcomes on brain functions in addition to numerous peripheral metabolic effects. There are two models that describe the connection between diabetes and Alzheimer’s disease. They include central insulin resistance and inflammation in the brain. Both of the models influence insulin sensitivity in the brain, which leads to B-amyloid accumulation and eventually to Alzheimer’s disease.
Insulin is primarily synthesized in the pancreas and has very important roles in metabolic homeostasis. There is evidence that insulin is also produced in the brain. It has important effects in the central nervous system, regulating key processes such as energy homeostasis, neuronal survival, as well as learning and memory. In patients with type 2 diabetes mellitus, the transport of insulin into the brain is reduced, which in turn decrease brain levels of insulin. Studies have linked the reduction of insulin in the brain with Alzheimer’s disease suggesting that the brain must be influenced by insulin levels and sensitivity. Another interesting aspect of the connection between diabetes and Alzheimer’s disease is the implication of glucose metabolism in Alzheimer’s disease. Utilization of glucose by the brain as a source of energy is important for many of the processes that the brain carries out. Abnormalities in the brain of Alzheimer’s patients are connected with alterations in brain metabolism. These alterations are often associated with impaired glucose utilization and energy metabolism, which are two features of type 2 diabetes mellitus.
I have never heard that type 2 diabetes mellitus is a significant risk factor for developing Alzheimer’s disease, so it was very interesting learning about the many factors that play a role in the connection between these two diseases. Learning about this connection has made me more aware and conscious of the decisions I make regarding how much and what types of food I consume.
Nuts and Bolts of the Akt/GSK3 Pathway
Over the past week in my neurochemistry class, we discussed and learned more about an important pathway in the brain. The pathway I am referring to is called the Akt/GSK3 pathway. In order to learn more about this pathway, we discussed the article, “Beyond cAMP: The Regulation of Akt and GSK3 by Dopamine Receptors.” Even after spending a week of learning about this topic, I still have many questions that have been unanswered. On the other hand, this past week has been very beneficial and has significantly advanced my understanding of this complex topic. The Akt/GSK3 pathway has implications in the actions of antipsychotic, psychostimulant, and antidepressant medications. It is also involved in schizophrenia, bipolar disorder, so it is important to understand the basics of this pathway.
The article begins by summarizing the mechanism of the Akt/GSK3 signaling cascade. Research has shown that dopamine may play a role in the regulation of Akt and GSK3 signaling. The D2R receptor is directly involved in this pathway and its activation stimulates the formation of an important signaling complex. This signaling complex is composed of three molecules: beta-arrestin 2, PP2A, and Akt. The formation of this complex results in increased inactivation of Akt. An important discovery by researchers is that lithium disrupts the formation of this complex and inhibits the activity of GSK3. Lithium is able to disrupt the complex by directly preventing the interaction of Akt and beta-arrestin 2. Inhibiting GSK3 is the mechanism of action that many antipsychotic medications utilize.
Here is a diagram of the Akt/GSK3 pathway, which will hopefully make the pathway a little clearer and easier to follow.
In addition to having implications in antipsychotic medications, the Akt/GSK3 signaling pathway plays a role in neurodegenerative diseases, such as Parkinson’s disease. Currently, it is unclear what the mechanism is behind the role that the Akt/GSK3 pathway has in Parkinson’s disease, but researchers have discovered two neurotoxins that play a role in this disease by studying model rats. Further research on the mechanism of Parkinson’s disease will hopefully lead to an effective way to prevent this disease.
Like I mentioned earlier, the Akt/GSK3 signaling pathways plays a role in the action of antipsychotics. Several antipsychotics have been shown to be able to activate Akt and inhibit GSK3. In my opinion, it is exciting that researchers are constantly discovering different ways to produce effective medications that are useful for various different diseases. The Akt pathway is only one pathway that is utilized in the production of medications. It will be important for researchers to continually produce medications, and it is exciting that researchers are working daily to produce new effective and efficient medications.
Over the past week, it has been very interesting to learn about this important signaling pathway in the brain and see how it can be utilized in the production of numerous medications. Discussing the article has made me aware of the fact that signaling pathways in the brain are very complex and can be difficult to completely understand.
