Pathophysiology And Management Of Alzheimer’s Disease: A Case Study

Pathophysiology of Alzheimer’s Disease

Question:

Discuss the Pathophysiology of Alzheimer’s disease in relation to the presenting signs and symptoms. Discuss the pharmacological Management in relation to symptom relief and ongoing Management.

As per the Alzheimer’s Association (2013), AD is an irreversible, progressive and neurological disorder that slowly impairs the thinking ability and memory and eventually the capability to perform normal activities.  The main characteristics of this disease are the aggregation of the Amyloid plaques and the neurofibrillary tangles in the brain. Another feature of this disease is the loss of communication between the neurons that transmits messages to the brain and different parts of the body.

This report discusses about the Pathophysiology of the disease, based on the symptoms and case history of the patient, Antonio Renaldi, who is suffering from mild to severe short term memory loss and few such problems related to AD.  The following report also aims at providing information about the different pharmacological treatments and the nonpharmacologicals treatment that are suitable for Antonio, as per his symptoms. Although the disease does not have any cure, researches are still going on how to decrease the death of the neuronal cells. Lastly an idea has been given regarding the proper management of the behavioral symptoms that can provide comfort to the AD patients, as it is seen that Antonio is also suffering from social widrawal and an idea has been given for making things easier for him.

Alzheimer’s disease is progressive, irreversible and a neurological disorder that results to impaired memory, loss of thinking skills and results in a cognitive decline (Nelson et al, 2012). This disease normally appears in the mid- 60s and worsen if treatment is not done properly. It is a common type of dementia. Many researches have taken place regarding the Alzheimer’s disease, but are the main reasons behind the reason why they occur is largely unknown (Birren et al., 2013).

According to the report the Patient has taken a CT of brain. Normally a CT of brain discloses the brain anatomy. A person having AD would show a loss in the brain mass, because the hippocampus of the brain would be atrophied. The mini mental assessment taken by the patient also shows a less score. The Mini–Mental Assessment (MMSE) or Folstein test involves a 30-point questionnaire which is used to measure the cognitive impairment. It is normally used in medicine to screen dementia. It is used to measure the degree of the cognitive impairment and is an effective way of understanding a patient’s response to the treatment. A score equal to or greater than 24 signifies better mental health. The mini-assessment score got by Antonio is quite low which clearly indicates impaired cognition. The following case study also says that the patient had taken a full blood test. A blood test could easily detect the AD before the symptoms could appear (Montine et al., 2012). A recent research done by the University of Otago has discovered a  marker in the blood that could help screen Alzheimer’s through a single blood test.  Recent researches have shown that the microRNAs found in the blood and the brain can easily detect AD with almost 86 percent accuracy (Denk et al., 2015).

Pharmacological Treatments

As per the information provided in the case study we have come to know that Antonio Renaldi is suffering from mild to severe short term memory loss which have caused due to the impaired communication between the neurons or neuronal death. AD is a very common type of dementia. The AD specialists can recognize the histopathological features within the brain. One histopathological feature involves the presence of the neurofibrillary tangles and amyloid plaques (Jiang et al., 2013). Amyloid β protein accumulates outside the neurons and a modified form of Tau protein aggregates inside the nerve cells. AD impairs the proper functioning of the synapses and neurons. Almost trillions of synapses allow nerve impulses to travel through the brain circuits. The accumulation of the β proteins prevents the communications between neurons and eventually the cell dies.  In AD the Tau tangles prevents the transfer of the nutrients in the neurons and ultimately causes cell death. In certain cases the brain can also show abnormal shrinkage due to the cell loss and debris due to the dying neurons. The damage occurs at first in the hippocampus portion of the brain, that stores the memory but finally the additional parts are also affected causing severe short term memory loss, as seen in the case of Antonio Renaldi. It has been reported that in some cases genetic mutations are also responsible for the cause of AD (Heppner, Ransohoff & Becher, 2015). Mutations in the gene expressing amyloid precursor proteins and Presinilin 1 and Presinilin 2 poteins potentially cause AD. Individuals suffering from AD often have difficulties in finding words to communicate with the people. Hence they detach themselves from social gatherings and often suffer from depressions. Patients with AD often suffer from sleeping disorders, so they sometimes wake up early. Antonio Renaldi is seen to have developed all these symptoms, which indicates the occurrence of AD.

