Alzheimer’S Disease: Dementia of the Brain

The brain is a complex organ that does a lot of communicating with our bodies. It can be considered the center of the nervous system. Since it serves many purposes our brains must be in good condition. When we have issues with our brain like dementia or then we have issues with our brain, like dementia, it impacts other parts of our body. Dementia is a disease that alters your brain and your life as well.

The first important thing to know is what is dementia? Dementia is not a specific disease; it is a term used to describe the inability to remember things, think, and make decisions (Center for Disease, 2019). There are different types of dementia much like there are different types of heart disease. The most common type of dementia is Alzheimer’s disease. Another type of dementia that is common is vascular dementia.

Since dementia is such a broad topic it can be hard in determining what exactly causes dementia. “The slow development of dementia is considered to be the result from accumulated loss of synapses or neurons” (Korczyn, 2002, p.129). In the past it has been hard to diagnose the onset of dementia. Overtime, with new technology it has made it possible to diagnose it without the person having to be dead. Now, doctors can use brain scans to determine dementia along with other symptoms. The brain scans can show any brain tissue that is deuterating. “The most common types of dementia begin with shrinkage of brain tissue. This means that each type of dementia tends to have early symptoms, depending on which part of the brain is affected“(Alzheimer’s Society, 2014).

There are different parts of the brain that are affected by each type of dementia. Alzheimer’s disease damages the hippocampus and its surrounding structures that are connected to it. Your hippocampus is in charge for memory and learning new things. When there is damage to this part of the brain it is hard for someone to learn new information and be able to store it. People with Alzheimer’s disease may have trouble remembering information like what they eat for lunch. However, they can possibly remember something that happened a couple years ago. Later in the diagnosis of Alzheimer’s the amygdala can be affected as well. “As Alzheimer’s disease spreads through the brain, additional parts of the brain can be affected. The cortex overall becomes thinner and the brain gradually shrinks” (Alzheimer’s Society, 2014).

“Early neurochemical analyses of Alzheimer’s disease brain tissue revealed that the enzymes that generate and metabolize acetylcholine are decreased. Although deficits in numerous neurotransmitters accumulate as the disease progresses, the early symptoms appear to correlate with dysfunction of cholinergic and glutamatergic synapses. In addition to the transmitter alterations, many other biochemical and morphological indicators suggest that Alzheimer’s disease represents, at least initially, an attack on synapses” (Selkoe, D. J., 2002).

The nucleus basalis is another part of the brain that is affected in having Alzheimer’s disease. It is also affected in other diseases like Parkinson’s disease. “The nucleus basalis receives information from the hypothalamus and basil ganglia. It then sends axons that release acetylcholine to widespread areas in the cerebral cortex” (Kalat, 2019, p.78). The nucleus basalis is key for attentions. Those who have Alzheimer’s struggle with attentions issues due to their nucleus basalis deteriorating.

Alzheimer’s has been linked with Down Syndrome. Those who have Downs Syndrome are almost likely to get Alzheimer’s disease as well. Those who have Down Syndrome have three copies of chromosome 21 rather than having the normal two. This led people to examine chromosome 21. Under the investigation it was found that there was a gene that is linked to many cases of early onset of Alzheimer’s disease. The early onset of Alzheimer’s disease is before age of 60 years old. “The genes controlling early onset of Alzheimer’s disease cause a protein called Amyloid-B accumulate inside and outside neurons and spread from cell to cell” (Kalat, 2019, p.390). The protein damages axons and dendrites. The damaged axons and dendrites then cluster into structures called plaques. The plaque structures damage the cerebral cortex, hippocampus, and other areas other brain.

Amyloid-B is not the only protein that researchers believe could be associated with Alzheimer’s disease. Tau protein is another protein that could explain damaged areas of the brain in those who have Alzheimer’s disease. Tau proteins supports structure of axons. High levels of Amyloid-B cause phosphate groups to attached to the Tau proteins. This enables the Tau protein to bind normally within the axons. Due to the unnormal binding it spreads to the cell body and dendrites.

