Alzheimer’s Disease is a complex and challenging health concern which impacts millions of older adults throughout the world. The pathophysiologic nature of this condition is difficult to treat and prevent further decline. Many patients suffer significant brain dysfunction and memory loss resulting from Alzheimer’s Disease; therefore, it is necessary to evaluate this condition from the perspective of a specific case study and the potential pathophysiologic causes of the disease. It is expected that the case study description will address further considerations that impact the patient’s condition and how to optimize treatment methods to manage the disease at a successful level. The following discussion will evaluate a specific case study and will recognize the importance of pathophysiology in the diagnosis and treatment of Alzheimer’s Disease for this patient population.
Alzheimer’s Disease is a condition that impacts the brain and leads to a gradual decline in cognitive function, including the loss of memory and the ability to perform routine activities (“Chapter 20”). Common symptoms include aphasia, visual disturbances, the ability to reason and concentrate, and other related factors (“Chapter 20”). Approximately 4.5 million cases of the disease currently exist in the United States and continue to challenge researchers and clinicians in their efforts to discover and utilize treatments for this condition. Case studies provide specific information regarding patients with this condition and the different treatments that are available to manage its symptoms more effectively in the context of alleviating symptoms through different methods.
The patient is a 76 year-old female who has recently become socially withdrawn and less than enthusiastic regarding her prior activities (Kongable, 2006). Recent events demonstrate her lack of clarity and significant confusion regarding different public events, in spite of having no recent bouts of illness or infection (Kongable, 2006). The patient was brought into the emergency department for an examination and was anxious upon arrival with normal vital signs and no signs of physical abnormalities (Kongable, 2006). Upon review of her laboratory results, normal values were identified; however, her MMSE demonstrated three types of cognitive deficits and memory impairment (Kongable, 2006). Furthermore, the Geriatric Depression Scale favored memory challenges, poor sleeping habits, an apathetic tone, and increased dependence on others (Kongable, 2006). These latter factors are typical signs of Alzheimer’s Disease for this population group (Kongable, 2006).
The pathophysiology of Alzheimer’s Disease is complex and may be attributed to four specific gene mutations, in addition to different types of tissue mutations that contribute to this condition, such as a reduced levels of choline acetyltransferase and cell death for some neurons (“Chapter 20”). In addition, there tends to be an expanded level of production of B-Amyloid in neuronal cells and interferes with learning and memory signaling (“Chapter 20”). These contributions to the disease become progressively worse over time and lead to severe cognitive deficits and other incapacities for many patients with this condition (“Chapter 20”). The interferlence of routine neuronal growth and function is likely to create deficits in cognition that are irreversible and difficult to treat in many ways (“Chapter 20”).
Alzheimer’s Disease is historically complex and difficult to treat. In addition, testing for this disease is not universal for all patients; rather, it is the responsibility of the clinician to determine this diagnosis by examining symptoms and evaluating existing profiles for the disease (Mayo Clinic, 2013). Furthermore, neuropsychological testing is necessary for some patients to determine the type and level of dementia that a patient is currently experiencing (Mayo Clinic, 2013). Finally, brain imaging is required in some cases, including CT Scans and MRI testing to form a definitive diagnosis (Mayo Clinic, 2013). In the case study, the patient has a number of classic Alzheimer’s symptoms; therefore, the diagnosis is Alzheimer’s Disease.
For this patient and for many other patients, the effective treatment of Alzheimer’s Disease is very difficult and challenging for a number of reasons. It is important for patients to be evaluated and diagnosed as early as possible so that they are provided with the best possible options for treatment (Salloway and Correia, 2009). Currently, there are five pharmacologic alternatives available to treat patients with Alzheimer’s Disease, including a group of cholinesterase inhibitors such as Tacrine, Donepezil and Galantime, along with Memantine (Salloway and Correia, 2009). It is known that “The main benefit of the cholinesterase inhibitors in clinical trials is an attenuation of decline over time rather than an improvement in cognitive or behavioral symptoms. This should be considered when judging whether there has been a positive effect” (Salloway and Correia, 2009). Therefore, it is necessary to determine how to best approach the treatment of Alzheimer’s Disease for patients not with the intent to cure the disease, but to delay or reduce the impact of its various symptoms for as long as possible (Salloway and Correia, 2009).