There are three stages of AD. They are- preclinical AD, dementia due to AD and mid cognitive impairment due to AD. The pre clinical stage involves with mild modifications in the brain. The blood diagnosis shows the signs of these disease but more important symptoms like the memory loss doesn’t appear at first. The presymptomatic stage may last for 20 years or more. Patients with mild cognitive impairment have very mild changes in the thinking capabilities that are normally recognizable to the patient’s family and friends, although this doesn’t prevent the patient from doing every day’s activity.

Non-pharmacological Treatments

Pharmacological treatment

They are treatments where medications are administered to prevent the illness or treat its signs. The medications that are normally given cannot stop the death of the neurons though the delaying of the process can be done (Salomon et al., 2012). There are certain drugs that can temporarily increase certain substances known as neurotransmitters. Acetyl-choline neurotransmitters are essential for learning and processing memory. In patients with AD the neurotransmitter is decreased. This deficit along with other presynaptic cholinergic deficits, and decreased activity of acetyl cholinesterase, emphasizes the cholinergic hypothesis of Alzheimer’s disease. This causes cognitive decline in AD patients and neuronal damage. Three cholinesterase are prescribed to treat mild to severe stages of Alzheimers. They are- Donepezil (Aricept) is prescribed for treating all the phases of Alzheimer’s. Rivastigmine (Exelon) and Galantamine (Razadyne) is prescribed for treating mild Alzheimer’s. The sleeping disorders that are found in AD patients like Antonio Renaldi,  the following medicines like Tricyclic antidepressants, such as nortriptyline and trazodone can be prescribed. Sleeping pills like zolpidem, chloral hydrate and zaleplon, Antipsychotics like quetiapine and risperidone can be given to Antonio as he had been suffering from sleeping disorders. Classical antipsychotics like haloperidol (Doody et al., 2013). The risks of medicines that induce sleep for elderly people shall be kept in to mind. There are risks like falls and accidents. If these medicines are even used, they should not be continued after the establishment of a regular sleeping pattern.  Non-drug methods should be tried before using medicines, as some medications might cause side effects.

Non pharmacological therapies

As per the informations given in the case study we have come to know that the person is suffering from social widrawal and depression. Therefore the health care providers or the family members should focus on the active management of the disease. Despite of the fact that AD does not have any proper treatment, studies have shown that an active management of the disease can improve the condition of the patients along the various stages of the disease. Active management involves 1) proper application of the treatment procedures 2) management of the condition that is already coexisting  3) Care and support provided by the health caregivers 3) Participation in many constructive, supportive activities (Burke et al., 2015).

Non pharmacological therapies involve cognitive training and things like behavioral interventions. The non pharmacological courses often   delay the brain ageing in the AD patients. The non pharmacological interventions are mainly useful to cope up with depressions, wandering, sleep disorders, aggression and agitation, that Antonio Renaldi is facing. There are researches that support the effectiveness of these non- pharmacological therapies (Horr, Messinger & Pillai, 2015).  This in some way would improve their quality of life, cognitive function, mood, behavior, performance of daily activities. Additional studies say that remaining socially and mentally active reduces the risk of AD and other dementia. Thus it can be said that proper management of this disease can make the quality of the life better and can extend the life span of the AD patients (Leon, Garci & Marco?Contelles, 2013).

