Introduction
Alzheimer’s disease (AD) is a psychological disorder that involves the progressive destruction of brain cells and reduction in the proper functioning of the brain (Altman, 2000). Alzheimer’s disease is a type of dementia that is characterized by degeneration of brain functions such as memory, speech, and comprehension. It affects people at a young age but signs and symptoms appear in old age.
The first sign of the disease is memory deterioration, which is characterized by memory loss and poor concentration (Altman, 2000). The disease is difficult to diagnose because its early signs can be easily confused with the effects of aging.
On the other hand, early symptoms of the disease can also be observed in other conditions such as depression, fatigue, continued use of certain medications, and grief. Alzheimer’s disease usually results in death due to the lack of a cure.
Even though certain medications are used, they only slow down the development of the disease and reduce the severity of symptoms. The pattern of AD’s development is different in individuals. However, its symptoms and effects are similar.
Causes
The main cause of AD has not yet identified. However, scientists have presented four main hypotheses to explain the causes. These include genetics, cholinergic hypotheses, tau hypotheses, and amyloid hypotheses.
Genetics and physiological contributions
Scientists have linked genetic inheritance to AD. According to scientists, three types of gene mutations cause the disease. They include mutations that encode presenilins 1, presenilins 2, and amyloid precursor protein (Foster, 2004). These mutations are responsible for the greatest percentage of autosomal familial Alzheimer’s disease.
The aforementioned mutations increase the secretion of a protein known as Aβ42, which plays an important role in the formation of senile plaques. Other mutations alter the ration of the protein to other forms of proteins without affecting the level of Aβ42. For that reason, presenilin mutations can cause AD without altering the level of protein Aβ42.
Cases that do not involve autosomal-dominant inheritance are referred to as sporadic AD. In those cases, the disease is caused by the inheritance of the ε4 allele. The genes are contained in a protein referred to as the apolipoprotein E. Studies have established that approximately 40-80 percent of people with Alzheimer’s disease possess the APOEε4 allele gene, which increases the risk factor of developing the disease (Foster, 2004).
Research has also found out that the TREM2 gene causes AD. Its mutation results in uneven regulation of beta amyloid in the brain that leads to accumulation of the protein in the brain.
Cholinergic hypothesis
According to the cholinergic hypothesis, Alzheimer’s disease results from low production of acetylcholine. Acetylcholine is a neurotransmitter that functions in the peripheral, autonomic, and central nervous systems (Brill, 2005).
The neurotransmitter is produced by the cholinergic system, whose damage results in Alzheimer’s disease. The hypothesis is not widely supported because medications that enhance production o acetylcholine do not alleviate the symptoms of the disease.
Amyloid and physiological contributions
According to the amyloid hypothesis, deposits of beta-amyloid (Aβ) cause Alzheimer’s disease. The hypothesis was based on the discovery that a large percentage of individuals with Down syndrome develop the disease. In addition, it was supported by the discovery that apolipoprotein4 was a risk factor for the disease. Apolipoprotein plays an important role in the dissolution of beta-amyloid in the brain.
However, certain forms of the protein promote the accumulation of the protein to toxic levels. The buildup of beta-amyloid damages brain cells and alters the proper functioning of the brain. Research studies have led to the development of a hypothesis that predicts that non-plaque Aβ aggregates are the cause of AD (Brill, 2005). Scientists have predicted that they bind to neuron receptors and inhibit communication.
Further studies suggested that a protein related to the beta-amyloid protein could be the cause of the disease. Even though scientists have not agreed regarding the cause of AD, studies show the involvement of beta-amyloid in the development of Alzheimer’s disease. Clumps of the protein interfere with neuronal communication between brain cells leading to their decline and death.
Tau and physiological contributions
According to the tau hypothesis, the tau protein is responsible for Alzheimer’s disease. The human brain depends on an internal system that transports nutrients and other essential elements to various brain cells and structures. This system relies on a protein knows as tau. The hyperphosphorylation of tau initiates the loss of its ability to bind to microtubules.
As a result, tau proteins bind to other tau filaments resulting in the formation of neurofibrillary twists that alter the transport and communication systems. Phosphorylation of tau protein is necessary for the proper function of the brain. However, uncontrolled rates of phosphorylation affect the proper functioning of the brain.
Hyperphosphorylation of tau proteins alters certain processes that maintain the activity of brain cells. For instance, hyperphosphorylated tau does not bind to neurotransmitters and does not initiate the assembly of microtubules thus causing their disintegration. Twisting of tau protein threads interferes with the proper functioning of the nutrient transport system thus leading to the death of brain cells (Lillrank & Collins, 2007).
Symptoms
Symptoms of AD are mild, moderate, and severe depending on the stage of development. Mild symptoms include mood swings, trouble completing daily tasks, problems with speech and language, and prevalent episodes of forgetting (Altman, 2000).
Moderate symptoms include sleep problems, delusions, difficulties with problem-solving, confusion, and restlessness (Brill, 2005). Severe symptoms include loss of ability to communicate, major confusion, intense mood swings, weight loss, and hallucinations (Budson & Kowall, 2011). Each group of symptoms appears at a certain stage in the development of the disease.
Pathophysiology
The main characteristics of AD include loss of communication between cells in the cerebral cortex, death of affected areas, and reduction in the size of certain brain parts (Budson & Kowall, 2011). Individuals with the disease possess amyloid plaques and tangles of tau protein in their brains.