“Another characteristic change in tissue feature of Alzheimer’s disease is the removal of neurofibrillary tangles within neurons. These abnormal proteins consist of flame-shaped, spiral deposits of hyperphosphorylated tau protein. Under normal physiological conditions, phosphorylation of tau protein helps to maintain cytoskeletal structure. In Alzheimer’s disease, there may be an imbalance between phosphorylating protein kinases and dephosphorylating protein phosphatases, leading to excessive tau phosphorylation, microtubule instability and cell death” (Danysz & Parsons, 2012).

“With increased frequency, clinical geneticists are asked for genetic advice on the heredity of dementia in families. Alzheimer’s disease is in most cases a complex disease but may be autosomal dominant inherited. Mutations in the PSEN1 gene are the most common genetic cause of early onset Alzheimer’s disease, whereas APP and PSEN2 gene mutations are less frequent” (Hokke, P. E. et al, 2012).

Amnesia is one of the most common symptoms associated with Alzheimer’s disease. Amnesia simply means memory loss. Those who have Alzheimer’s disease learn procedural skills better than learning facts like you learn in school. Alzheimer patients can learn new skills but surprise themselves when they do it because they do not remember learning it. As time passes with those who have Alzheimer’s disease memory loss gets more severe. Memory loss can progress to confusion, depression, restlessness, and loss of appetite.

“Vascular dementia occurs when cells in the brain are deprived of oxygen. A network of blood vessel supplies the brain with oxygen. If a blockage occurs in the vascular system, blood may be prevented from reaching the brain. As a result, cells in the brain die, leading to symptoms of dementia” (Zhang et al., 2013).

Vascular dementia has a wide range of symptoms. Vascular dementia symptoms are more widely ranged than any other type of dementia. Vascular dementia may follow a stroke or mini strokes. After a stroke the blood supply is cut off which causes one side of the brains tissue to die resulting in Vascular dementia. If this happens some of the common symptoms are problems thinking and concentrating. If Vascular dementia is followed mini strokes each stroke creates an infarct in the cortex. Problems with episodic memory is a symptom associated with mini strokes. (Alzheimer’s Society, 2014)

There are other psychological issues that are prevalent in dementia. Once of those is sleeping disorders. Sleeping disorders are common in those who have Alzheimer’s disease. Another thing that is common with Alzheimer’s disease and dementia are sundowning. Sundowning is where those who have dementia have confusion in the late day into the night. There are symptoms that are associated with sundowning. Some of them are anxiety, restlessness, mood swings, pacing, and rocking.

All forms of dementia are mostly common among the older population. With dementia affecting the older population it makes them more dependent and vulnerable. Th symptoms that are associated with dementia increase their vulnerability. People with dementia struggle socially, mentally, and physically. This develops challenges for our society and health care systems to learn how to overcome. The diagnosis of dementia is not precise. It can occur and develop in individual’s differently. This is another challenge associated with dementia. (Ulster Medical Society, 2015)

“There has been research and studies showing that there may be a possible way to diagnose Alzheimer’s early. There is non-invasive test that can be used to diagnose degenerative dementia by using biomarkers. However, there are no validated extracerebral diagnostic markers for the early diagnosis of Alzheimer disease are available” (Jellinger, Janetzky, Attems, & Kienzl, 2008).

“Testing blood is also another way that could be used to test for early onset of Alzheimer’s disease. In an initial trial group using the blood test, one in five healthy participants with no memory complaints tested positive. On further medical investigation using brain-imaging techniques, these patients showed signs of degeneration in the brain resembling Alzheimer’s disease features. The high accuracy of this blood test for the brain disorder comes from the ability to harvest protected bubbles of genetic material, called microRNA, found circulating in the bloodstream. Those with Alzheimer’s disease contain a certain set of microRNAs which distinguishes them from healthy people” (Alzheimer’s disease, 2014).