Management of Behavioral Symptoms

Conclusion

In the above case study, the patient has been suffering from short term memory loss, depression, sleeping disorder and loss of confidence, thus widrawal from the society. His age and the symptoms thus indicated dementia. The CT reports of the brain have shown the shrinkage in brain due to the loss of neuronal cells. The blood tests conducted also indicated towards the Alzheimer’s disease. Further histopathological analysis of his brain had also indicated the formation of the neurofibrillary tangles and amyloid plaques that prevents the flow of the nerve impulse through the neurons, ultimately resulting in the death of the neuronal cells.  Although there are certain medications that could be used to reduce the problems faced by Antonio, like sleeping disorders, memory loss and more, but emphasis is also given on the non-drug treatment, as per the age of the patients. Henceforth it can be concluded that active management of the disease, like 1) suitable application of the treatment options 2) management of the coexisting conditions 3) Care and support given by the health care provider, caregivers 3) Participation in many constructive, supportive activities could at least make their journey through the different stages of the disease, a bit easier and happier.

References

Alzheimer’s Association. (2013). 2013 Alzheimer’s disease facts and figures. Alzheimer’s & dementia, 9(2), 208-245.

Birren, J. E., Cohen, G. D., Sloane, R. B., Lebowitz, B. D., Deutchman, D. E., Wykle, M., & Hooyman, N. R. (Eds.). (2013). Handbook of mental health and aging. Academic Press.

Burke, A., Hall, G. R., Yaari, R., Fleisher, A., Dougherty, J., Young, J., … & Tariot, P. (2015). Pocket Reference to Alzheimer’s Disease Management. Springer Healthcare Limited.

Denk, J., Boelmans, K., Siegismund, C., Lassner, D., Arlt, S., & Jahn, H. (2015). MicroRNA profiling of CSF reveals potential biomarkers to detect Alzheimers disease. PLoS One, 10(5), e0126423.

Doody, R. S., Raman, R., Farlow, M., Iwatsubo, T., Vellas, B., Joffe, S., … & Aisen, P. S. (2013). A phase 3 trial of semagacestat for treatment of Alzheimer’s disease. New England Journal of Medicine, 369(4), 341-350.

Heppner, F. L., Ransohoff, R. M., & Becher, B. (2015). Immune attack: the role of inflammation in Alzheimer disease. Nature Reviews. Neuroscience, 16(6), 358.

Horr, T., Messinger-Rapport, B., & Pillai, J. A. (2015). Systematic review of strengths and limitations of randomized controlled trials for non-pharmacological interventions in mild cognitive impairment: focus on Alzheimer’s disease. The journal of nutrition, health & aging, 19(2), 141.

Jiang, T., Yu, J. T., Tian, Y., & Tan, L. (2013). Epidemiology and etiology of Alzheimer’s disease: from genetic to non-genetic factors. Current Alzheimer Research, 10(8), 852-867.

Leon, R., Garcia, A. G., & Marco?Contelles, J. (2013). Recent advances in the multitarget?directed ligands approach for the treatment of Alzheimer’s disease. Medicinal research reviews, 33(1), 139-189.

Montine, T. J., Phelps, C. H., Beach, T. G., Bigio, E. H., Cairns, N. J., Dickson, D. W., … & Nelson, P. T. (2012). National Institute on Aging–Alzheimer’s Association guidelines for the neuropathologic assessment of Alzheimer’s disease: a practical approach. Acta neuropathologica, 123(1), 1-11.

Nelson, P. T., Alafuzoff, I., Bigio, E. H., Bouras, C., Braak, H., Cairns, N. J., … & Duyckaerts, C. (2012). Correlation of Alzheimer disease neuropathologic changes with cognitive status: a review of the literature. Journal of Neuropathology & Experimental Neurology, 71(5), 362-381.

Salomone, S., Caraci, F., Leggio, G. M., Fedotova, J., & Drago, F. (2012). New pharmacological strategies for treatment of Alzheimer’s disease: focus on disease modifying drugs. British journal of clinical pharmacology, 73(4), 504-517.