Alzheimer's Disease



Alzheimer's Disease


Dementia prevalence is growing with the increase in life expectancy. Dementia is one of the leading disabilities among the elderly resulting in dependency and considerable financial burden. According to the Framingham Study, Alzheimer’s disease is the most prevalent etiology of dementia (Satizabal et al., 2016). Alzheimer’s disease is an acquired behavioral and cognitive impairment. Currently, this is an incurable disease associated with devastating occupational and social disabilities.

In Alzheimer’s disease, plaques deposit deep in the brain (hippocampus) in the areas responsible for memory, thinking, and decision-making. It is still unknown whether the plaques cause the disorder or just behave as markers of the disease. In the current paper, data on epidemiology, key aspects of etiology, pathophysiology, diagnostics, and treatment of Alzheimer’s disease will be discussed.

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Incidence/Prevalence and Factors that Influence the Impact

Alzheimer’s disease accounts for 60 percent of all cases of adult dementia (Yiannopoulou & Papageorgiou, 2013). The Centers for Disease Control and Prevention reports that currently, more than 10 percent of adults aged above 65 years have Alzheimer’s disease, which makes five million people in the U.S. (Korolev, 2014). More than half of those beyond 85 years suffer from this condition (Sun, Jin, & Ling, 2012). This is the fifth leading cause of death among adult Americans, while more than 500 billion USD are spent annually to support the affected individuals across the country (Huang & Mucke, 2012; Korolev, 2014).

Worldwide, 35 million people live with Alzheimer’s disease, and considering the current trend towards aging of the population, by the year 2030, there will have been 65 million (115 million by 2050) of such patients (Korolev, 2014). Therefore, the prevalence of dementia is significant. Nevertheless, the recent reports from the Framingham Study suggest that the incidence of dementia in the elderly is currently declining (Satizabal et al., 2016).

The authors of this investigation explain the reducing incidence by the enhanced effects of antihypertensive agents. As for Alzheimer’s disease, the Framingham Study indicated an independent decline in its incidence over the previous five decades among the high school graduates. Better diet, general cardiovascular health, physical activity, and unknown factors might contribute to the new evidence (Satizabal et al., 2016).

Finally, the incidence of Alzheimer’s disease seems to be declining due to yet unstated factors, but its prevalence is considerable and is likely to continue increasing in the future.

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The exact etiology of Alzheimer’s disease is unknown, but it is recognized as a multifactorial malady. According to the common approach, a combination of genetic and environmental factors provokes a pathophysiological cascade that causes dementia over the years. Both modifiable and non-modifiable etiological factors are involved. Advancing age is a strong determinant of Alzheimer’s disease. The risk to acquire the disease doubles every five years after 65, while only 5% of Alzheimer’s disease appears before 65, which is also called ‘early Alzheimer’s disease’ (Korolev, 2014).

Family history is another potential factor. Autosomal dominant mutations are detected in families with Alzheimer’s disease. Clients with Down’s syndrome (trisomy 21) are at a higher risk of developing Alzheimer’s disease (Huang & Mucke, 2012; Korolev, 2014). The mutations are related to the genes of amyloid precursor protein (chromosome 21), presenilin 1 (chromosome 14), presenilin 2 (chromosome 1), and apolipoprotein E4 (chromosome 19) (Huang & Mucke, 2012; Nye et al., 2016).

Females tend to live longer and have Alzheimer’s disease more often. Alzheimer’s disease is associated with a low educational level. Perhaps, education stimulates the brain and opposes dementia. Other risk factors include obesity, hyperlipidemia, arterial hypertension, diabetes, smoking, history of head injury, syphilis, herpes, depression, pesticides (Korolev, 2014; Sun et al., 2012). Out of these factors, arterial hypertension is the best-studied modifiable factor. Autopsy data from those who took beta-blockers and antihypertensives found that in the cases of controlled arterial blood pressure, the Alzheimer’s plaques were less frequent (Satizabal et al., 2016).


Alzheimer’s disease causes disruption of the brain structure and function. On the microscopic level, the pyramidal neurons are progressively lost, while the synapses between the neurons disarrange so that circuits responsible for the memory and cognitive function are disabled.