The Concussed
When a concussion occurs, the first few hours are when the neurological damage really occurs, and the weeks after the injury are when the side effects start to be noticed. Neurons are forced to work overtime due to the rapid metabolism of glucose after a concussion. Hypometabolism occurs in the first few hours of the injury, and the recovery time of this hypometabolism is dependent on the degree of the concussion. This metabolism rate is not the only dependent on intensity of the concussion; the amount of damage the axonal cell membranes endure is also related to how bad the concussion is, and this axonal injury is connected to spatial learning and memory deficits. It makes sense that with worse injuries, the patient’s memory is at more risk.
The effects repeat concussions have on the brain is very influential to the person’s memory, learning ability, etc., which is why it is extremely important to make sure that a person is completely recovered before they are put back into a situation where they could potentially get another concussion. Thankfully there have been regulations limiting the amount of concussions a person can have before they can no longer play a sport. However, this poses the problem that some concussions go unreported. For many athletes playing in a game is more important at the time than their long term health.
Concussions have been a topic of debate that has essentially changed the way contact sports are played. Although many of the changes are beneficial and were necessary, I do believe that the game has changed so drastically that we may be doing more damage than good. It’s not a secret that with new padding and equipment players are more likely to use more force when coming into contact with another player. Comparing how hockey is played in 2013 and how it was played 60 years ago, the only obvious commonality they have is that it is played on ice. I’m sure the reported amount of concussions in the 1950’s would not be accurate, and neither would the amount of reported concussions in 2013, but I believe for completely different reasons. An athlete can only report so many concussions before they are out of the game, whereas in 1950 it may not have been sociably acceptable to have a concussion, both cases leading to an inaccurate number of reported concussions and an athlete that is at risk for permanent long term memory defects. As we learn more about the long lasting effects of concussions, sports are bound to change even more, which may be met with resistance, but hopefully it will help athletes in the long run.
I think you were dropped on your head as a child.
Source:http://www.maafirm.com/library/dallas-fort-worth-concussion-injury-lawyer.cfm
What is the real meaning behind this common saying? Usually, this saying is used when a person says or does something that isn’t very intelligent. The rationale behind this statement is that the hit to the head of a child is likely to cause brain damage, likely through a concussion. Concussions are becoming increasingly scary to the general public as more research is able to demonstrate their negative long-lasting effects, as demonstrated in the article The Molecular Pathophysiology of Concussive Brain Injury.
The problem with concussions is that many times, people are unaware they even had one. There are different intensity levels of concussion, ranging from minor headache and grogginess, to entire loss of consciousness. If someone experiences a minor concussion, it is possible that they won’t realize it could have serious consequences. The other problem facing concussion is that physical contact sports, like football and hockey, are becoming increasingly more intense and rough for both males and females of all ages. Return to play policies seem to be on qualitative evaluation of symptoms rather than quantative measurements of brain health or recovery. Experiencing multiple concussions in a row greatly increases the chance for long-lasting, severe damage. But if healing occurs between concussions, the risk is much lower.
Most people understand that a concussion occurs from a hit to the head. The hit could be from a sport, falling, car accident, or really anything that causes the brain to crash into the skull. When this happens, brain cells become damaged. The membranes become permeable to many ions. This causes nonspecific depolarization of the cells, which leads to random action potentials firing. This causes the release of neurotransmitters which excite other molecules. This excitation causes an overabundance of potassium to rush into the cell. This causes the ion pumps in the cell membrane to work extremely hard to restore the cell to its normal condition. This requires an extreme amount of energy in the form of ATP. In order to compensate for the extreme energy need, the brain goes into hyperglycolysis mode. This means the cell is taking glucose through glycolysis, breaking it down into two molecules of pyruvate, and then into lactate and ATP. The ATP is used by the brain, but the lactate builds up in the brain as lactic acid. This is unfortunate because the buildup of acid in the brain is quite detrimental. Next in the process, calcium influx occurs which causes the oxidative metabolism in mitochondria to become impaired. The mitochondria are then unable to produce enough ATP for the brain, which leads to a decrease of available energy. This activated calpain and apoptosis, or cell death.
The axons of neurons in brain also experience extreme negative side effects as the result of a concussion. The axolemma responds negatively to the previously described calcium influx by disrupting its normal behavior. Its neurofilaments become compacted due to phosphorylation or cleavage of the sidearm chains. This causes the axonal organelles to accumulate as the microtubules of the axon begin to aggregate. All this disruption leads to severe swelling of the axon and eventual death.
