Stress and anxiety are part of life—but while a little bit of stress (good stress) may keep us active and alert, and sometimes even motivate us, the long-term type (bad stress or chronic stress) can have negative effects on our health. Chronic stress “is the grinding stress that wears people away day after day, year after year. Chronic stress destroys bodies, minds and lives. It wreaks havoc through long-term attrition. It’s the stress of poverty, of dysfunctional families, of being trapped in an unhappy marriage or in a despised job or career. Chronic stress comes when a person never sees a way out of a miserable situation. It’s the stress of unrelenting demands and pressures for seemingly interminable periods of time. With no hope, the individual gives up searching for solutions.” Broadly speaking, chronic stress can be mentally visualized as the perception of environmental demands that are believed to exceed one’s resources for adapting to the situation.
Image credit: Bernard Goldbach, CC BY 2.0
Chronic stress leads to the development of so-called “stress-related disorders.” Elevated blood pressure, heart disease, psychological impairments and depression are just some examples of these disorders. Scientists have known for years that chronic stress influences the inflammatory response—our first line of defense against infectious microbes. It is the inflammatory response that, in turn, may worsen heart disease, increase the risk of heart attack and stroke, and lead to cognitive disorders— those that affect learning, memory, perception, and problem solving.
Now, results from a new study show that chronic psychosocial stress promotes short-term memory loss. The study (Neuroinflammatory Dynamics Underlie Memory Impairments after Repeated Social Defeat), published a few days ago (March 2, 2016) in the Journal of Neuroscience, was carried out using a mouse model known to recapitulate the key physiological, immunological, and behavioral changes that humans undergo when exposed to chronic psychosocial stress.
For the study, mouse were exposed to repeated social defeat stress: non-aggressive mice were repeatedly subjected to bouts of social defeat by a larger and aggressive mouse placed in the same cage. The results show that mice that were repeatedly exposed to the aggressive intruder had a hard time recalling where the escape hole was in a maze they had mastered prior to the stressful period. Jonathan Godbout, senior author of the study, said in a press release: ““The stressed mice didn’t recall it. The mice that weren’t stressed, they really remembered it.”
Repeated social defeat stress promoted inflammation in the hippocampus, a region of the brain involved in the formation, organization and storage of new memories. Presence of inflammation was characterized on the basis of proinflammatory gene expression, monocyte trafficking, and activation of microglia. Microglia are the primary immune cells of the central nervous system, and are highly similar to peripheral macrophages. John Sheridan, one of the study co-authors, said in the press release: “Stress releases immune cells from the bone marrow and those cells can traffic to brain areas associated with neuronal activation in response to stress. They’re being called to the brain, to the center of memory.”
Minocycline, an anti-inflammatory agent and purported microglia inhibitor that was given to the mice, prevented memory loss and recruitment of monocytes. The study authors conclude that, together, their findings open up possibilities for novel immune interventions in the treatment of cognitive and mood disturbances
The sympathetic system of our body mediated by cortisol and catecholamines produces a stress response to our brain to instantly alert us of danger and undergo allostasis – a means to achieve stability through change. Acute stress can indeed have its positive effect in our overall well-being but an allostatic load, a repeated stress or chronic stress, can dramatically affect our health. Not only does prolonged stress cause the activation of microglia but also inflammation of the hippocampus is the major issue in short-term memory loss. The psychological comparison of the mouse model and human in this study in response to stress is primarily due to the function of the hippocampus when inflamed. A study demonstrated how stress acts on neurogenesis by causing a rapid and prolonged decrease rate of cell proliferation of the hippocampus. But if the hippocampus is responsible for the formation of new memories, how come older adults tend to have more memory loss than teenagers or younger adults? How would the same exposure to stress be different in elders and young adults? The same study experimented on rats suggest that adrenal steroids, primarily glucocorticoids responsible for calcium homeostasis in the hippocampal neurons, are less responsive to negative feedback regulation due to aging. Young adults, however, have a natural mechanism that regulates the glucocorticoid feedback by reducing its signal. We cannot only implement immune interventions but hormone regulations as well when it comes to age differences and how our body function, as we get older.
