Pathophysiological Studies of Alzheimer

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Understanding the pathophysiology of Alzheimer’s disease is vitally important. This disease currently threatens to affect at least 30% of all individuals presently alive in twelve most developed countries, unless effective interventions are found to treat or prevent the disease (Perry, 2006, p. 123). Despite the fact that memory loss is the major symptom of Alzheimer’s disease, the pathophysiological mechanisms that lead to Alzheimer-specific cognitive impairments have been understood only to a limited extent (Perry, 2006, p. 123).

At the same time, without fundamental understanding of Alzheimer’s disease, no adequate progress in accurately diagnosing and successfully treating Alzheimer’s can be made. In this sense, although scientists’ understanding of the mechanism of this disease is still evolving, agreement exists among many researchers about the key steps in the disease development and impacts on the brain (Jackson-Siegal, 2005). This paper will trace the current understanding of pathophysiology of Alzheimer’s disease, focusing on the known pathophysiological mechanisms that cause its symptoms and affect the brain.

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First, it is necessary to clarify what a pathophysiology of Alzheimer’s disease is. Pathophysiology of Alzheimer’s studies the changes taking place as a result of Alzheimer’s and how a human will function as a result of this disease. This is made up of biological and physical manifestations that are more commonly known as symptoms and signs. Just as pathophysiology of Alzheimer’s disease consists of pathology and physiology, where pathology accounts for studying the disruptions in human body condition, i.e. “changes in the human body caused by the disease and how it affects a normal person’s behavior and characteristics,” whereas physiology accounts for full understanding how exactly and why the brain gets affected by Alzheimer’s (Ali, 2015, p. 11).

Pathophysiology of Alzheimer’s disease is understood to be complex and involving multiple neurotransmitter systems along pathophysiologic processes. The central and well-known factors in Alzheimer’s neurodegenerative process are its long-held hallmarks: β-amyloid plaques, neuronal cell death, and neurofibrillary tangles (also known as NFTs) (Jackson-Siegal, 2005, p.126).

As for amyloid plaques, also known as plaques of β-amyloid protein, their important role amongst numerous pathophysiological processes of Alzheimer’s disease neuronal degeneration has been well established. It is known that plaques are present in all people as they become older, yet in Alzheimer’s disease, the density is higher. Also, the plaque distribution is found to correlate with certain areas of neuronal degeneration and specific clinical symptoms. Importantly, β-amyloid plaques are multiple clumps of insoluble peptides which come as a result of the aberrant cleavage of APP or amyloid precursor protein, which is a transmembrane protein. APP gets cleaved by 3 enzymes (β secretase, α secretase, and γ secretase), and in normal conditions, cleavage by β secretase, which is followed by γ secretase, is known to yield a 40 amino acid peptide, which is essentially soluble (Jackson-Siegal, 2005).

However, in Alzheimer’s disease, a variant form of γ secretase conducts the cleavage of APP at a wrong place, which results in 42 amino acid peptide Aβ 42 or simply Aβ. This peptide is insoluble and thus aggregates into easily identifiable clumps that are termed β-amyloid plaques. Finally, it needs to be said that an important role in Alzheimer’s disease pathophysiology for amyloid is also implied by the fact that those proteins that are encoded by APP, SorL1, PS1, ApoE, and PS2, are all closely associated with amyloid generation, trafficking, or processing. At the same time, some evidence exists today that amyloid plaques may not be the key cause of Alzheimer’s (Jackson-Siegal, 2005). This is because amyloid plaques are also sometimes found in cognitively healthy adults, because amyloid plaque burden does not correlate with the actual degree of cognitive degeneration in persons with Alzheimer’s disease dementia, as well as because amyloid plaques are linked to cognitive improvement in some Alzheimer’s disease mouse models.

Next, if to consider neurofibrillary tangles, they are seen as dead or dying neurons. NFTs come as a result of neuronal microtubules destruction caused by certain modifications of their supportive protein tau. Just as microtubules are essential ingredients of the structure of neuronal cells delivering nutrients and helping with synaptic transmission alongside the length of the neuronal axon, the harm done by tau lies in its disruption of its bonds to microtubules after tau proteins become hyper-phosphorylated during Alzheimer’s pathogenesis. In this way, the structure of microtubules collapses, thus destroying the neuron’s communication and transportation systems. As a result, neuronal cell death happens (Jackson-Siegal, 2005).

Last but not least, several other pathophysiologic processes are linked to Alzheimer’s disease progression. In particular, neuron and synapse loss has been one of them. The distribution of death of neuronal cells as well as synapse loss occurs similarly to neurofibrillary tangles. In typical Alzheimer’s disease, neuron death within the nucleus basalis of Meynert causes a deficit in acetylcholine. That is a neurotransmitter which is involved in memory. In the brainstem, the loss of locus ceruleus neurons and median raphe loss cause deficits in norepinephrine and serotonin respectively. As a result, abnormal adrenergic activity and cerebral serotonergic activity are thought to contribute to insomnia and dysphoria in Alzheimer’s (Jackson-Siegal, 2005).

All these and other mechanisms of Alzheimer’s disease progression lead to the following symptoms: loss of memory, skills, intellect, ability to learn, while the disease itself leads to depression and anxiety. A brain affected by Alzheimer’s, in its turn, is characterized by considerable shrinkage of tissues, so that it becomes smaller gradually. As the grooves widen and the folds shrivel so that gaps appear in the outer layer of the brain and important nerve fibers get lost, a person loses the ability to control feelings, reasoning, and movements. Short-term memory and function of speech deteriorate. Besides, the impact on amygdala leads to a person’s loss of control of the feelings of anger and fear. Impact on the brain stem leads to the deterioration of heart rate, blood pressure, and breathing. As the frontal lobe gets damaged, the person is unable to perform complex processes such as logical thinking or cooking, and is subject to lethargy. Damage of parietal lobes leads to loss of ability to read, write, calculate, and adequately perceive space. Damage of the temporal lobes results in incapability to recognize familiar places, people, and things, as well as in hallucinations (Ali, 2015).

This paper has looked into the pathophysiology of Alzheimer’s disease. It first defined the essence of Alzheimer’s pathophysiology and then focused on the exact pathophysiological and neurotransmitter processes that are neuropathologic mechanisms of the disease: β-amyloid plaques, neuronal cell death, and neurofibrillary tangles. Then it focused on how the brain is affected by the disease, and what the result is. Hopefully, more discoveries in pathophysiology of Alzheimer’s disease will be done, so that effective cures are found.

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