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Introduction
Alzheimers disease is a degenerative disease of the brain. It is categorized by the WHO into the broader Dementia family of brain syndromes, along with vascular dementia, front temporal dementia, and dementia with Lewy bodies (Duthey 6). Like other forms of dementia, Alzheimers Disease is characterized by an impairment of cognitive functions, including orientation, judgment, comprehension and memory, learning capacity, and language. The distinction between these dementia subtypes is often ambiguous or arduous to identify, and different forms may often co-exist (Duthey 6). This paper will look into Alzheimers Disease, including its symptoms and effects, risk factors, causes and prevalence, and eventually, treatment and medications.
Physiology and Anatomy
A healthy human brain contains innumerable neurons. These are specialized cells tasked with the processing and transmission of signals via chemical and electrical signals (Scammell et al. 186). Neurons will transmit signals between different areas of the brain or from the brain to the various organs and muscles in the human body. Alzheimers disease leads to the degeneration of these neurons through disruption of intercommunication between them, leading to loss of function and eventual cell death.
A basic neuron comprises three parts; a cell body, multiple dendrites, and an axon. The cell body itself houses the nucleus, which essentially contains the genetic makeup that regulates and directs the cells activities. Dendrites are branch-like structures that protrude from the cell body and are receptors of information from other neurons (Scammell et al. 186). Finally, the axon is a cable-like structure on the cell body opposite the dendrites and transmits signals to other neurons (Scammell et al. 186). The basic structure of the neuron is outlined in Figure 1 below.
The survival and continued functionality of neurons are dependent on several critical biological processes, primarily communication, metabolism, and repair, remodeling, and regeneration (Duthey 18). Upon receiving a signal from another neuron, the axon conducts an electrical charge down its length and across a synapse, a tiny inter-neuron gap in the form of neurotransmitter chemicals. This is the basic working of communication between neurons. Metabolism involves the breaking down of nutrients and chemicals within a cell, which is essential to cell survival and healthy cell function. Finally, neurons have consistently evolved to be rather long-living, remodeling their synaptic connections and adjusting based on the stimulation received from other neurons. Adult brains will also generate new neurons through neurogenesis (Duthey 22). This remodeling, repair, and regeneration are essential for cognitive functions such as learning and memory.
Symptoms and Effects
The brain will shrink to some extent during healthy aging. However, it does not lose neurons in a significant number. Alzheimers disease disrupts processes critical to neuron functioning and their networks, primarily communication, metabolism, and repair (Duthey 17). The result, in comparison, is catastrophic on the brain, and damage becomes widespread as neurons lose functionality, connections and eventually die.
Initially, Alzheimers disease affects neurons, and neuron communication, in sections of the brain influencing memory. These include the hippocampus and the entorhinal cortex (Eratne et al. 350; Duthey 24). As the disease advances, it attacks areas in the cerebral cortex that are responsible for social behavior, reasoning, and language. The disease progresses gradually, wreaking damage on the brain until the affected person with Alzheimers loses their ability to function independently (Duthey 11). The disease is ultimately fatal.
Symptoms of Mild Alzheimers Disease
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Memory loss
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Loss of initiative and the sense of spontaneity
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Poor reasoning and judgment
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Loss of spatial awareness
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Taking unreasonably long in completing mundane tasks
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Mood and personality changes
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Trouble doing basic arithmetic, such as handling money.
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Increased aggression and anxiety.
Symptoms of Moderate Alzheimers Disease
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Exacerbated confusion and memory loss.
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Inability to comprehend and learn new things.
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Difficulty with reading, language, and arithmetic.
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Shortened attention span
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Inappropriate bursts of aggression.
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Impulsive behavior, including vulgar outbursts.
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Difficulty reasoning logically.
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Anxiety, aggression, restlessness, and tearfulness.
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Repetitive movements and muscle twitches.
Symptoms of Severe Alzheimers Disease
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Severe weight loss.
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Seizures.
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Skin infections.