http://www.sciencedirect.com/science/article/pii/S0197458002000271
You pose an interesting research topic of evaluating stress responses in both elders and young adults. The decreased negative feedback regulation in older individuals was a great explanation to this topic. However, it would be interesting to determine the effects of diabetes, a chronic disease that influences large percentages of our population in people of all ages. In particular, this disease results in hyperglycemia which, when left unmanaged, can cause detrimental effects on the vascular system. In the article, “Low-Density Lipoprotein Postsecretory Modification, Monocyte Function, and Circulating Adhesion Molecules in Type 2 Diabetic Patients With and Without Macrovascular Complications” the authors determine that there was an increase in IL – 1 beta secretions and monocyte adhesion to endothelium. If examined further, research could potential gage whether diabetes induced monocyte adhesion could play a role in the increase likelihood of monocyte trafficking within the blood brain barrier.
S. Devaraj, PhD; I. Jialal, MD, PhD. “Low-Density Lipoprotein Postsecretory Modification, Monocyte Function, and Circulating Adhesion Molecules in Type 2 Diabetic Patients With and Without Macrovascular Complications.” http://circ.ahajournals.org/content/102/2/191.short
In your primary response TBui you mention how acute stress can have a positive effect in our overall well-being. That to me was interesting in the fact that I didn’t know that acute stress could be beneficial. I thought any kind of stress always had negative impact on us physically and mentally. To expand on your statement I did some research on this idea and there seem to be a good amount of evidence that supports the idea that acute stress can not only be a positive but a positive for our immune system. One acute stress study conducted by researchers involved mice. Type IV hypersensitivity also known as delayed hypersensitivity tension is a reaction that is known to be antigen specific and a cell mediated immune response. Mice that went under acute stress before being exposed to antigen had enhance delayed hypersensitivity tension of the skin. The study also showed that acute stress can impact leukocyte mobilization. Acute stress can lead to significant mobilization of leukocyte to areas infections. In another study involving rats that were under acute stress, researchers found that the stem cells in the brains of these rats became nerve cells. Once the nerve cells mature within a couple week, the mental performance of these rats were noticeably better. Results from these studies can help alleviate the common notion that stress has immunosuppressive function.
http://www.ncbi.nlm.nih.gov/pubmed/11268419
http://news.berkeley.edu/2013/04/16/researchers-find-out-why-some-stress-is-good-for-you/
Just to further expand on Patrick Nguyen’s statement about stress not only being immunosuppressive but also that it can be immune-protective. Most of the benefits of short-term stress is sometimes overlooked and in a research done, it was discovered that mice subjected to acute stress and then immunized had enhanced immune response after re-exposure. This research further elaborates on the positive effects of short-term or acute stress on people’s lives. Acute stress experienced before immunization can induce a long lasting increase in immunologic memory. And this is important in that it increases the effects of both T and B memory cells to respond to secondary exposures. Enhancement of immunological response could be of great significant especially in vaccine development. So basically stress is not the underlying problem but that lack of management of stress could be detrimental. And that continuous exposure to the stressor just like the mice in the blog post above can negatively affect both the behavior, neurological and immune response.
http://ajpregu.physiology.org/content/289/3/R738.short
As a person who suffers of diagnosed stress induced generalized anxiety disorder, I was very relieved to read an article on a study performed in an effort to actually address, rather than simply control, the physical and psychological issues brought about by stress and anxiety. Nowadays doctors send patients home with a selective serotonin reuptake inhibitor (SSRI) that functions to block the reuptake of serotonin levels and call it a day. If the patient returns to the doctor complaining that the medication did not work, the doctor prescribes the patient with yet another SSRI, ultimately with the same function. Weeks pass and patients begin to feel calmer, less irritable and less restless. However, the problem is only solved as long as the patient remains on the medication.
This study conducted an experiment that revealed that stress induced mice displayed inflammation of the hippocampus, which resulted in monocyte diapedesis and the activation of microglia, which caused short-term memory loss. A possible solution for short-term memory loss was proposed using an anti-inflammatory agent and a microglia inhibitor. Based on my background knowledge, I know that microglia function to protect neurons from damage and infiltrating pathogens, ultimately acting like the brain’s macrophages. A study revealed that the activation of microglia at early stages of Alzheimer’s disease has proven to protect neurons. With microglia being the first line of defense of the brain, I am curious to know if using a microglia inhibitor would cause more harm than good? Would the benefits outweigh the consequences? It sounds like a matter of picking and choosing battles.
