All Nonfiction
- Bullying
- Books
- Academic
- Author Interviews
- Celebrity interviews
- College Articles
- College Essays
- Educator of the Year
- Heroes
- Interviews
- Memoir
- Personal Experience
- Sports
- Travel & Culture
All Opinions
- Bullying
- Current Events / Politics
- Discrimination
- Drugs / Alcohol / Smoking
- Entertainment / Celebrities
- Environment
- Love / Relationships
- Movies / Music / TV
- Pop Culture / Trends
- School / College
- Social Issues / Civics
- Spirituality / Religion
- Sports / Hobbies
All Hot Topics
- Bullying
- Community Service
- Environment
- Health
- Letters to the Editor
- Pride & Prejudice
- What Matters
- Back
Summer Guide
- Program Links
- Program Reviews
- Back
College Guide
- College Links
- College Reviews
- College Essays
- College Articles
- Back
A New Approach To Alzheimer's Disease
Alzheimer’s Disease (AD) is one of mystery. Since its discovery in 1906 by Dr. Alois Alzheimer who studied a female patient suffering from an odd mental illness that included memory loss, language problems, and unpredictable behavior, scientists have been scratching their heads as to how this disease starts and why it can’t be stopped. Despite that AD was discovered over 110 years ago, it remains one of the most confusing and misunderstood illnesses that medical science has ever encountered. The statistics are frightening and depict a widespread, growing epidemic. Today there are an estimated 5.4 million Americans living with this disease, 200,000 of whom are under the age of 65. The number of people with Alzheimer’s continues to grow exponentially in spite of intense medical research. The current forecast is grim. By mid-century someone will develop AD every 33 seconds just in the United States. By 2050, unless there is a medical breakthrough, more than 16 million Americans will be afflicted with Alzheimer’s disease.
While there are countless numbers of researchers dedicated to finding what factors cause or trigger AD; how to cure it; or at least ameliorate its symptoms, to date no effective relief is in sight. In fairness, there are numerous drugs on the market that damp down the symptoms of AD, but they in turn, have the side effect of dumbing down the patient. Besides the mental and physical incapacitation experienced by the patient with AD and the emotional anguish of family caregivers, the financial effects are crippling. The average cost to tend to a person suffering from Alzheimer’s is roughly $60,000.
The following presentation concerning this tragic disease is based on current research, rationality untainted by pre-conceived notions and intimate, long-standing observation of a typical Alzheimer’s patient.
A Different Approach
The supposition underlying (the new approach of) The Originating Cause of Alzheimer’s Disease recognizes the very real (if overlooked) possibility that the corner stone of this disease is set well before there are any symptoms. Indeed, it is quite possible that this disease can be traced all the way back to a patient’s early life. Within that framework, therefore, the basis of this understanding necessarily includes viewing the afflicted person holistically, i.e., understanding that everything within the physiology, psychology and environmental factors of a particular human life is interrelated; and therefore is represented/expressed by the state of health of the whole entity. That viewpoint demands more extensive research than what is common in the usual professional assessment of Alzheimer’s where each person falls into a statistical classification.
The historic lifestyle of a patient is needed, that is, examining how a person experienced and lived life from the earliest years. This is relevant because the underlying theme of this presentation is that chronic stress and the toll it takes on the person (known as allostatic load) is the major contributing factor to the cascade of cellular dysfunction that ultimately results in AD.
First, we must define chronic stress. What is it? How does it affect us? If we look at that part of our nervous system known as the Autonomic Nervous System (ANS), we see that the ANS controls all of our involuntary processes, such as heartbeat, gastric secretion, breathing, etc. The Autonomic Nervous System is divided into two parts depending on its function. One side is the sympathetic nervous system (SNS) and the other, the parasympathetic nervous system (PNS). Their effects are opposite. One side causes relaxation, the other stimulation.
The SNS is well known to most; when in a heightened state of activation, it is otherwise referred to as the fight or flight response. The fight or flight response is an evolutionary process. Its main function is to enhance a particular being’s ability to survive in moments of peril. For instance, if you were being chased by a lion, you would rely on the automatic activation of your SNS to keep you alive.
