Alzheimer’s Thesis Statement

Alzheimer’s Thesis Statement

What is Alzheimer’s disease?

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Alzheimer’s disease (AD) is a neurological disease framed in the group of neurodegenerative (are those that produce degeneration of the essential cells of the nervous system, neurons). It is the disease that most frequently causes senile dementia (loss of mental faculties in the elderly). This has led to equal senile dementia to EA and vice versa.

Page Contents

Alzheimer’s thesis statement: age and neuronal degeneration
    Thesis statement about Alzheimer’s: causes of the disease
    The symptoms of Alzheimer’s disease
    The three phases of Alzheimer’s
Thesis statement for Alzheimer’s: current Alzheimer’s treatments

Alzheimer’s thesis statement: age and neuronal degeneration

Alzheimer’s thesis disease has a peak of onset (incidence) increasing from 70 years of age. It is relatively rare below 65 years, although there are cases described with onset, exceptionally atypical, in youth. The fact that it affects more elderly people has mistakenly matched aging to Alzheimer’s disease. Not all the elderly suffer Alzheimer’s, nor does Alzheimer’s disease occur only in the elderly. The fact that there are diseases with a preferential age target is not something rare: there are diseases that only occur in childhood, some that occur with maturity, etc.

Alzheimer’s disease produces a neuronal degeneration that mainly affects highly specialized neurons responsible for performing the functions that most characterize us as human beings. In fact, Alzheimer’s disease as such seems typical of humans. Behavioral changes have been described in elderly companion animals, but the alterations in their brains are not similar to those of Alzheimer’s disease. We must bear in mind that humans are terrestrial mammals with the longest average longevity.
Thesis statement about Alzheimer’s: causes of the disease

It is not completely known what the causes of Alzheimer’s are and why the disease occurs. In the brains of people afflicted with dementia due to Alzheimer’s disease, abnormal deposits of two proteins that form aggregates and inclusions have been identified, deconstructing the brain architecture. These proteins are called beta-amyloid and tau protein.

Beta-amyloid protein and tau protein

According to the thesis statement about Alzheimer’s the beta-amyloid protein is denatured and caked, forming insoluble aggregates between brain cells. These aggregates, only visible under a microscope, are called senile plaques or amyloid plaques. This process of denaturation is similar to what occurs when boiling an egg. The egg white is basically formed by a protein called albumin. Under natural conditions, it is soluble in water and we can easily separate it. When we heat it solidifies, it changes color, we cannot separate it and, what is more important, denaturation process is irreversible: even if it is cold, it does not look the same as when we opened the egg. We do not know yet what it is that causes the beta-amyloid protein to denature.

Another interesting aspect of thesis statement on Alzheimer’s is that there is no direct correlation between the total amount of added proteins and symptoms that the patient suffers. There are people affected by AD with a relatively small lesion load and other people with a very acceptable functioning and who autopsy their brain is found to have large accumulations of beta-amyloid protein. Therefore, tau and beta-amyloid protein aggregates are sufficient to cause dementia due to AD, but there may be mechanisms of defense or of cerebral compensation that minimize the impact that these deposits have on performance in our daily activities.
The symptoms of Alzheimer’s disease

The symptoms of Alzheimer’s disease involve the progressive loss of the brain’s own functions and allowing us to relate to the environment. They are collectively called cognitive functions (literally, “thinking functions”) and include, among others, memory, language, visual and temporal orientation, attention and planning.

It also affects emotional and behavioral abilities such as motivation, mood, perception of reality and sleep. The symptoms develop gradually and progressively.

Large number of people afflicted with Alzheimer’s disease, the first symptoms of which occurs in relation to their ability to memorize new things. This cognitive function is called episodic or autobiographical memory. The person is not able to remember recent events and also does not substantially increase their ability to remember if we help with clues or put the fact to remember within a context.

To these memory symptoms, a certain character change is usually associated with apathy. Later, symptoms such as:

Disorientation in time.
Inability to draw and copy figures.
Inability to name common objects.
Disability to discriminate well things or people, delusions, hallucinations and agitation.

Finally, the most basic functions of the human being are affected, such as the motor function and those of regulation of our internal organs.
The three phases of Alzheimer’s

Phase 1: Duration of the disease from 1 to 3 years

This first stage in line with statements about Alzheimer’s has an approximate duration of 3 years and it shows a gradual deterioration in episodic memory, especially. The person forgets recent events, it does not matter that 10, 15 or 20 minutes of a given event have passed. You may not remember that you already ate or forget the conversation you had with your child minutes before. Likewise, the perception of their environment is diminished, just as memory in terms of time and space is affected.

Phase 2: Duration of the disease from 2 to 10 years

In this second stage, all aspects of memory progressively begin to fail. This stage lasts approximately 3 years, during which important changes in brain function occur with the appearance of more worrisome or more attention-grabbing symptoms. Problems of language (aphasia), learned functions (apraxia) and recognition (agnosia) begin to arise.

Aphasia is difficulty in the language. The person has difficulty talking, expressing and making themselves understood. The person cannot or does not know how to dress, does not know how to use cutlery, etc. Agnosia is a loss of ability to recognize the people with whom you live.

The person begins to do repetitive acts bordering on the obsessive. He wanders, goes around the house, orders clothes or papers several times a day, his eyes change. At this stage, it is obvious that the capacity for abstract thinking and the ability to carry out calculation operations disappear completely. They cannot perform the simplest operations, although they do, perhaps, recite the multiplication tables from memory.

Phase 3: Duration of the disease from 8 to 12 years

In this third and final stage, there is a broad and marked involvement of each and every one of the intellectual faculties. The cerebral symptoms are aggravated, accentuating the muscular rigidity as well as the resistance to the postural change. There may be tremors and epileptic seizures.

The Alzheimer’s patient does not recognize his relatives and may even not recognize his own face in the mirror. The personality that always accompanied the person changes greatly. They are deeply apathetic, losing the automatic abilities acquired such as washing, dressing, walking or eating.
Thesis statement for Alzheimer’s: current Alzheimer’s treatments

Before starting to talk about medicines it is necessary to clarify what is meant by a curative treatment and a symptomatic treatment:

A curative treatment is one that returns the individual to the state that was present before the onset of the disease. The classic example is antibiotics for infections.

A symptomatic treatment is one that relieves the symptoms or even makes them disappear even if the disease is still there. An example would be anti-inflammatories for the pain of knee osteoarthritis.

That said, if we focus on the EA, today there is no curative treatment. There are drugs and non-pharmacological treatments that have been shown to slow the progression of the disease, although they are not capable of reversing it.

A controversial issue is when to withdraw drugs for AD throughout the course of the disease. The response is complicated in very severe phases. Treatment with these drugs should be stopped when the patient stops’ benefiting from its use, but this is difficult to determine in individuals with advanced AD, when patients hardly relate to their relatives or caregivers. If no adverse effects are seen, their withdrawal can be assessed carefully and individually. In this situation, each case must be considered independently, there being no consensus guidelines for action.

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