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3699675/
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3277080/
As it appears, Solito and Sastre and Xiang et al. have something in common. They believe that Alzheimer’s disease may be caused by an over inflammatory response in the brain. But as Solito and Sastre stated in their original article, it is until an older age when this occurs. So I am wondering, could chronic stress be the fine line between over activation of microglia and the initiation of Alzheimer’s disease? Chronic stress can last for years, and the older individuals get, the longer their chronic stress can last. Some of the sources for chronic stresses in the elderly include income reduction, being a caregiver to their partner, losing their spouse, moving into a nursing home, etc. I wonder if this longer term of stress is also interfering with glucocorticoid feedback as TBui mentioned above. If so, it seems as if chronic stress is attacking the hippocampus from multiple angles: via the immune system response and by over production of glucocorticoids which have been shown to cause hippocampus atrophy. These affects would in turn lead to memory loss.
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3277080/
http://www.ncbi.nlm.nih.gov/pubmed/16410654
http://www.medicineonline.com/articles/s/2/Stress-and-the-Elderly/Stress-and-Seniors.html
http://archpsyc.jamanetwork.com/article.aspx?articleid=481654
I was also curious of how blocking microglial cells would prevent memory loss as microglial cells are important in fighting bacteria and viruses of the brain. Microglial constitutes about 10-15% of cells in the brain, primarily immune cells more than nerve cells themselves. An article published by Stanford University School of Medicine brought up the relationship of microglial function to Alzheimer’s disease. The main contribution to Alzheimer’s is the buildup of A-beta – clusters of proteins that turns to soluble molecules that becomes highly toxic to nerve cells. The job of microglial is to clear off the accumulation of A-beta to prevent toxicity/inflammation of the nerve cells. Without proper functioning of the microglial, toxic inflammation occurs and can lead to Alzheimer’s. So from this article proposing the affects of inhibiting microglial to prevent memory loss, what about the prevention of Alzheimer’s disease if the microglial are inhibited? What other cells in the immune system might be able to take over the responsibility of microglial function in “garbage collecting” debris of the brain?
http://med.stanford.edu/news/all-news/2014/12/blocking-receptor-in-brains-immune-cells-counters-alzheimers.html
Although my previous blog states that a study was conducted in which the activation of microglia during early stages of Alzheimer’s disease seemed to function as a defense mechanism, I would not doubt that prolonged stress over a long period of time could lead to the over activation of microglia and the beginning of Alzheimer’s disease. A study was conducted to prove that chronic stress disrupts the glucocorticoid negative feedback system, which in turn alters the limbic system resulting in stress-related disorders such as depression and PTSD. So now we know that the limbic system is also taking part in these stress-induced disorders. As you mentioned, Juan, chronic stress seems to be attacking the hippocampus from multiple angles! One factor leads to another. Although stress is often times inevitable due to the fast paced world we live in, I wonder if maybe creating a drug that functions to maintain the glucocorticoids in balance could perhaps help avoid stress-related disorders?
http://journal.frontiersin.org/article/10.3389/fnbeh.2013.00061/full
I believe that the inhibition of microglia cells will do more harm than good, as you’ve mentioned earlier, microglia cells function to protect the brain damage from macrophage as well as phagocytizing debris. Many articles I read mentioned a correlation between chronic stress and Alzheimer’s disease. Many students especially pre-professional students go through stress on a year round basis especially when enrolled in a summer class and I was wondering whether this will makes us susceptible to the disease.
Although pre-professional students at a young age may not show signs of memory loss due to coping of the stress from cortisol hormone, age might actually change this by having a negative effect on our body if students to continue to have long-term stress. As we age, our body system becomes weakened and most of our body’s organ will begin to function less than when we are at our younger age. A study done from the University of Iowa suggests that cortisol helps us cope with stress but not for long-term stress especially as we age. Their findings suggest to decrease memory loss by decreasing the amount of cortisol in the body for those who are susceptible to memory loss.