Continuous cell and axon death in the brain can lead to long-term damage. Unfortunately, no real medical or pharmacological treatments for concussions are available. The best, and essentially only, treatment for a concussion is rest and minimizing brain usage. Students shouldn’t attend school or attempt homework until they are symptom-free for at least 24 hours. This is a harsh reality to face since concussive symptoms can last for weeks. For high school students, this might be a huge problem, but to a college science student, missing weeks of school could mean the necessity of repeating classes and potentially not graduating on time and paying for an extra semester, likely without financial aid. This may seem like an extreme consequence, but it is a very real scenario. Missing a month of college science classes would be terribly hard to learn on your own, plus you can’t even keep up with the work while you are out sick because studying causes the brain to work too much during recovery. As for athletes, missing a month of practice could also be career ending. Most coaches wouldn’t allow a person to play after missing a month of practice. Plus, a month of staying in bed as much as possible is likely to lead to loss of muscle mass.
If concussions can have such serious negative effects, effecting both physiology and life style, what can be done to prevent them? Helmets are an obvious, but they can’t protect everyone at all times. Even state of the art helmets lead to concussions in the NFL and other professional athletic leagues. What about people who experience concussions in everyday life from slipping on ice or falling off a ladder? In that case, education on the essential resting period after a concussion is the best medicine. People need to realize the extreme effects that are consequential of improper concussion treatment. Too early return to play, school, or regular brain function can increase the risk of experiencing an additional concussion. There is a terrible period of brain vulnerability after concussion. It is also nearly impossible to turn off brain function, so the healing process is consequently slowed down.
The most important things to gain from this specific article are: The mechanism of concussive brain damage, the negative long-lasting effects of concussion (ex. Dementia like symptoms), and the importance of healing and prevention of further concussions. Hopefully, this article leads to thoughts and conversations as to which types of activities that leads to concussions outweigh the possible brain defects that can come from them. Conversations and brainstorming ways to properly deal with concussion are necessary for all people since concussions can happen to anyone.
Iron and Parkinson's Disease: Why We Should Keep Our Bodies Balanced
Two weeks ago in class, we talked about the importance of iron levels in the development and progression of Parkinson’s disease. As most of the public knows, Parkinson’s is a movement disorder that is characterized by muscle weakness as well as rigidity. As the disease involves a process of progressive neurodegeneration, resulting in concomitant worsening of symptoms, research in preventing damage at the earliest possible stage of disease has been of utmost importance. But where does iron come into the picture? Well, some recent findings have pointed to the role of iron homeostasis, or rather the alteration thereof, in the initiation of the cascade of events leading to Parkinson’s pathology. Iron is a very important element in the human body as it serves as a co-factor and electron carrier in many reactions; a great example of this is hemoglobin function. Iron also plays a role in cellular metabolic processes and is therefore of utmost importance in every area of the body, but we’ll focus on the brain. A significant increase in brain iron levels of Parkinson’s patients. Generally, iron accumulates in the brain over time, but its concentration is balanced by the action of several proteins. An imbalance of iron in the brain can lead to larger amounts of free radicals and subsequent reactive oxygen species in the brain. Free radicals cause a protein called α-synuclein to aggregate, leading to a cascade of events that result in cell death. This cellular mishap is accelerated by increased levels of iron which stabilizes the α-synuclein aggregates and even leads to increased expression of the protein.
Given these findings, it would be therapeutic for treatments to target this iron imbalance in its early stages to prevent the progression of symptoms. Iron-chelating drugs are currently being developed by independent researchers and pharmaceutical companies with some success in halting neurotoxicity. One very interesting finding is that a major catechin protein in green tea, called (-)-epigallocatechin 3 gallate or EGCG for short, has shown highly potent ability to prevent neuronal death by scavenging reactive oxygen species as well as binding/chelating excess iron to form an inactive complex.
How should the average citizen use this information? Given oxidized species build up in the body over time due to declining antioxidant activity, it would be very beneficial to combat this and prevent the buildup of potentially dangerous chemicals in our bodies before they become a problem. Some research suggests that products containing antioxidants possess a fair amount of value. Others state that simple remedies such as green tea hold very little clinical value. Either way, the average person doesn’t have much to lose by switching out coffee for green tea once in a while.