There are several theories explaining Alzheimer’s disease:

  1. Cholinergic dysfunction of the central nervous system. Cholinergic neurons loss in the hippocampus and cortex leads to cognitive deficits.
  2. The amyloid cascade hypothesis. Normally, the amyloid precursor protein is cleaved by the β-secretase; if it fails, the amyloid-beta (Aβ) accumulates in the brain. Aβ is toxic and disrupts the calcium channels in the neurons. The insoluble Aβ is the substrate for the amyloid plaques found in the brains of patients with dementia. The amyloid plaques are of high diagnostic value in the alive patients, but they do not correlate with the clinical prognosis.
  3. Neuroinflammation. The deposition of Aβ results in chronic inflammation, which further disrupts healthy neurons and leads to brain mass loss.
  4. Other. Presenilin 1, 2 mutations cause hypercholesterolemia, which is associated with Alzheimer’s disease. Apolipoprotein E4 is a natural anti-inflammatory agent so that its mutations shift the balance towards inflammation (Huang & Mucke, 2012; Korolev, 2014; Sun et al., 2012).

As a result, the brain mass is reduced (especially the neurons in the cortex and hippocampus) and its function declines. The degeneration starts from the temporal areas and speeds to the parietal lobes approaching the frontal areas in the advanced stages. The anatomical pattern of neurodegeneration correlates well with the clinical deficits (speech, memory, visual function, executive, reasoning). The loss of synapses and dendritic spines reflects the depth of cognitive deficits even better than the loss of neurons (Huang & Mucke, 2012). Finally, emotional or personality disturbances compose a psychiatric picture (Korolev, 2014; Sun et al., 2012).

Signs and Symptoms

Dementia is a decrease in the ability to think, talk, and remember, while consciousness is not affected. Dementia interferes with the work, as it represents a decline from previous levels, and cannot be explained by delirium or a major psychiatric disorder (Korolev, 2014; McKhann et al., 2011). The cognitive impairments include:

  1. Inability to acquire and remember new information revealed in repetitive questions, misplacing personal belongings, forgetting events, and getting lost on a familiar route.
  2. Poor handling of complex tasks or judgment expressed in poor understanding of safety risks, inability to manage finances and inability to plan complex activities.
  3. Impaired visuospatial abilities, namely inability to recognize faces or common objects or to find objects, inability to operate simple implements, or orient clothing to the body.
  4. Impaired language functions, namely difficulty recollecting common words while speaking, as well as speech and spelling errors.
  5. Changes in personality, namely uncharacteristic mood fluctuations, impaired motivation, apathy, decreased interest in previous activities, loss of empathy, and engagement in socially unacceptable behaviors (McKhann et al., 2011).

Clients with Alzheimer's disease have a history of memory loss. Memory troubles are progressive and with time, are added with cognitive disorders. Typically, Alzheimer's dementia starts after the age of 65 years, beginning with memory loss, having gradual onset and deterioration, and showing no motor impairment in physical characteristics until the late stages. Mild forms of the disease develop in the same way, albeit with less obvious presentation (Korolev, 2014; McKhann et al., 2011). The clinical diagnosis of Alzheimer's disease is not an easy task and its accuracy hardly approaches 70-90% (Korolev, 2014).

The current recommendations of the National Institute on Aging and the Alzheimer’s Association workgroup classify Alzheimer’s disease into probable and possible Alzheimer’s dementia in terms of practical issues. Both meet the criteria for dementia as described earlier. Probable Alzheimer’s disease has a gradual onset, history of progressive cognitive decline, and no evidence for another cause of cognitive impairment. Possible Alzheimer’s disease is revealed in the atypical clinical course or in mixed etiology (McKhann et al., 2011).

Physical examination involves the assessment of attention, concentration, memory, language, praxis, and visuospatial function. Neurological exams and mental evaluations need to be addressed. A complete mental evaluation is the basics for understanding the disease's progress. The neurological examination should exclude other causes of dementia, such as stroke or Parkinson’s disease.

The most reliable way to diagnose Alzheimer's disease is to perform a postmortem examination of the brain in the common areas and to detect amyloid plaques and the neuronal damage (Korolev, 2014; McGhee et al., 2014). Lab investigations are of low diagnostic help; any known biomarkers are not helpful in the estimation of this condition, even if taken from the cerebrospinal fluid (McGhee et al., 2014). Brain imaging with CT or MRI helps to exclude other etiologies of dementia and indicate atrophy of the hippocampi (McKhann et al., 2011). Genetic testing for the amyloid precursor protein, presenilin 1, 2, and apolipoprotein E4 is promising (Nye et al., 2016).

Depression is the most obvious differential diagnose of Alzheimer's disease because it also meets the loss of memory, concentration, and a decrease in motivation. The other conditions include posttraumatic encephalopathy. In chronic posttraumatic encephalopathy, the brain degenerates after repeated head injuries (for example, among football players). Atherosclerosis of the carotid arteries is the underlying etiology of the cerebrovascular disease. In the case of the cerebrovascular disease, stroke severely damages certain lobes of the brain with subsequent loss of psychological skills.