http://now.uiowa.edu/2014/06/stress-hormone-linked-short-term-memory-loss-we-age
You guys do have a point there. Blocking microglial cells completely might be more detrimental than anything. Not only will you have a suppressed innate immune response in the brain, but there will also be an accumulation of toxic materials and cellular debris. However, an over accumulation of microglial cells in the hippocampus, which can lead to memory loss, was seen in the hippocampus of postmortem brains of Alzheimer’s patients. Similar results were seen in the mice of the original post. Mice with repeated social defeat stress showed signs of inflammation in the hippocampus. One of the cells that was involved in the inflammation of these mice was the microglial cell. If we could limit this hyperactivity, just like we do with allergic reactions, the inflammatory response that targets the hippocampus involving microglial cells can be reduced. This might lead to an over accumulation of the A- beta molecules. However, what if we rely on chemistry to remove the A- beta molecules rather than other cells? The article that you posted, TBui, also mentioned that A- beta molecules are actually abundant, and become dangerous when they clump together. If we can prevent this clumping, we can stop its toxicity in the brain. I am thinking of a system that flushes the brain from these chemicals. Just like alcohol crosses the blood brain barrier to reach our brains and then eventually exits in urine, we can come up with a system that traps the A- beta molecules before they clump, carries them out of the brain through the blood brain barrier, and eventually out of our bodies as urine. By decreasing the hyperactivity of microglial cells and accumulation of A- beta molecules in the brain, the hippocampus will remain healthy, and it will reduce memory loss. Of course, this is all hypothetical.
http://www.ncbi.nlm.nih.gov/pubmed/16410654
As we know, the immune system is set up to protect its host from infections and cancerous cells. It can be viewed as a personal army. However, there are cases where the immune system may be more damaging to the host than it is helpful such as in autoimmune diseases. Autoimmune diseases occur when cells of the immune system attack healthy cells of the host. Rheumatoid arthritis, celiac disease, and multiple sclerosis are a few examples of autoimmune diseases. In general, the inflammatory response initiated by cells of the immune system can inevitably damage healthy host cells. In the presented study by McKim et al., inflammation in the hippocampus caused by repeated social defeat stress led to spatial memory loss in mice. Inflammation of the hippocampus in these mice was characterized by activation of microglia, monocytes migrating to brain, and proinflammatory gene expression. Can stress really cause inflammation in the brain? In a different study, Xiang et al. used Human Leukocyte Antigen- DR immunochemistry to detect microglia activation in postmortem brain sections of individuals with Alzheimer’s disease. As in the mice, there was an increase of microglia activation in the hippocampus. This inflammation could be causing the memory loss and spatial disorientation that characterizes Alzheimer’s disease since the hippocampus is associated with memory storage including spatial memory. In fact, research has linked stress as a contributing factor to Alzheimer’s disease. The information provided by Xiang et al. and McKim et al. can open doorways to new therapeutic approaches for treating Alzheimer’s disease. For example, safe microglia blockers could be developed to slow down or even reverse Alzheimer’s disease. These microglia blockers could also be accompanied by behaviors that are known to reduce stress in the Alzheimer’s patients such as daily meditation. However, there can be consequences for this form of treatment. By blocking microglia, the central nervous system can be more easily hijacked by pathogens, but antibiotics, antivirals, and other cells of the immune system can help in these situations.
http://www.ncbi.nlm.nih.gov/pubmed/16410654
It’s remarkable to see how a system meant to protect us in a specific manner, unknowingly harms what it’s guarding. Reading the study, I too, perceived the effect of repeated social defeat as an autoimmune illness. Autoimmune illnesses have the capability of causing rheumatoid arthritis, psoriasis, and even irritable bowel disease. Most interesting, is a study that shows autoimmune disorders causing neuropsychiatric issues. Neuropsychiatry focuses on mental illness accompanied by brain disease. Lupus, an autoimmune disease that can cause inflammation anywhere in the body, presents with neuropsychiatric symptoms. These symptoms include cognitive dysfunction, like confusion and mood changes, and depression. The causative factor is inflammation in the central nervous system, primarily because of cytokines released by the microglia in the brain. The relationship between the immune system and the brain is deeper than we thought. Also, the immune system is not as strict and rigid as we may perceive.