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Increased need for sleep
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Loss of bladder and bowel control.
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Inability to communicate.
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Difficulty with swallowing.
Causes and Risk Factors
Researchers and scientists do not fully comprehend the causes of Alzheimers Disease in the majority of the population. However, speculation revolves around the combination of age-induced brain changes, along with lifestyle, environmental, and genetic factors (Eratne et al. 348). The significance of any of these predisposing factors varies on an individual basis.
Old age does not directly cause Alzheimers Disease. However, it is the most significant known risk factor for the disease. Research is still ongoing on how age-related brain changes may harm neurons and other brain cells, leading to Alzheimers Disease-induced damage (Eratne et al. 351). However, these age-induced changes that have been identified as potentially risky include atrophy, or the shrinkage of several parts of the brain, vascular damage, inflammation, and production of free radicals or unstable molecules (Mathys et al., 336). However, many people will go well into their 90s without incidence of the disease or any other form of dementia.
Genetic makeup also increases the risk of developing Alzheimers Disease. For instance, the incidence of the disease in the hereditary lineage increases the risk of Alzheimers in descendants. Genetic risk factors are changes in genes that expound the risk of contracting a disease. The prevalence of late-onset Alzheimers Disease may involve a gene called APOE [4, while early-onset Alzheimers Disease is usually passed through inherited genes (Mathys et al. 334; Duthey 48). Therefore, genetic makeup is considered a significant risk factor for Alzheimers Disease incidence.
There has also been significant research that shows factors beyond genetics and age play a role in the development of Alzheimers Disease. For instance, there has been scholarly interest in the relationship, correlative or causative, between vascular conditions such as stroke, heart disease, and hypertension (Eratne et al. 352). There is also interest in the effect of metabolic conditions, including diabetes and obesity, on the prevalence of Alzheimers Disease. This research helps outline the efficacy of interventions meant to alleviate the risk of Alzheimers Disease.
Statistics
Alzheimers disease is a highly prevalent form of dementia. It comprises approximately 60-70 percent of diagnosed dementia cases, with the number of individuals with the ailment doubling every five years past 65 years of age. Further, about a third of all people beyond the age of 85 may have Alzheimers Disease (Alzheimers Association, 389). In the United States, Within the timeframe of 2000 to 2015, deaths from Alzheimers Disease increased by 123 percent, with caregivers and family members estimating 18.4 billion hours of care provided to people with Alzheimers (Alzheimers Association 399-400). The care is at an estimated value of more than 232 billion USD, with an exacerbated risk of emotional and mental distress among care providers (Alzheimers Association 401). The toll of Alzheimers Disease is increasing and, therefore, there is increased interest in preventative and curative measures for the disease.
Treatment and Medications
There is currently no known cure for Alzheimers Disease or to alter its progressive course. However, there exist numerous proposed interventions and treatments being investigated in clinical trials. Much can be offered to improve the quality of life for people who have Alzheimers Disease and other forms of dementia and their families, including early diagnosis, optimizing physical and cognitive health, and treating accompanying physical and psychological symptoms.
Works Cited
Alzheimers Association. 2018 Alzheimers disease facts and figures. Alzheimers & Dementia, vol. 14 no. 3, 2018, pp.367-429.
Duthey, Béatrice. Background paper 6.11: Alzheimer disease and other dementias. A public health approach to innovation, vol. 6 no.1, 2013, pp. 1-74. Web.
Eratne, Dhamidhu, et al. Alzheimers disease: clinical update on epidemiology, pathophysiology and diagnosis. Australasian Psychiatry, vol. 26 no. 4, 2018, pp.347-357.
Mathys, Hansruedi, et al. Single-cell transcriptomic analysis of Alzheimers disease. Nature, vol. 570 no.7761, 2019, pp. 332-337.
Scammell, Thomas, E. et al. Histamine: neural circuits and new medications. Sleep, vol.42, no. 1, 2019, pp.183-198. Web.
World Health Organization. Dementia. WHO, 2019, Web.
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