A Shift in the Perspective on Endocannabinoids and Marijuana
According to the United Nations Office on Drugs and Crime, marijuana is the most-used illicit drug in the world. In the United States, it is classified as a Schedule I drug, which is defined as “a substance or chemical which has no currently accepted medical use and a high potential abuse.” These are considered to be the most dangerous drugs, and a user is severely at risk for psychological or physical dependence. Marijuana is joined on this list by other substances such as heroin and ecstasy. Schedule II drugs are also relatively dangerous, but are considered to carry less potential for abuse than the schedule I drugs. A few examples from this list include cocaine, methamphetamine, and oxycodone. (For more information, see http://www.justice.gov/dea/druginfo/ds.shtml)
If one takes a look at the current marijuana use laws across the country, or even just takes a second to listen to those arguing in the popular debate, it is easy to see that the legal classification of marijuana as a Schedule I drug with “no currently accepted medical use” is somewhat out of line with the twenty states that currently allow marijuana for medical use. Though federal law still prohibits its use, the Department of Justice has announced that as long as those states which have legalized it for recreational use regulate it tightly, it will not challenge the laws in Colorado and Washington at this time. (http://www.justice.gov/opa/pr/2013/August/13-opa-974.html)
The American public has historically been opposed to the legalization of Marijuana, but a recent Gallup poll shows that for the first time, a majority of Americans are in favor of legalizing Marijuana.
I have always been on the fence regarding the legalization of marijuana, even for medical purposes. However, after reading an article recently regarding the biochemistry of the endogenous cannabinoids (substances made in the body which bind to the same receptors that the active substances in marijuana do), my opinion has changed. There are many different mechanisms and pathways by which the substances in the endocannabinoids may act, and these may be useful targets in the treatment of certain conditions. For instance, endocannabinoids are involved in vasodilation, which might be important in the treatment of high blood pressure. They can also mediate the effects of pain and inflammation. Perhaps the most surprising actions to me were those that targeted the treatment of cancer both directly and indirectly. The binding of anandamide and 2-arachidonoylglycerol (two substances found in marijuana) to the CB1 receptor in the body can induce apoptosis, or programmed cell death, which is essentially the goal in treating many types of cancer. Indirectly, substances in marijuana can also play a role in the treatment of cancer as well. Often, those undergoing chemotherapy for the treatment of cancer experience a loss of appetite, and substances in marijuana can help to induce someone to have an appetite. This can also be useful in treating anorexia.
Of course, we still cannot completely ignore the more harmful effects marijuana exhibits. There are certainly issues like the potential for addiction which caused it to be classified as a Schedule I drug in the first place. However, after learning of all the potential medical uses for marijuana, I cannot help but think that we need to rethink its classification as a Schedule I drug with “no currently accepted medical use.”
Iron Overload
I have always viewed Parkinson’s disease as something that only effected a person’s movements. After this week, I have learned that it effects to much more than that. There are many differences in the brain from a person who has Parkinson’s disease, and a person who does not.
Parkinson’s disease is characterized mainly by the loss of dopaminergic neurons, and the formation of Lewy bodies that reside in the remaining dopaminergic neurons. These Lewy bodies replace other elements within cells. Lewy bodies are not the only disruption in cells that a person with Parkinson’s disease has; there are also neurofibrillary tangles (NFTs) present within PD patients. NFTs and Lewy bodies are very representative of PD patients, but it was interesting to learn that the amount of iron in people with PD is significantly higher than people who do not have PD.
This raised an interesting question: does the food a person eats play into the likelihood he or she will develop PD? As a class, there have been many topics that relate neurological disease to the food that is put into our body. The relation with type 2 diabetes and Alzheimer’s disease, as well as green tea being extremely beneficial to PD patients in helping reduce oxidative stress, thus increasing the amount of properly working biological functions, has shown that what we feed ourselves may have a drastic effect on our brain’s health.
Although it should be no surprise, it is still fascinating that what we eat really does determine how healthy we are, both physically and mentally. Food and water are the resource for most of the functions our body conducts. As time has gone forward, we have discovered that food is an important factor in our livelihood, but it takes a lot of effort to eat what our body truly needs, as well as being able to afford it. With this dilemma, companies have capitalized by selling pills, tablets, etc. to keep a person at optimal health without having to worry about what else is being put into his or her body.
This relates back to Parkinson’s disease in that those with PD have a much higher concentration of iron than those who do not have PD; is this due to an individual’s diet? There have been many studies conducted showing the benefits of a Mediterranean diet or an Oriental diet (a real Oriental diet, not one consisting of deep fried chicken smeared in some sugary sauce—it is delicious, but not very comparable to what is actually eaten in the Orient) compared to a typical diet of those who live in the United States.