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC4302271/
http://www.pni.org/neuropsychiatry/
http://www.mayoclinic.org/diseases-conditions/lupus/basics/definition/con-20019676
Alzheimer’s disease is another scientific mystery. There are generally two types of Alzheimer’s, Early onset and late onset. Typically in early onset, scientist suggest in most cases patients caused by an inherited change in genes, different single-gene mutations on chromosomes 21, 14, and 1. The mutations on the chromosomes cause abnormal proteins to be formed which can trigger early onset Alzheimer’s. In the late onset, the cause is generally unknown but scientist speculate that indeed inflammation of the hippocampus and other immune overreactions can lead to this disease, but other factors of environment and genetics can predispose an individual to Alzheimer’s disease. Stress is a very important angle to finding out the cause of many diseases because simply when your brain is overworked and an increase of chemicals is released, something is bound to malfunction and cause disease.
The article is very intriguing as it combines phycosocial/psychological and biological evaluation to determine the cause of short term memory loss. As stress is a chronic disorder that plagues many individuals in our society, it is interesting to consider its contribution to the actual mechanism of short term memory loss presented in the article. The primary research article attributes this short term memory loss to neuroiflammation of the hippocampus, it even goes further as to provide three characteristics with which inflammation was evaluated. These characteristics include presence of proinflammatory gene expression, microglia activation, and monocyte trafficking (diapedesis). Futhermore, minocycline, an anti-inflammatory, was shown to decrease microglia activation and monocyte recruitment, thus decreasing the negative effects of stress on the hippocampus. As a result, the authors suggest the implication of immune system intervention for treatment of cognitive and mood disturbances.
In the article, “A novel chronic stress-induced shift in the Th1 to Th2 response promotes colon cancer growth” the authors determine that chronic stress cause a shift in Th1 immune response to Th2 immune response, is related to the development of cancer. The idea is that a decrease in Th1 immune responses will decrease the activity of cytotoxic t-cells, which play a primary role in apoptosis of cancer cells. Do you think that this stress induced shift from Th1 to Th2 could also increase nueroinflammation in the brain either through primary or secondary measures? If so, how exactly would you combat this shift and restore the th1/th2 balance?
Hou N1, Zhang X, Zhao L, Zhao X, Li Z, Song T, Huang C. “A novel chronic stress-induced shift in the Th1 to Th2 response promotes colon cancer growth.” Biochemical and Biophysical Research Communications. Volume 439, Issue 4, 4 October 2013, Pages 471–476. http://www.sciencedirect.com/science/article/pii/S0006291X13014599
Russell Puckett,
It’s a well known fact that Tcells can be both cancer promoters and suppressors. But I did not know that the actual ratio of Thelper cells 1 and 2 is a factor among this concept. I also don’t know the answer to your question if a change in the ratio would cause more inflammation in the brain. Your second question, returning the ratio back to normal, could possibly be answered through articles about pregnant women. I say this because this imbalance of Th1 and Th2 happens during pregnancy as well, and can also promote or harm the process of fetal development (1). Maybe a similar pathway to rebalance Th1 and Th2 levels that a mother’s immune system takes can be applied to cancer patients. However, My actual response to your post is about a similar imbalance of a completely different molecule, macrophages. It was presented in a study that just like Tcells, macrophages can be divided into M1 and M2 groups as well (2). Interestingly enough, if this ratio is thrown off, M1 cytokines have a tumor-supressing effect while M2 cytokines have a tumor-promoting effect. A key difference between macrophages (class 1 and 2) and Tcells (class 1 and 2) is a macrophage’s class is decided by a physical characteristic and not by differentiation from a naive precursor like Tcells. Therefore, Tcell class is pre-determined and permanent. So an interesting question to this whole “class 1 or 2” concept that macrophages raise is that once a macrophage is deemed class 1 or 2, does it die after doing its job similarly to Tcells or become naive again to perform other functions? This question is unanswered due to the lack of long-term experiments, but if macrophages perform some type of mechanism that evens out that classes this concept could be similar to Th1 and Th2 balancing back out.
1. http://www.ncbi.nlm.nih.gov/pmc/articles/PMC1905376/
2. http://www.ncbi.nlm.nih.gov/pmc/articles/PMC4201108/
According to the article, there were 3 means of characterizing inflammation namely; based on proinflammatory genes, activation of microglia cells and monocyte trafficking to the brain. Inhibition of monocytes to the brain could also be a technique to reduce neuroinflammation as it works in a cycle with microglia cell activation. Some immune cells typically APC’s secrete the chemokine CCL2 (Chemokine C-C motif ligand 2) which calls in monocytes to the brain and plays a part in neuronal degradation. It was discovered by Mark Swain and colleagues that blocking the signaling of CCL2 (probably by blocking its CCR4 or CCR2 receptors) led to the inhibition of monocyte entry into the brain thus less inflammation. It was also discovered that inhibiting TNF-α also led to the down-regulation of CCL2 and less monocyte entry into brain. In my opinion, learning about the mechanisms behind stress and inflammation is extremely important but the immune response is as a result of the psychosocial stress i.e. stress is the core of the problem. It would make sense to try to get rid of the main problem and have these chemokine inhibitory methods when that is not possible.
