Cobbers on the Brain

Endocannabinoid signaling is the signaling that mediates the affects of cannabis (marijuana). The ethical question here is whether or not marijuana should be legalized as a medical treatment or not. Endocannabinoid signaling occurs throughout the body, and mediates many different types of functions in the body. When this signaling is active, it is known to increase appetite, improve memory, and induce sleep. So why not have marijuana legalized as a medical treatment? Marijuana stimulates the endocannabinoid system and can have all of these positive effects on the body. For example, someone who has had cancer and has lost a significant amount of weight. They are now cancer free and trying to recover. If the stimulation of endocannabinoid signaling can increase their appetite and help them gain weight, wouldn’t it be a good treatment? Medical marijuana can be used to treat all sorts of different diseases/ailments, but it should be legalized for the specific situations it would be helpful in. I know there is a lot of ethical questions surrounding the legalization of marijuana as a medical treatment, but wouldn’t it be helpful to have it legalized as a medical treatment for special cases?

Dopamine is a neurotransmitter that is normally found in the brain. It plays a large role in the body’s mechanisms for reward, motor control and motivation. Dopamine can also be given as a supplement to treat many different things. Dopamine has many effects throughout the body, including in the immune system, in the digestive system, and in the renal system. Because dopamine cannot cross the blood-brain barrier, dopamine given supplementally will not have any affect on the brain chemistry. A good example of dopamine as a treatment is in a person who does not produce enough dopamine in their kidneys. These people will generally have high blood pressure and reduced sodium excretion in the urine. If these people are supplemented with the correct dosage of dopamine, their blood pressure problems can be alleviated. Who knew dopamine had so many affects outside of the brain?

Bipolar disorder is characterized as a mental illness in which a person exhibits episodes of mania followed by episodes of depression. Between those episodes, the person may also have a mixed version where mania and depression are exhibited at the same time. People with a more severe form of bipolar disorder may show signs of suicide during their depressive states and make impulsive decisions when they are in their manic state. Many people with bipolar disorder are misdiagnosed with schizophrenia because their symptoms are seen as psychotic. Mental illnesses have a heavy stigma in our society. Whether you are talking about eating disorders, depression, or any other mental illness, the stigma in our society just makes it more difficult for the person suffering with the mental illness to live their life and eventually recover. People need to have a better understanding about mental illnesses in general. Mental illnesses are not something that the person can control. It is very difficult for the person to change their (sometimes abnormal) behavior, and requires treatment and psychotherapy. If people had a better understanding of mental illnesses, they would not judge mentally ill people the way they do. Sometimes all the person needs is a little bit of understanding and someone kind to talk to. The stigma in our society should be changed for the better of everyone in the community.

Throughout the week of November 10^th, my neurochemistry class and I learned about and discussed a topic that is currently very prevalent in the United States. The topic we discussed is obesity and whether or not it can be considered a brain disease. Throughout the United States, many people are considered to be overweight and many of these people are considered to be obese. Severe health consequences are associated with obesity such as, increased risk of type II diabetes, heart disease, and strokes, so it important for people to keep their weight in check and also the types of food they are consuming. Recent research has been carried out in order to determine if the brain is involved in the pathogenesis and perpetuation of obesity. Throughout this blog, I will hopefully effectively explain how the brain is actually involved in obesity.
Overnutrition or overeating is a biological trap and it is not simply a willful choice. This means that is not an individual’s choice of how much they eat. Their brain elicits a response that causes them to eat more and thus experience obesity. Eating a diet that is high in fat disrupts the blood brain barrier in the hippocampus exposing the brain tissue to potentially damaging circulating factors that cannot normally interact with brain cells. Chronic high fat intake can lead to inflammatory changes in the brain cortex, which is evidenced by high concentrations of nicotinamide adenine dinucleotide phosphate (NADPH). Along with having structural changes in the brain during periods of high fat intake, there are other affects that overnutrition has on the brain.
It has also been determined that overnutrition has important implications in the hypothalamus by inducing inflammation and dysfunction of the hypothalamus. In response to a high fat diet, proinflammatory cytokines, such as TNF-α and interleukin-1 beta, were shown to be released and activate apoptotic signaling in the hypothalamus. Proinflammatory cytokines play important roles in the immune system by inducing inflammation, so the release of them in the hypothalamus causes inflammation within this region of the brain. Inflammation causes the depletion of neuronal cells in the hypothalamus and can lead to cognitive dysfunction. Inflammation can also lead to dysfunction in metabolic processes that include neural and endocrinal regulation, such as energy balance, glucose metabolism, and cardiovascular homeostasis. Hypothalamic inflammation also affects insulin release and action. It causes a disruption in normal insulin sensitivity and reduced peripheral insulin sensitivity.
Sleep deprivation has also been determined to play a role in the spread of obesity. Sleep deprivation in normal weight adults leads to increased overall neuronal activation in response to food. Obesity also interferes with normal sleep, most commonly by causing sleep apnea and daytime sleepiness. Regarding obesity and overnutrition, it is important for a person to get an adequate amount of sleep.
Since obesity and overnutrition is so prevalent in the United States today, it is important to know and understand the negative affects that they have on the brain. Obesity does much more than just cause a person to be unhealthy. It has important implications in the brain and can induce cognitive dysfunctions. The cognitive dysfunctions often come in the form of inflammation of the hypothalamus that has a variety of negative affects throughout the brain. Overall, it has been very interesting learning about obesity and its affects in the brain.
 

