Introduction
Alzheimer’s Disease (AD) is a neurological disorder caused by many factors, which usually affects older members of the population. AD is a form of dementia that includes cognitive impairment, behavioral changes, and impairment of daily activities (Waldemar & Burns, 2016). The disorder is not new to medical science. Nevertheless, it was not until the beginning of the 20th century that attempts to explain its causes and forms began to appear (Waldemar & Burns, 2016). AD is a challenging issue for research; despite more than a hundred years of research, it cannot be stopped or prevented. However, with existing approaches in diagnosis and treatment, it is possible to slow down the development of AD.
Causes of Alzheimer’s Disease
According to the American Psychiatric Association (as cited in Waldemar & Burns, 2016, p. 1), “Dementia is a clinical syndrome operationally defined as cognitive impairment in at least two domains interfering with activities of daily living.” The first report of AD is dated 1906 in Alois Alzheimer’s observations of a patient displaying dementia (Waldemar & Burns, 2016). Castrillo and Oliver (2016) spoke of the multifactorial nature of AD, defining “a combination of genomic, epigenomic, interactomic and environmental factors” (Castrillo & Oliver, 2016. p. 3) that influence the development of this disorder. Lazarov and Tesco (2016) presented models of cognitive decline in healthy aging compared to the asymmetric cognitive decline in preclinical AD, stating that neuropathological changes develop a long time before any clinical symptoms of this disorder become evident, and it can be diagnosed.
Symptoms and Signs
AD is rarely diagnosed at an early stage since clinical symptoms and characteristic signs can appear years after neuropathological changes begin (Lazarov & Tesco, 2016). Because the development of the disorder is individual for every person, the observation of symptoms is even more complicated. The majority of patients observe AD symptoms for the first time after the age of sixty (National Institute of Aging, n.d.). Waldemar and Burns mention that the prevalence of AD “increases exponentially between 65 and 85 years, doubling for each successive 5-year age group” (2016, p. 27).
Susceptibility to AD is observed among older people, those who have a family history of AD, women rather than men, people with a lower education level, patients suffering from cerebrovascular disease or earlier head injuries, and the presence of the APOE-ɛ allele, among other factors (Waldemar & Burns, 2016).
The first symptoms of AD vary and are often misinterpreted. They can be confused with the consequences of taking a new medication, an operation, or a febrile disease (Waldemar & Burns, 2016). AD presents both cognitive and behavioral symptoms. Cognitive symptoms include the progressive loss of episodic memory, while old memories remain uninfluenced for a long time. Waldemar and Burns also mention “deficits in frontal, occipital, or parietal functions” as frequent initial symptoms in about 15% of AD cases (2016, p. 28). Visuospatial deficits, signaling right hemisphere dysfunction, are another sign of AD. Patients experience problems in visuospatial orientation, can feel unsafe in new places, or not be able to use some tools and objects. The reduction of executive functions, which include initiating, planning, sequencing, and monitoring activities, is also observed in the early stage of AD. Moreover, patients with AD usually do not recognize cognitive deficits (Waldemar & Burns, 2016).
The majority of AD patients (90%) demonstrate behavioral disturbances (Waldemar & Burns, 2016). Thus, behavioral symptoms include “agitation, hallucinations, delusions, sleep disturbances, depression, distractibility, apathy, aberrant motor behavior, and wandering” (Waldemar & Burns, 2016, p. 29). Usually, behavioral symptoms progress over the course of illness. They usually mean bad prognosis and negatively influence the quality of life.
Diagnosing Alzheimer’s Disease
Successful diagnosis depends on the early detection of symptoms. It enables timely intervention that may prolong the preservation of life quality and postpone nonreversible changes (Castrillo & Oliver, 2016). Unfortunately, it is when cognitive symptoms become evident that dementia can be clinically diagnosed. Diagnosing AD is challenging for physicians because it is important not to confuse it with impairment as a symptom of depression, delirium, toxic conditions, drain infections, or substance abuse (Waldemar & Burns, 2016).
AD diagnosis demands a complex approach. It is necessary to interview both the patient and a person who can give additional information since the patient can be unaware of cognitive or behavioral problems. Diagnosis also includes physical and neurological observation, cognitive tests, a psychiatric assessment of daily activities and other symptoms, a set of laboratory tests, and investigation of the brain through computed tomography or magnetic resonance imaging (Waldemar & Burns, 2016).