http://www.natap.org/2009/HIV/031009_07.htm
http://www.ncbi.nlm.nih.gov/gene/6347
I have to agree with you that chemokine inhibition is another method for treatment especially inflammatory cytokines and chemokine. An article I found also studied a similar chemokine like CCL2 that you mentioned called MIP-1α/CCL3 and its function in hippocampal synaptic transmission, plasticity and spatial memory. CCL3 is a hippocampal neuromodulator involved in learning and memory function that showed memory impairment when the researchers injected CCL3 to lab rats. I believe not only inhibiting chemokine to improve spatial memory, we should also focus on inhibiting inflammatory cytokines as well. However, I wonder if it is safe to inhibit both mechanisms at the same time and how it would affect the immune system if inhibited long term.
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC4625372/
It’s sad to see that the increasing expectations to excel and become more efficient has induced psychological problems in individuals. More and more adults are sacrificing their health due to their chronic stress. It’s not only the adults who suffer, either. Studies have shown the stress that parents suffer affects their children in varying degrees. As explained, many consequences arise from continued chronic stress over time. One consequence being the inflammation of the hippocampus. However, the hippocampus is not the only area that is affected by stress-induced immune reactions. Stress indicates to the body that the immune system should prepare to act. Chronic stress leads the immune system to be perpetually active to some degree. This is evident by observing the presence of cytokines in overly stressed individuals.
While it’s important that the symptoms exhibited by chronic stress are addressed by administering medication, the bigger picture must also visualized in order to fully fight this phenomenon. I believe that it’s impossible to approach the problems that chronic stress introduces without studying the reasons as to why some people seem to handle stress better than others. If a correlation is found in people who are more tolerant of chronic stress, then maybe it’s possible that this correlation can be used to prevent health problems before they become apparent. A relevant study has been done on mice where the relationship between the amygdala and the prefrontal cortex was observed. It turns out that there is more activity between the two brain areas in mice more prone to chronic stress. This information magnifies the need for further studies on individual tendencies to succumb to chronic stress. It could be that there is a correlation that parallels the one found in the mice. It could also be that the immune systems of more stress-tolerant people are better able to determine the degree to which a response should be taken. For now the possibilities are endless.
http://www.apa.org/monitor/2011/01/stressed-america.aspx
http://www.usatoday.com/story/news/nation/2014/07/29/study-underlying-cause-stress/13321593/
You bring up an excellent point when you say that some individuals tolerate stress better than others. Although we do realize that this is a major factor to take into consideration, finding a common solution to stress is simply not reasonable. Stress does not solely stem from present day challenged, but also from previous experiences. Perhaps someone lived a rough life growing up in low socioeconomic environments where they maybe saw or experienced things as a child that shouldn’t be seen at such a young age or perhaps someone suffers of PTSD from a traumatic event that occurred earlier in a person’s life, the list is endless! Causes and severities of stress cannot be generalized. Every person has their own story that help shape who they are. Traumatic events can often times also affect memory. A study was conducted where victims of sexual abuse were interviewed 12-21 years after the abuse took place. They their found that individuals with PTSD remembered abuse accurately due to the networks formed in the brain as a result of chronic stress. These memories can also lead to long term stress. With that being said, the study you mentioned analyzing the correlation between the amygdala and prefrontal cortex, two key players in the limbic system, seems to be a great start to begin to address this issue! Because the limbic system regulates behavior and also functions to determine emotion, it may be a good idea to expand this idea and analyze the structures of the limbic system to determine which structures are impacted by particular stressors. Perhaps this could open doors to new medication that can target these affected areas to help control stress and ultimately the inflammation that lead to a plethora of problems.