The amount of red meat a person in the United States is extraordinary. This could result in a high concentration of iron in the brain, thus being an influence on developing Parkinson’s disease. It is probably not going to fix the problem entirely if people change the way they eat, but it could be beneficial, just as drinking green tea has been shown to do.
"Light it up and Take a Puff, Pass it to me Now"
For years marijuana has been used both medicinallly as well as recriationally. These days society has made a huge commotion about this drug, trying to determine if it is an “okay” thing to allow people to use. There is plenty of evidence to suggest that this drug is being used more and more frequently whether it is legal or not. For instance a lot of artists, espcially in the rap and hip hop industry, have used references to marijuana use in their songs. These songs are being listened to everyday by millions of people. Often times the main listeners of this music are impressionable young children or young adults. This makes me wonder what kind of impact this is having on the youth of America in whether or not they are using marijuana. Not only that but why are people using the product; is it because getting high is cool and fun, or could it actually help these younger people feel more calm, get more sleep, eat better, etc.? I think this is why it is such a hot topic and why some states have decided to legalize this drug where others say it is too dangerious or unhealthy to allow.
Since the use of marijuana in the United States is such a controversial issue, have you ever found yourself asking why? or what makes a plant, of all things, something to argue over? If you have, you may want to first understand what makes this plant a drug. Endocannabinoids were the topic our neurochemistry class discussed this week by reading and anylizing the article “Endogenous cannabinoids revisited: A biochemistry perspective”. We discovered that the plant Cannabis sativa (marijuana) contains more than 400 chemical components, 60 of which belong to the cannabinoid class. Recently the main cannabinoid psychoactive component in marijuana was discovered. This is what we know as THC. THC does produce many psyhoactive effects in ones brain. Research has found that these cannibinoids act on the CB-1 and CB-2 receptors in our brain causing a person to feel “high”. Although this is largely frowned upon, recent research has been focussing on how the chemical components in marijuana may be more beneficial than harmful if used properly. For example we discussed that one study found that a certain strain of the drug, that had lower THC levels, can be used to treat people with epilepsy. The reason that a strain like this works better than other strains is becuse there is a cannibinoid called cannibidol in marijuana that is linked with health benefits and is less psychoactive than the THC. By consuming a strain that has less THC and more cannibidol in it, a perosn would have reduced psychoactive effects and possibly have more health benefits from the drug. There is a lot of research going on today that is trying to find out how using cannibinoids in different treatments would work and how they would be beneficial to society. Treatments for a lot of things are blossoming such as: treating cancer and cancer symptoms, helping with eating disorders, slowing down the effects and controlling the symptoms of HIV and AIDS, helping with depression, reducing headaches, and aiding in many pain disorders. I think people warm up to this idea because it is a “natural” solution to very difficult problems we face in the health problems we are experienceing today. A lot more research needs to be conducted in order to pinpoint specific treatments using endocannibinoids, cannibinoid receptors, etc. however, I do think scientists are going in the right direction to discover how marijuana can be considered a treatment not just a drug.
The significance of the Atk-GSK3 pathway
Of the countless neurotransmitters associated with the human central nervous system, dopamine is perhaps one of the most crucial neurotransmitters to understand in its pathways and signaling. Dopamine is utilized in a variety of different regions of the central nervous system, including cognition, locomotion, and emotional behaviors.
The regulation of dopamine is crucial to the well being of human health. As soon as the pathways that govern dopamine signaling, uptake, and various other aspects of its existence in the central nervous system start to get out of whack, things can start heading downhill pretty quickly.
Given the complexity and variability of dopamine pathways and signaling, it is absolutely miraculous that dopamine-related disorders aren’t more common. There are many different signaling pathways that each contain different chemical interactions that illicit responses. Specifically, the Atk-GSK3 pathway is of great importance. Disruptions in this pathway have been linked to the development of disorders such as schizophrenia, bi-polar disorder, depression, Parkinson’s disease, and many others.
In the grand scheme of things, chemical reactions occurring at the molecular level seem minuscule compared to the implications that arise from a disease like Parkinson’s or schizophrenia. However, if we wish to treat these disorders to the best of our ability, we need to focus on the underlying mechanisms that produce the effects we see. Completely understanding these pathways will hopefully allow us to treat these disorders in the most optimal way and possibly even provide methods of curing diseases that have previously been incurable. Research continues to uncover more and more information about dopamine and other important neurotransmitters, and it is crucial that we keep funding and supporting this type of research.