It works by secreting adrenaline (epinephrine) through the organ known as the adrenal medulla. The adrenaline courses through the blood stream to rev you up to fight or flee. It also causes your heartbeat to race, your breath to become fast and shallow and a number of other processes that increase your awareness of the danger and pump you up for either battle or to provide the energy for an escape. Have you ever heard the stories about people lifting up cars to save their children or other super-human acts that save lives? Yes? Well that is all thanks to the activated SNS.
The body and the mind work together. When the mind determines that a situation is dangerous, the body responds by instant and appropriate activation of the sympathetic side of the ANS. The mind also registers when the danger is passed; in turn the body de-activates the flight or fight response. Normalcy returns and the person relaxes.
Our whole being (body/mind) is designed to thrive when activation of the SNS is sporadic, i.e., only rarely provoked in true life or death settings. The healthy scenario describes a being who is able to react to the fear quickly and then once the danger has passed to return to a state of calm or homeostasis. Balance between the two sides of the ANS is called homeostasis and describes an alert but relaxed entity.
Stress is the opposite of balance. It describes a continuously nervous person whose SNS is on heightened but inappropriate alert most of the time. That is, there is the perception of danger although it is non-existent, and this mis-perception can even be at an unconscious level.
Stress then can be said to be caused by fear, whatever the fear may be, losing your job, not being able to support your family, etc., or subtler underlying issues, such as feelings of inferiority. Realizing that stress and fear go hand and hand, with one there is another, it is true that the SNS is also wakened as a result of stress. In modern society, more than half of Americans claim to be chronically nervous or worried (stressed) which reveals the epidemic of constant activation of the SNS. In such prolonged or chronic activation of the SNS, the same chemicals course through the bloodstream as when a lion is chasing us.
Continuous activation of the SNS results in damaging effects to the entire body that greatly increases risk for heart attack, stroke, obesity, etc. The physiological consequences of chronic exposure to fluctuating or heightened neural or neuroendocrine responses that result from chronic stress is referred to as the allostatic load. As noted before, the allostatic load is simply the toll that chronic stress takes on the body. While chronic stress does have major, negative implications for the entire body, this presentation will focus on the brain as it impacts Alzheimer’s Disease.
Activation of the SNS results in stimulation of the Endocrine System. Continuous activation of the SNS stimulates the Endocrine system repeatedly. Relevant to this presentation, is that function of the Endocrine System known as the Hypothalamic-Anterior Pituitary Adreno-medullary axis (HPA). Activation of the HPA axis releases the stress hormone cortisol, which is a glucocorticoid (GC), a hormone designed to stop inflammation.
Understanding how glucocorticoids work also means understanding inflammation, diminutively speaking. Starting with a point of injury, maybe you closed your finger in a door. That initial point of injury ignites a sequence of events. The first event being the damaged cells of that area becoming stimulated. This stimulation activates a protein complex that controls transcription within the cells. This protein complex will than trigger genes in each of the cells to produce mRNA that will be translated for molecules that activate the inflammatory response. GC’s however, work by entering into the cells and inhibiting the protein complex activity, making it inactive. Therefore, stopping the leading up factors that trigger the inflammatory response.
In the case of chronic stress, the inflammation is the Endocrine’s System response to continuous perception of danger. GC’s can have many unhealthy side effects when released in abundance. Although the purpose of GC’s is to stop inflammation, when it is secreted by way of continuous SNS activation, the levels increase to the state of Endocrine Imbalance.
Higher than normal levels of GCs can cause major damage to the Immune System, including immune cells developing a tendency toward a chronic inflammation state. This effect is due to the cells actually becoming resistant to GC’s. Through an extremely complex set of events that even the best scientists do not completely understand, the cells build up a tolerance to the chemicals so they no longer have the desired effect, a sort of desensitization.
Normally, inflammation is a protective feature of the body that includes dilation of local blood vessels so as to allow an increased outflow of fluid and immune cells to the tissue surrounding the injury. This is the normal swelling/inflammation that is visible and temporarily a discomfort that resolves on its own. In some cases, though, inflammation is the disease. This occurs with the absence of injury only to continue without resolution as a side effect to heightened GC levels.
