Alzheimer's Disease Case Study
INTRODUCTION
Approximately 36 million individuals have Alzheimer’s disease (AD) worldwide which is the common cause of dementia in the range of higher ages (Alzheimers.net, 2014). About 5% to 8% of people aged above 65, 15% to 20% of people aged above 75 and 25% to 50% of those aged above 85 are affected by Alzheimer’s disease (Duthey, 2013). Alzheimer’s disease is an irreversibly progressive disease of the brain characterised by gradual loss of memory, change in personality and a decline in cognitive functions such as language, perception and reasoning. An individual with Alzheimer’s disease would lose all mental and memory abilities in later stages (National Institute of Aging, 2011). It is believed that Alzheimer’s disease is caused by the
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One of the principal treatments approved by the Food and Drug Administration (FDA) for Alzheimer’s disease is a drug named Rivastigmine (Exelon®). The beginning of this essay starts with how the neurons relay messages in the central nervous system followed by the pathophysiology of Alzheimer’s disease then illustrates the function of Rivastigmine to reduce the effect of Alzheimer’s disease.
PATHOPHYSIOLOGY
Neurons communicate with each other by relaying electrical and chemical signals across the synapses (Stufflebeam, 2008). Synapses are places usually formed between the axon terminals and dendritic spines. The presynaptic neuron is the neuron that transmits the signal whereas the postsynaptic neuron receives the signal. For transmission of signal across a chemical synapse, neurotransmitters are produced and stored in vesicles in axon terminals
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Alzheimer’s disease is caused by the low levels of concentration of neurotransmitter acetylcholine which aids in neurotransmission as a chemical messenger due to the two hallmarks of Alzheimer’s disease which are the accumulation of beta amyloid plaques and neurofibrillary tangles. There is yet for a cure to be found for Alzheimer’s disease however the use of the drug Rivastigmine has been verified to help relieve the symptoms of Alzheimer’s disease by inhibiting the enzyme acetylcholinesterase so that the neurotransmitter acetylcholine is not
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