The first step in diagnosing AD is the confirmation of dementia syndrome. Dementia is diagnosed according to the following criteria identified by the World Health Organization (as cited in Waldemar & Burns, 2016, p. 44), including evidence of a decline in memory and other cognitive abilities; awareness of the environment being preserved during a long period; decline in emotional control or motivation or a change in social behavior; emotional lability; irritability; and apathy. It is underlined that the mentioned symptoms should be observed for at least six months.
Typical AD can be diagnosed if two aspects of diagnostic criteria are exhibited. First, the particular clinical phenotype should be considered. The presence of early and significant episodic memory impairment with “gradual and progressive change reported by patient or informant over more than six months” and “objective evidence of and the amnestic syndrome” revealed with the help of the episodic memory test are the evident signs of AD (Waldemar & Burns, 2016, p. 46). Second, it is necessary to study the in-vivo confirmation of AD. This includes “decreased Aβ1-42 together with increased T-tau or P-tau in CSF; increased tracer retention on amyloid-PET; or mutation (PSEN1, PSEN2, APP) present (Waldemar & Burns, 2016, p. 46).
Possible Treatment Strategies
With a timely diagnosis of AD in the initial stage, early symptomatic treatment is possible. AD treatment is challenging for several reasons. First, there is currently no actual cure, but only the possibility of reducing symptoms and postponing irreversible changes. Second, the patient’s age is a risk factor in treatment. AD is a disorder of the elderly, age 65 and older, who likely already have some chronic disease. It is crucial to consider the patient’s general condition when selecting a treatment strategy.
The conditions observed by patients with AD can be managed through pharmacological treatment. Four drugs are currently used in AD treatment: tacrine, donepezil, galantamine, and rivastigmine (Waldemar & Burns, 2016). However, none of them can stop the progress of the disease. Their choice depends on the stage of the disease, the set of symptoms, and the strategy selected by a medical institution. Overall, the strategies for AD treatment include symptomatic cure, combination therapy, and care of behavioral and psychological symptoms (Waldemar & Burns, 2016).
Another aspect related to treatment is the patient’s nutrition. There is evidence that certain nutritional elements can decrease AD risk (Lazarov & Tesco, 2016). Products rich in antioxidants are considered to have a positive influence.
The prognosis for patients with Alzheimer’s Disease
At present, prognoses for AD patients are not favorable. Despite many years of research, there are still no preventive measures or strategies for efficient treatment (National Institute of Health, n.d.). However, new research is being carried out to discover new approaches to diagnosis and to develop new, more effective drugs (National Institute of Health, n.d.). For example, the particular attention of researchers is focused on the investigation of the role of exercise and the study of genetic factors in AD prevention. Present-day perspectives of patients with AD include symptomatic treatment, life-long care, and support. Current treatment strategies in the case of early diagnosis can provide preservation of life quality and reduce cognitive and behavioral changes.
Conclusion
Currently, there is no effective cure for AD or other forms of dementia. However, there is a possibility to slow the development of the disease. It demands particular attention to early symptoms because the treatment is more successful when the changes in cognitive functions and behavior are still reversible. As soon as serious symptoms are revealed, it is necessary to provide a thorough examination to prove or disprove AD diagnosis. The role of the family is crucial in diagnosing AD. Since a patient is maybe not aware of changes, the information from a person close to the individual can prove decisive in diagnosing. Overall, the success of treatment depends on the accessibility of care and the cooperation of the patient’s family with health-care providers.
References
Castrillo, J.I., & Oliver, S.G. (Eds.). (2016). System biology of Alzheimer’s disease. New York, NY: Humana Press.
National Institute of Aging. (n.d.). About Alzheimer’s disease: Symptoms.
Lazarov, O., & Tesco, G. (Eds.). (2016). Genes, environment and Alzheimer’s disease. San Diego, CA: Elsevier.
National Institute of Health. (n.d.). The dementias: Hope through research.
Waldemar, G., & Burns, A. (Eds.). (2016). Alzheimer’s Disease. (2nd ed.). Oxford, UK: Oxford University Press.