For each patient who is diagnosed with Alzheimer’s Disease, it is important to evaluate the strength of different treatment methods and how they might support improved symptom management over time. For the case study patient, a cholinesterase inhibitor is likely to lead to the improvement of symptoms, but also depends on the stage of the condition at the time of diagnosis (Shah et.al, 2008). For current patients with the disease, the limited number of pharmacologic treatments that are available is likely to be troublesome; however, the progression of the disease and its specific causes lead to complex underlying issues that are difficult to manage, particularly when changes to the genetic makeup of neurons are evident (Shah et.al, 2008). Establishing an effective treatment plan for a given patient is challenging because the outcomes at best are the delayed onset of symptoms in some cases (Shah et.al, 2008).
Future directions for Alzheimer’s Disease represent a challenge to researcher and clinicians alike due to the complexities of this condition. It is known that “AD and other neurodegenerative disorders are associated with oxidative and inflammatory stress and mitochondrial dysfunction… In the neurobiology underlying the development of AD, there is a progression of hyperphosphorylated tau-bearing tangles appearing initially in the entorhinal cortex and hippocampus, then progressing to neocortex of the temporal, frontal, and parietal cortices. An optimal disease-modifying strategy should interfere with this cascade either by interfering with an upstream causal event (thought by many to be generation of Aβ) or targeting tangle formation directly” (Rafii and Aisen, 2009). Under these circumstances, it is necessary to continue research in order to develop new treatment methods for Alzheimer’s patients at different stages of the disease (Rafii and Aisen, 2009).
Patients with Alzheimer’s Disease are very challenging to clinicians and researchers alike because the ability to manage the disease has been realized for some patients, while others faced advanced cognitive impairment that cannot be alleviated or reversed (“Chapter 20”). Under these conditions, it is expected that disease progression will move forward on a gradual basis and will impact each patient in different ways. Nonetheless, the continued development of B-amyloid therapeutics is the primary objective of many scientists as a means of reducing the time progression of the disease (Rafii and Aisen, 2009). It is important for scientists to examine specific tissue forms and neurons to determine functionality and any mutations that exist in order to develop treatments that will slow these actions as best as possible to achieve optimal treatment outcomes for these patients (Rafii and Aisen, 2009).
Understanding Alzheimer’s Disease as a complex condition with many variables is perhaps the most effective means of recognizing the severity and devastation of the disease. Its pathophysiology has been determined to be the cause of genetic mutations and neuronal cell changes that contribute to eventual cell death and cognitive decline (“Chapter 20”). Therefore, it is important to evaluate each case individually and to determine the extent of the symptoms and the stage of the disease (“Chapter 20”). It is important to evaluate these considerations and the steps that are necessary to provide effective treatment to patients according to their specific symptoms and level of cognition.
For the patient in the example case study, due to the patient’s level of cognition and memory loss, she should be prescribed a cholinesterase inhibitor such as Tacine or Donepezil to treat the condition and to reduce the production of B-amyloid as best as possible. If this treatment method is successful, it will reduce the severity of current symptoms and prolong the condition for a longer period of time so that the patient’s quality of life is not minimized in a significant manner. From a non-pharmacologic perspective, it is also important to provide the patient with the means to preserve her quality of life as best as possible by attempting to provide a sense of normalcy and encouragement, in spite of her memory and cognitive deficits. This is perhaps the most relevant means of promoting a greater quality of life for the patient with the current state of her condition.
“Chapter 20: Alzheimer Disease.” 283-290.
Kongable, G. (2006). Case Study: Alzheimer Disease.
Raafi, M.S., and Aisen, P.S. (2009). Recent developments in Alzheimer’s Disease therapeutics. BMC Medicine, 7(7), 1-4.
Salloway, S., and Correia, S. (2009). Alzheimer disease: time to improve its diagnosis and treatment. Cleveland Clinic Journal of Medicine, 76(1), 49-58.
Shah, R.S., Lee. H.G., Zhu, X., Perry, G., Smith, M.A., and Castellani, R.J. (2008). Current approaches in the treatment of Alzheimer’s Disease. Biomedicine & Pharmacotherapy, 62(4), 199-207.