Throughout the week of November 3^rd, my neurochemistry class and I learned about and discussed an important treatment that has been utilized to treat bipolar disorder for over half a century. The particular treatment that we explored is lithium. Along with having neuroprotective effects against bipolar disorder, it has also been discovered that lithium reduced cognitive deficits in other neurodegenerative diseases such as, strokes, amyotrophic lateral sclerosis, fragile X syndrome, Huntington’s disease, Alzheimer’s disease, Parkinson’s disease, and many others. Within the body, lithium performs a variety of mechanisms which it utilizes in order to reduce the symptoms associated with the many different neurodegenerative diseases that I just mentioned. Throughout this blog, I will try to explain these complex mechanisms as effectively as possibly in order to help you understand them.
Lithium is a monovalent cation that has been the standard pharmacological treatment for bipolar disorder for over 60 years. It is often used in conjunction with mood stabilizers, antidepressants, and antipsychotics in order to reduce the symptoms associated with numerous neurodegenerative diseases. Lithium has a narrow therapeutic range and outside of this range a patient can experience minor to severe side effects, so it is important to monitor the dosage that a patient takes. Several minor side effects occur at lithium levels ranging from 0.6 to 1.2 mEq/L. Symptoms that occur at lithium levels above 1.5 mEq/L are generally mild and include tremor, nausea, diarrhea, vertigo, and confusion. At lithium levels above 2 mEq/L a patient will experience severe symptoms such as, seizures, coma, cardiac dysrhythmia and permanent neurological impairment at lithium levels greater than 2.5 mEq/L.
When a patient is given the correct dosage of litium, it carries out a variety of mechanisms in order to display many neuroprotective effects on the brain. As a class, we came to the conclusion that the inhibition of GSK-3 was the most important pathway that lithium carries out. GSK-3 is a serine/threonine protein kinase that is mediator of signaling pathways and is involved in a variety of cellular functions. GSK-3 activity is regulated by a wide variety of kinases and systems including Akt, protein kinase A, protein kinase C, MAP kinases, and the Wnt pathway. Lithium inhibits GSK-3 by phosphorylating it at the 21/9 serine residue. Another important aspect of the inhibition of GSK-3 is the stabilization of β-catenin. In response to the inhibition of GSK-3, the levels of β-catenin increase, which is a novel therapeutic strategy for treating mood disorders.
The inhibition of NMDA receptor-mediated signaling is another important mechanism that plays a role in the treatment of bipolar disorder by lithium. Glutamate induced excitotoxicity has been found to be an important contributor to bipolar disorder. It has been determined that lithium significantly reduces excitotoxicity, which in turn reduces the symptoms associated with bipolar disorder. Along with reducing excitotoxicity that is induced by glutamate, lithium also reduces excitotoxicity that is induced by calcium by inhibiting the entry of calcium into NMDA receptors.
As you can see, lithium is a very important treatment for bipolar disorder as well as many more neurodegenerative diseases. It affects a variety of different pathways and mechanisms in order to reduce the symptoms that are associated with the disorder. I have very little previously knowledge of bipolar disorder and how it is treated, so it was interesting learning about it and how lithium can be used as a treatment.