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2917081/
Chronic stress has become a greater concern because there are more and more people being affected from chronic stress than before. It takes a toll on the immune system through inflammation, which can affect the rest of the body, including the brain. Ultimately, chronic stress degrades you bit by bit, and taking a cycle of medications will not help cure it. It is great to see how many studies have come out and focused on the immune part of the chronic stress, and one word caught my eye – minocycline. It seems that this is the cure for test animals when undergoing stress. Therefore, by constantly testing minocycline in various ways, there is a great possibility that minocycline is very safe to be used in humans.
Similar to the primary article, this study is based on microglial activity and minocycline, a microglial activity inhibitor. In this study, scientists took de-stressed rats and reconstructed the microglial structure in their medial prefrontal cortexes to determine whether activity would increase. As predicted, the microglial activity was increased significantly. After giving a dose of minocycline, the microglial activity had slowed down the activity of the microglial activity, thereby reducing stress significantly.
Although increased inflammation was not observed, there was an increased expression in beta1-integrin, which is a key protein in microglial activity. If scientists could make drugs that would target microglial structure and function in chronic stress patients, then there would be significant decrease in the number of patients over the next several years, possibly even within the next decade.
https://cercor.oxfordjournals.org/content/early/2012/06/16/cercor.bhs151.full
This article talks about the impact of chronic stress not only to our immune system but also its effect on short term memory. This is interesting because stress is found in most of people’s daily life’s and if left uncontrolled could become chronic and create a lot of problems that weren’t there before. Knowing how to prevent or learn how to manage chronic stress could help prevent most’s of the problems stress is associated with. Although this article mentions about the negative impact of chronic stress on memory, a research done on mice found that coupling of exercise and stress improved mice’s memory of what-where-when memory. A combination of both voluntary exercise and then followed by chronic stress treatment counteracted the effects of stress induced deficits in neurogenesis and behavior. Additionally, coupling of these two contributed to increase cell survival, neuron maturation and apoptosis in the dentate gyrus- a region of hippocampus that plays critical role in memory, learning etc. This is in contrast to what the article states and further shows us what role exercise places not only in our immune cells but also to our memory. And indeed, this could be a way to for instance manage chronic stress in our daily lives.
http://www.sciencedirect.com.ezproxy.gsu.edu/science/article/pii/S1074742713002499
The effects of stress can be overwhelming but I don’t always think that drugs are the way to treat everything. Exercise as a method to treat stress was addressed in the article by Peter Salmon’s Effects of physical exercise on anxiety, depression, and sensitivity to stress: a unifying theory. Exercise in combination with anti-inflammatory therapy may be the solution for addressing stress and short-term memory.
Salmon, P. (2001). Effects of physical exercise on anxiety, depression, and sensitivity to stress: a unifying theory. Clinical psychology review, 21(1), 33-61.
When first reading this article about the relationship shared by chronic stress and short term memory, the first thing that I thought about was a test-taking experience. I know a lot of people that stay up stressing all night before an exam, or maybe they lead stressful lives. Then when it is time to perform well and remember things for an exam they “blank out”. This type of activity is named test anxiety, however I’m questioning is if the loss of short term memory caused by chronic stress in this article is related to the chronic stress and anxiety of test taking? Does test anxiety along with chronic stress cause the inflammation of our memory compartment of the brain; the hippocampus? Does the short term loss of information gathered overnight for an exam align with chronic stress and anxiety?
Well research shows in the article below that chronic stress and anxiety damages the brain, specifically causing deterioration of the hippocampus in addition to the prefrontal cortex and an overactive amygdala. These effects can eventually lead to dementia. So similar to chronic stress, chronic test anxiety could also lead to short term memory loss, and the feeling of “blanking out”. Dementia is usually a disease that adults get later in life. Further questions would be is this chronic stress and test anxiety causing what I would term a “short term dementia episode” for students taking exams? In addition to that, because these short term episode are causing effects that aren’t 100% reversible, could the repetition of these episodes lead to a permanent diagnosis of dementia later in life?
It almost seems that stress and anxiety are one in the same. However, based on the second source below, in stress there must be a factor present, causing it. However with anxiety, even when the factor is not present, the body is still responding to that factor. Extended adrenaline amounts can also cause anxiety.
Sources: https://www.sciencedaily.com/releases/2016/01/160121121818.htm
https://www.healthstatus.com/health_blog/depression-stress-anxiety/how-is-anxiety-different-from-stress/