1. Compare and contrast the pathophysiology between Alzheimer’s disease and frontotemporal dementia.
The exact cause of Alzheimer’s Disease is unknown. Failure to process and clear amyloid beta protein leads to the formation of diffuse neuritic plaques, disruption of nerve impulse transmission, and death of neurons. Misfolded and aggregated proteins trigger immune responses with activation of glial cells and release of cytokines leading to neuroinflammation. Neuritic plaques and neurofibrillary tangles are more concentrated in the cerebral cortex and hippocampus. The loss of neurons results in brain atrophy with decreases in weight and volume. Loss of synapse, acetylcholine, and other neurotransmitters contributes to decreased memory and attention and loss of other cognitive functions associated with AD. With frontotemporal dementia, there is a familial association with an age onset of less than 60 years. The majority of cases involve mutations of genes encoding tau protein or progranulin. The specific pathogenesis is unknown (Heuther & McCance, 2019).
2. Identify the clinical findings from the case that support a diagnosis of Alzheimer’s disease.
Clinical findings from the case that support the diagnosis of Alzheimer’s are reports of worsening memory and how he has been found wandering in the neighborhood where he has lived for 35 years. His wife is concerned about his ability to make decisions as he was convinced to buy a home security system, which they already have. The patient has trouble dressing himself and balancing the checkbook. There is a family history of Alzheimer’s; his father died at 78 from AD. The patient scored a baseline MMSE score of 12 out of 30, suggesting moderate dementia. The MRI shows hippocampal atrophy.
3. Explain one hypothesis that explains the development of Alzheimer’s disease.
One hypothesis that explains the development of AD is the excitotoxic hypothesis. Glutamate is the excitatory neurotransmitter in the brain that is responsible for synaptic plasticity and processes related to memory and learning. It is produced over several signaling pathways within the CNS and the hippocampus. This neurotransmitter has two types of receptors, inotropic and metabotropic, and they play an essential role in the development of cognitive disorders, especially with AD, since they participate in the process of formation of modulation of memory. In patients with AD, there is a hyperexcitability of the channels of these receptors caused by deficient recycling of glutamate released in the synaptic cleft. This causes the neurotransmitters to keep acting on the receptors, chronically activating them and triggering an influx of excessive calcium ions in the neuronal cell. This increase in calcium damages the cell, causing cell degeneration and death (Schwab et al., 2022).
4. Discuss the patient’s likely stage of Alzheimer’s disease.
Based on the case, the patient’s likely stage of Alzheimer’s Disease would be the moderate stage. In this stage, behavioral disturbances can include wandering, outbursts of anger, and aggression towards caregivers. The patient may struggle with independent eating, dressing, and bathing (Olczak et al., 2022). The wife reports that the patient has difficulty dressing himself. She also reports that the patient becomes angry and defensive when asked about wandering in the neighborhood. In the general physical exam, the patient is alert and angry but cooperative.
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