The biochemistry of Alzheimer’s disease involves the accumulation of beta-amyloid and tau proteins to levels alter certain brain functions. Hyperphosphorylation of tau proteins results in abnormal aggregations that kill brain cells (Grossberg & Kamat, 2010). On the other hand, the accumulation of beta-amyloid proteins also kills brain cells.
Diagnosis
Alzheimer’s disease is diagnosed through a comprehensive medical evaluation. Diagnosis involves an analysis of a patient’s medical history and mental status, as well as physical and neurological examination (Gauthier, 2006). In addition, blood tests and brain imaging are conducted to aid in proper diagnosis.
The main symptoms that all patients exhibit include confusion, poor memory, the decline in communication skills, and difficulties in executing daily activities. Medical practitioners conduct thorough assessments in order to rule out related or unrelated conditions that have similar symptoms (Grossberg & Kamat, 2010). Mental tests involve answering a set of questions in order to test a patient’s memory and thinking capabilities (Lillrank & Collins, 2007).
Physical examination and blood tests aid in the identification conditions that could be the cause of certain symptoms (Gauthier, 2006). Brain imaging identifies conditions such as strokes and tumors that could be the cause of memory loss and confusion. Major types of brain scans include computerized axial tomography, magnetic resonance imaging, and single photon emission computerized tomography (Gauthier, 2006).
Treatment
AD is incurable. However, certain medications slow the development of the disease. Medications that are commonly used include Cognex, Donepezil, Exelon, Razadyne, and Memantine (Grossberg & Kamat, 2010). Cognex is rarely used because it causes liver damage. Memantine prevents nerve damage and improves mental function.
Prevention and management
Prevention of AD involves medication, lifestyle changes, and choosing the right diet. Research has revealed that people who use non-steroidal anti-inflammatory drugs are at a lower risk of developing Alzheimer’s disease compared to people who do not use the drugs (Shankle & Amen, 2005). In addition, the drugs reduce inflammations that are caused by reactions of beta-amyloid proteins.
Before technological advancements, hormone replacement therapy was used to prevent AD. However, research studies later revealed that the remedy increases the risk of developing the disease. Lifestyle is an important factor in the prevention of AD. Individuals who develop the habits of reading, socializing, and completing intellectually challenging puzzles lower the risk of the disease (Grossberg & Kamat, 2010).
According to the cognitive reserve theory, working the brain enhances the performance of the neural system. Finally, physical exercise keeps the brain active and healthy. Proper diet plays a vital role in the prevention of Alzheimer’s disease. Legumes, fruits, vegetables, unrefined cereals, fish, and diets rich in flavonoids are recommended (Lillrank & Collins, 2007). In addition, moderate consumption of wine and dairy products reduces the risk of AD.
Conclusion
Alzheimer’s disease (AD) is a psychological disorder that alters the proper functioning of the brain. The main symptoms of the disease are memory loss and language problems. It is most common among old people even though its onset occurs during the middle ages.
Causes of AD include genetics, accumulation of beta-amyloid proteins, and twisting of tau proteins. Also, scientists predict that low production of acetylcholine and mutations that encode presenilins 1, presenilins 2, and amyloid precursor protein contributed towards the development of AD.
Symptoms of the disease include mood swings, difficulty in completing daily tasks, problems with speech and language, prevalent episodes of forgetfulness, sleep problems, delusions, difficulties in solving problems, confusion, and restlessness. Other symptoms include loss of ability to communicate, major confusion, intense mood swings, weight loss, and hallucinations.
The hyperphosphorylation of tau results in the loss of the protein’s ability to bind to microtubules. As a result, it binds to other tau filaments resulting in the formation of neurofibrillary twists that initiate the breakdown of microtubules. Mutations that encode presenilins 1, presenilins 2, and amyloid precursor protein increase the secretion of a protein known as Aβ42, which plays an important role in the formation of senile plaques.
Correct diagnosis of AD involves analysis of a patient’s medical history, physical and neurological examination, and evaluation of mental status. In addition, tests such as blood tests and brain imaging are carried out to aid in proper diagnosis. Prevention and management of AD involve medication, lifestyle changes, and eating a healthy diet.
References
Altman, L. J. (2000). Alzheimer’s Disease. New York: Lucent Books.
Brill, M. T. (2005). Alzheimer’s Disease. New York: Marshall Cavendish.
Budson, A. E., & Kowall, N. W. (2011). The Handbook of Alzheimer’s Disease and Other Dementias. New York: John Wiley & Sons.
Foster, H. D. (2004). What really Causes Alzheimer’s Disease. New York: Trafford Publishing.
Gauthier, S. (2006). Clinical Diagnosis and Management of Alzheimer’s Disease. New York: CRC Press.
Grossberg, G., & Kamat, S. (2010). Alzheimer’s: The Latest Assessment & Treatment Strategies. New York: Jones & Bartlett Learning.
Lillrank, S., & Collins, C. E. (2007). Psychological Disorders: Alzheimer’s Disease and Other Dementias. London: Infobase Publishing.
Shankle, W. R., & Amen, D. G. (2005). Preventing Alzheimer’s: Ways to Help Prevent, Delay, Detect, and Even Halt Alzheimer’s Disease and Other Forms of Memory Loss. New York: Penguin.