Those who have a form of dementia may also struggle with their emotions. They may have less control over their emotions. They not only have trouble controlling their emotions but also expressing them. This causes difficulty for those that care for those who have dementia. It is hard to help patients when they do not know how to express what they are feeling. It could be difficult to tell if a patient with dementia is hurting, having anxiety, or depressed. Caregivers may underestimate a situation while the patient is “overreacting.” (Alzheimer’s Society, 2015)

“Managing the behavioral and psychological signs of dementia is a major problem for healthcare professionals. Neuroleptic drugs are the mainstay of pharmacological treatment, although their use is justified largely based on clinical anecdote, and they have many harmful side effects. Dementia is a common condition, and those who suffer have a particularly high risk of adverse treatment responses. It is important to have clear evidence that treatments are both effective and safe. Given current knowledge, unless symptoms are unbearable it would seem appropriate to monitor the disturbances for at least one month before starting pharmacological treatments” (Ballard, C., & O’Brien, J., 1999). The monitoring period allows those to determine who really needs medication versus those who may just need some therapy to cope with their issues.

As of right now, there is no cure for Alzheimer’s disease. There are no medications that are highly effective for Alzheimer’s disease. There are medications that help with certain symptoms of Alzheimer’s like anxiety, but not treat Alzheimer as a whole. One explanation for failure of medications is the diagnosis is too late for medications to work. The damage is too progressed for medications to work. That is why it is important for doctors to learn how to diagnose Alzheimer’s as early as possible.

References

1. Alzheimer disease; blood test developed to diagnose early onset alzheimer’s disease. (2014, Nov 15). Medical Imaging Week Retrieved from http://proxy.ncwc.edu/login?url=https://search-proquest-com.proxy.ncwc.edu/docview/1620620383?accountid=12726
2. Alzheimer’s Society United Against Dementia. (2015, February). The psychological and emotional impact of dementia. Retrieved from https://www.alzheimers.org.uk/get-support/help-dementia-care/understanding-supporting-person-dementia-psychological-emotional-impact
3. Alzheimers’s Society United Against Dementia. (2014, September). Dementia symptoms and areas of the brain. Retrieved from https://www.alzheimers.org.uk/about-dementia/symptoms-and-diagnosis/how-dementia-progresses/symptoms-brain
4. Ballard, C., & O’Brien, J. (1999). Treating behavioural and psychological signs in alzheimer’s disease. BMJ : British Medical Journal, 319(7203), 138. doi:http://dx.doi.org/10.1136/bmj.319.7203.138
5. Centers for Disease Control and Prevention. (2019, December 19). What Is Dementia? Retrieved from https://www.cdc.gov/aging/dementia/index.html
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7. Danysz, W., & Parsons, C. G. (2012). Alzheimer’s disease, β‐amyloid, glutamate, NMDA receptors and memantine – searching for the connections. British Journal of Pharmacology, 167(2), 324-352. doi:10.1111/j.1476-5381.2012.02057.x
8. Delong, Z., Liu, B., Chen, J., Peng, X., Liu, X., Fan, Y., . . . Huang, R. (2013). Determination of vascular dementia brain in distinct frequency bands with whole brain functional connectivity patterns. PLoS One, 8(1) doi:http://dx.doi.org/10.1371/journal.pone.0054512
9. Hokke, P. E., Elting, M. W., Pijnenburg, Y. A. L., & van Swieten, J. C. (2012). Genetics of dementia: Update and guidelines for the clinician. American Journal of Medical Genetics Part B: Neuropsychiatric Genetics, 159B(6), 628-643. doi:10.1002/ajmg.b.32080
10. Kalat, J. (2019). Biological Psychology 13h ed., Cengage Learning, 78-79.
11. Kalat, J. (2019). Biological Psychology 13h ed., Cengage Learning, 390.
12. Korczyn, A. D. (2002). Mixed Dementia—the Most Common Cause of Dementia. Annals of the New York Academy of Sciences, 972(1), 129-134.
13. Selkoe, D. J. (2002). Alzheimer’s disease is a synaptic failure. Science, 298(5594), 789-91. Retrieved from http://proxy.ncwc.edu/login?url=https://search-proquest-com.proxy.ncwc.edu/docview/213580113?accountid=12726
14. Ulster Medical Society. (2015, May). Dementia. Retrieved from https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4488926/?tool=pmcentrez&report=abstract