Paper On Alzheimer's Disease

1192 Words 5 Pages
Ronald Reagan was diagnosed with Alzheimer 's disease in 1994, which was after his presidential term. Alzheimer 's disease (AD) is an incurable and debilitating chronic progressive neurodegenerative disorder which is the leading cause of dementia worldwide (Kazim and Iqbal, 2016). Many of Reagan’s speech characteristics changed and can be associated with the neurological structures such as the myelination of the neurons as well as specific genes and the thickness of the surrounding cells of the neuron.

A Study done on molecular neurodegeneration states, “Finally, we document that the loss of BIN1 significantly correlates with the extent of demyelination in multiple sclerosis lesions” (De Rossi et al, 2016). The study provides information
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For now, I can say that the slurring of his speech is due to the initial loss of communication between the neurons. The slower behavioral changes would also be a result of the neurons not connecting or making action potentials at the correct or appropriate time. This would be a result of the loss of synaptic connections, or the alterations in the BIN1 gene and presence of the Aβ or tau pathologies.

Moreover, people affected by Alzheimer’s disease face many challenges, such as not being able to complete a daily task like dressing one-self or having no recollection of a loved one. This disorder is a progressive disease that deteriorates the neurons in the brain as time passes which lead to the decline of cognitive function and eventually death. Some of the most common symptoms include mental decline, memory loss, changes in personality and confusion (Fattahi & Mirshafiey,
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Some of the major pharmaceuticals that are used today include donepezil, galantamine, memantine and rivastigmine. Of these, galantamine is one of the most commonly prescribed and used. Research published in Psychopharmacology examined the effects that galantamine had on patients with Alzheimer 's disease and concluded that people treated with galantamine have improved cognitive function ( Ellis et al, 2009). This is because galantamine enhances cholinergic function by restricting acetylcholine-degrading enzyme, AChE, and the binding sites of nAChRs. There was a 27% increase in verbal learning and language in some patients with this treatment. However, galantamine failed to enhance other cognitive functions such as attention, orientation, and short-term recall. This may be a result of galantamines poor ability to regulate α4 β2

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