Alzheimer’s disease is a form of dementia (Kumar et al., 2022). It is a progressive neurodegenerative disease that affects a persons cognitive function (Kumar et al., 2022). According to McCance & Huether (2019), there are 3 different forms of alzheimer’s disease (AD). There is early onset familial AD, early onset AD, and nonhereditary sporadic or late-onset AD (McCance & Huether, 2019). The most common is late-onset AD while early onset AD is the least common (McCance & Huether 2019). When looking at the pathophysiology of alzheimer’s disease, the cause is unknown (McCance & Huether, 2019). Both early onset familial AD and late onset AD have been linked to chromosomal mutations (McCance & Huether, 2019). Early onset familial AD is linked to 3 genetic mutations on chromosome 21, while the genetic mutations for late-onset AD are on chromosome 19 (McCance & Huether, 2019). There is no genetic association for sporadic late onset AD (McCance & Huether, 2019). However, the alterations in the brain are the same as early onset familial AD and late onset AD (McCance & Huether, 2019). These alterations include abnormally folded tau proteins and amyloid betas, tangles of the intraneuronal neurofibrillary, accumulation of plaques, and degeneration of cholinergic neurons (McCance & Huether, 2019). There is a disruption of nerve impulse transmission, neuron deaths, and neuritic plaques due to these changes (McCance & Huether, 2019). All of these disruptions contribute to the loss of cognitive function in Alzheimers disease (McCance & Huether, 2019).

Frontotemporal dementia (FTD) is also a form of dementia (McCance & Huether, 2019). However, contrary to Alzheimers, this dementia focuses on the frontal lobes (McCance & Huether, 2019). Under imaging, atrophy of both the frontal and temporal lobes has been seen (McCance & Huether, 2019). Just like AD, the pathogenesis is also unknown (McCance & Huether, 2019). Additionally, most of the cases involve gene mutations like AD (McCance & Huether, 2019). Under the frontotemporal dementia branch, there are 3 different syndromes including, behavior variant of frontotemporal dementia, progressive nonfluent aphasia, and semantic dementia (McCance & Huether, 2019). McCance and Huether (2019) mention that there is no specific treatment for this.

2.
The clinical findings that support diagnosis include angry but cooperative upon physical exam, an MMSE of 12, and hippocampal atrophy. Additionally, the wifes concerns of worsening memory aid in the diagnosis. The wife mentioned that he has recently been getting lost in his neighborhood of 35 years, has been found wandering, and becomes angry and defensive when questioned about certain situations. He also allowed unknown people into the home and purchased a home security system despite already having one. He cannot balance his checkbook and is also having difficulty dressing himself.

3.
When looking at ADs risk factors, age and familial history are the most prevalent risk factors (McCance & Huether, 2019). Additionally, other risk factors include smoking, diabetes, hypertension, hyperlipidemia, obesity, depression, head trauma, sedentary lifestyle, elevated cholesterol levels, neuroinflammation, and oxidative stress (McCance & Huether, 2019). Other factors such as being female, being estrogen deficit, or being cognitively inactive are also predisposing factors (McCance & Huether, 2019). In this scenario, this patient has a family history of his father expiring at 78 due to AD. Additionally, the patient himself is 76, so he is of older age. However, he is a retired lawyer meaning he was not cognitively inactive. He practiced golf at least twice per week, meaning he tried to incorporate physical activity into his life. Is negative for depression and head injuries. Also, negative for hypertension and hyperlipidemia. Denies smoking and is not obese. Based on this information, my hypothesis is that this patient developed AD due to some sort of genetic mutation passed on from his father which caused him to develop late-onset AD. However, there are so many different factors that could have played a role throughout his life and thus is hard to pinpoint what may have caused it.

4.
When looking to stage AD, it is important for the NP to take a family and caregiver history as the patient may not be a good historian due to their disease (Kumar et al., 2022). In this case, with the wifes information, the likely stage of AD is middle stage (McCance & Huether, 2019). This is because the patient is showing significant forgetfulness, i.e. not remembering where he lives although he has been there for 35 years (McCance & Huether, 2019). He is also forgetful of events, such as forgetting they already had that security system in the home (Alzheimers Association, 2024). He is also moody, as per the physical assessment showing he was angry but cooperative (Alzheimer’s Association, 2024). The wife mentioned he is having trouble dressing himself and is considering hiring a day-time caregiver to help with certain activities of daily living. That would also be indicative of the middle stage as it includes instrumental activities of daily living-dependent and is having some activities of daily living problems (McCance & Huether, 2019). He is also showing an increased tendency to wander and become lost as he was brought home by neighbors due to wandering (Alzheimers Association, 2024). In this stage, the Alzheimers Association (2024) mentions that these patients can still participate in daily activities, however, with assistance. They also recommend considering respite care to allow the caregiver to take a break from caregiving (Alzheimers Disease, 2024).

Second discussion:

Compares and contrasts the pathophysiology between Alzheimer’s disease and frontotemporal dementia.

Alzheimers disease and frontotemporal dementia are the most common neurodegenerative early-onset dementias (Israr & Orlando, 2023). Alzheimer’s disease is a neurodegenerative disease with insidious onset and progressive impairment of behavioral and cognitive functions including memory, comprehension, language, attention, reasoning, and judgment (Kumar et. al., 2022). There is no known cause of Alzheimer’s disease, however, it is characterized by an accumulation of abnormal neuritic plaques and neurofibrillary tangles. Plaques are spherical microscopic lesions that have a core of extracellular amyloid beta-peptide surrounded by enlarged axonal endings. Neurofibrillary tangles are fibrillary intracytoplasmic structures in neurons formed by a protein called tau. In Alzheimer’s disease, due to aggregation of extracellular beta-amyloid, there is hyperphosphorylation of tau which then causes the formation of tau aggregates (Kumar et. al., 2022). Alzheimer’s disease can be inherited as an autosomal dominant disorder with nearly complete penetrance. The autosomal dominant form of the disease is linked to mutations in 3 genes: AAP gene on chromosome 21, Presenilin1 (PSEN1) on chromosome 14, and Presenilin 2 (PSEN2) on chromosome 1 (Kumar et. al., 2022).

Frontotemporal dementia is a sporadic disease that targets brain areas that are responsible for personality, behavior, language learning, motivation, abstract thinking, and executive function (Isar & Orlando, 2023). Frontotemporal dementia has three distinct clinical syndromes based on the underlying pathologic mechanism characterized by intracellular deposition of abnormal proteins aggregates in the frontal and temporal lobes resulting in the degeneration of neurons, micro-vacuoles formation, and astrocytosis (Isar & Orlando, 202). Genetics play a key role in his disease cases are found to be an autosomal dominant inheritance. Most cases involve mutations of genes encoding protein tau and progranulin (Isar & Orlando, 2023).

2. Identifies the clinical findings from the case that supports a diagnosis of Alzheimer’s disease.