When researching inflammation and AD what you will find is an abundance of studies and research in the field of looking at how inflammation manifests after the diagnoses of AD. This is to say that most modern medicine is looking at inflammation as a result of AD, whereas this approach includes flipping the tables and looking at inflammation as the leading factor to the development of AD.
This “different approach” has been given merit in accordance with the fact of allostatic load. That is that heightened levels of GC’s cause a limited amount of neurogenesis (growth of new brain cells), an increase in cell apoptosis (death of cells), and an increase of atrophy to the hippocampus (one of the first parts of the brain that is affected by AD) via perpetual inflammation of immune cells. These factors which stretch from the initial inappropriate activation of the SNS all the way to the atrophy of the hippocampus can be encompassed by the term allostatic load, driving the conclusion of this unemphasized view that unceasing or prolonged inflammation without resolution in the brain leads to the development of AD.
Of course, when inflammation is called upon, it does serve a very necessary purpose. So what is the healthy way it is supposed to work? Say you drop a brick on your pinky toe. That causes damage to the tissue and possibly infection, as well as the vulnerability of some foreign entity invading the damaged tissue. White blood cells and other molecules then rush into the area, wall it off, and attack any invaders. This process causes the damaged area to become red, hot, swollen, and painful. After the fight has finished, clean up cells come in and gobble up the remains. Once the damage has been controlled the inflammation then subsides.
The unhealthy effects of this inflammation state include the collateral damage that is done, that is, a sort of friendly fire. The exact same process that got rid of foreign agents also kills good cells. While those cells die there is a trigger effect of further inflammation. For reasons that remain unclear, this sometimes provokes a vicious cycle of self-sustaining, cascading, and lethal damage.
Now take that information and apply it to the brain. This domino effect of pure destruction, if given the proper emphasis, could quiet possibly cause the first chemial imbalance of the brain, the initial hippocampal damage, the first indication of neuronal damage, and even the beginnings of the cellular dysfunction we see in AD patients. From this point of view, it appears that inflammation, at a chronic level, is in fact what encourages the development of AD, not what results from AD.
In Conclusion
Alzheimer’s Disease remains an unsolved puzzle. A slow but aggressive attack on not only one’s physical ability, but also upon the mental outlook as well as the spiritual component of a person. This disease is unmerciful in its attack which ends only with the final breath. Cruel and harsh indeed, although there is hope. Science and medical research grow with every single day and for this paper shall serve as the spark that lights the flame of further research in psychological issues relating to the physical world in depths that have never been considered.
The most weight for the devastating affliction of AD is placed on chronic stress. The motivation for writing this paper is to encourage a further examination of how psychological disarray can have major implications on the physical body, even resulting in diseases such as Alzheimer’s. While the focus has just been on chronic stress it is also important to recognize the specific diseases of depression, PTSD, bipolar disorder, etc. These all have similar consequences to the person and must be studied more closely.
References
Mcewen, B. "Allostasis and Allostatic Load Implications for Neuropsychopharmacology." Neuropsychopharmacology 22, no. 2 (2000): 108-24. doi:10.1016/s0893-133x(99)00129-3.
"Alzheimer's & Dementia Risk Factors | Alzheimer's Association." Alzheimer's & Dementia Risk Factors | Alzheimer's Association. Accessed December 29, 2016.
Chen, Hui, Shuai Liu, Lu Ji, Tianfeng Wu, Yong Ji, Yuying Zhou, Miaoyan Zheng, Meilin Zhang, Weili Xu, and Guowei Huang. "Folic Acid Supplementation Mitigates Alzheimer’s Disease by Reducing Inflammation: A Randomized Controlled Trial." Mediators of Inflammation 2016 (2016): 1-10. doi:10.1155/2016/5912146.
Clougherty, Jane E., Christina A. Rossi, Joy Lawrence, Mark S. Long, Edgar A. Diaz, Robert H. Lim, Bruce Mcewen, Petros Koutrakis, and John J. Godleski. "Chronic Social Stress and Susceptibility to Concentrated Ambient Fine Particles in Rats." Environmental Health Perspectives 118, no. 6 (2010): 769-75. doi:10.1289/ehp.0901631.
Cummings, J., and K. Zhong. "Trial design innovations: Clinical trials for treatment of neuropsychiatric symptoms in Alzheimer's Disease." Clinical Pharmacology & Therapeutics 98, no. 5 (2015): 483-85. doi:10.1002/cpt.190.
Danese, Andrea, and Bruce S. Mcewen. "Adverse childhood experiences, allostasis, allostatic load, and age-related disease." Physiology & Behavior 106, no. 1 (2012): 29-39. doi:10.1016/j.physbeh.2011.08.019.
García-Casal, J. Antonio, Andrea Loizeau, Emese Csipke, Manuel Franco-Martín, M. Victoria Perea-Bartolomé, and Martin Orrell. "Computer-based cognitive interventions for people living with dementia: a systematic literature review and meta-analysis." Aging & Mental Health, 2016, 1-14. doi:10.1080/13607863.2015.1132677.
Greulich, Franziska, M. Charlotte Hemmer, David A. Rollins, Inez Rogatsky, and N. Henriette Uhlenhaut. "There goes the neighborhood: Assembly of transcriptional complexes during the regulation of metabolism and inflammation by the glucocorticoid receptor." Steroids 114 (2016): 7-15. doi:10.1016/j.steroids.2016.05.003.
Juster, Robert-Paul, Bruce S. Mcewen, and Sonia J. Lupien. "Allostatic load biomarkers of chronic stress and impact on health and cognition." Neuroscience & Biobehavioral Reviews 35, no. 1 (2010): 2-16. doi:10.1016/j.neubiorev.2009.10.002.
Leurent, C., and Md Ehlers. "Digital technologies for cognitive assessment to accelerate drug development in Alzheimer's disease." Clinical Pharmacology & Therapeutics 98, no. 5 (2015): 475-76. doi:10.1002/cpt.212.
Mcgeer, Patrick L., Joseph Rogers, and Edith G. Mcgeer. "Neuroimmune Mechanisms in Alzheimer Disease Pathogenesis." Alzheimer Disease & Associated Disorders 8, no. 3 (1994): 149-58. doi:10.1097/00002093-199408030-00001.
Netzer, N., P. Werner, I. Jochums, M. Lehmann, and K. P. Strohl. "Blood Flow of the Middle Cerebral Artery With Sleep-Disordered Breathing : Correlation With Obstructive Hypopneas." Stroke 29, no. 1 (1998): 87-93. doi:10.1161/01.str.29.1.87.
Rabasa, Cristina, and Suzanne L. Dickson. "Impact of stress on metabolism and energy balance." Current Opinion in Behavioral Sciences 9 (2016): 71-77. doi:10.1016/j.cobeha.2016.01.011.
Recio, Alberto, Cristina Linares, José Ramón Banegas, and Julio Díaz. "Road traffic noise effects on cardiovascular, respiratory, and metabolic health: An integrative model of biological mechanisms." Environmental Research 146 (2016): 359-70. doi:10.1016/j.envres.2015.12.036.
Sun, X., G. He, H. Qing, W. Zhou, F. Dobie, F. Cai, M. Staufenbiel, L. E. Huang, and W. Song. "Hypoxia facilitates Alzheimer's disease pathogenesis by up-regulating BACE1 gene expression." Proceedings of the National Academy of Sciences 103, no. 49 (2006): 18727-8732. doi:10.1073/pnas.0606298103.
Takano, Takahiro, Guo-Feng Tian, Weiguo Peng, Nanhong Lou, Ditte Lovatt, Anker J. Hansen, Karl A. Kasischke, and Maiken Nedergaard. "Cortical spreading depression causes and coincides with tissue hypoxia." Nature Neuroscience 10, no. 6 (2007): 754-62. doi:10.1038/nn1902.
Wallace, Anna, and Romola S. Bucks. "Memory and Obstructive Sleep Apnea: A Meta-Analysis." Sleep, 2013. doi:10.5665/sleep.2374.
Similar Articles
JOIN THE DISCUSSION
This article has 0 comments.
About 7 years ago my grandfather was diagnosed with Alzheimer's disease. We were very close, in fact, at that time he may have been one of the most important people in my life. Alzheimer's Disease stole my grandfather from me. After having a first hand witnessing of Alzheimer's disease, the destruction it causes, I became inpired to change the field of study around it.
The historical experiences of pychological disarray I speak of in this paper were all true of my gradfather.