Alcohol abuse, especially in advanced stages is characterized by apathy, loss of coordination, and poor memory. Hearing or visual impairment from ear or eye pathologies may sometimes be confused with the psychiatric anomaly. In the case of hypoglycemia, the client is slow and sleepy. Parkinson’s disease may mimic the symptoms of dementia. Other conditions for the differential are thyroid dysfunction and polypharmacy from sedatives (Lakhan, 2016).


Alzheimer's disease cannot be cured; the only symptomatic approach is recognized. Approved drugs alleviate the symptoms, but cannot slow down the speed of disease progression.


The key approach of the pharmacological intervention is aimed at enhancing the neuro transmitting between the neurons:

  • Acetylcholinesterase inhibitors (Donepezil, Rivastigmine, Galantamine) increase the concentration of acetylcholine, improving cognitive results, and function. These drugs block acetylcholinesterase, a natural enzyme that breaks down the acetylcholine resulting in the increased activity of the neurons in the hippocampus and neocortex. The initiation of these drugs at the early stages is recommended by the FDA. Donepezil is metabolized in the liver (55% of oral intake) and excreted with the feces (21%) and urine (79%);
  • Partial N -methyl-D-aspartate (NMDA) antagonist (Memantine) eliminates ‘noise’ to the neuron and protects the cell from calcium overload. As a result, the nerve damage is mitigated. The FDA approves this drug for moderate and severe conditions, but it is not effective against mild symptoms. Memantine is excreted with the urine almost unchanged, while 20% of the absorbed drug is metabolized in the liver;
  • M1 receptor agonists mitigate the symptoms and slow the disease progression;
  • Anti-A drugs are the most promising; they include calcium antagonists (protect the neurons from calcium overload of the neurons), antioxidants (protect the nerves from Oxygen toxic free radicals), nonsteroidal anti-inflammatory drugs (reduce inflammation in the brain), hypolipidemic drugs (reduce the cholesterol), iron chelators (remove excess iron from the brain). However, all these agents are non-specific and lack evidence support. Currently, the only specifically engineered anti-A the drug that has entered the clinical trials is tramiprosate, a compound that interferes with A;
  • β-secretase inhibitors may enhance the natural breakdown of amyloid; this area is under investigation;
  • Nicotine injected intravenously enhances neuron survival and results in the improvement of cognitive tasks among patients (Hong-Qi, Zhi-Kun, & Sheng-Di, 2012; Sun et al., 2012; Yiannopoulou & Papageorgiou, 2013).


Vaccination with the agent that provokes the production of antibodies against Aβ prevents Alzheimer's disease in experiments (Sun et al., 2012). Injections of monoclonal antibodies against amyloid are potentially effective but are associated with significant side effects (Hong-Qi et al., 2012).

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Gene Therapy

Transplantation of acetylcholine-rich neurons into experimental rats with Alzheimer's disease ameliorates deficits (Hong-Qi et al., 2012).

Secondary Conditions

Secondary symptoms in Alzheimer's disease include sleep disorders, depression, and hallucinations. Conventional psychotropic medications are used for secondary conditions:

  • Antidepressants, selective serotonin uptake precursors alter the degradation of serotonin and increase its concentration in the brain neurons.
  • Anxiolytics inhibit anxiety by enhancing the effects of the neurotransmitter γ-aminobutyric acid resulting in relaxation effects.
  • Neuroleptics manage hallucinations by blocking dopamine-dependent chains of the brain (Korolev, 2014).

Patient Teaching

Recent research suggests that a healthy lifestyle reduces the risk of developing Alzheimer's disease (Satizabal et al., 2016). Routine exercises and regular physical activity can protect from its progression and have a general defensive effect on the brain. In the case of the mild form of the disease, physical exercising correlates with higher hippocampal volumes (Lakhan, 2016). In any effort, the environment should be friendly to prevent accidental falls or trauma. It is recommended to have contacts with the encirclement – parks, restaurants, museums to support behavioral skills.

Health Promotion

The client is recommended to modify risk factors:

  1. Dietary recommendations include vegetables, fresh fruit, nuts, fish and omega-3 rich oils, complex vitamins (B12, B6, folic acid, vitamin E), and a limited amount of meat or dairy products.
  2. Reduction of alcohol consumption to a low-moderate level
  3. Engagement in regular physical exercises and social activities
  4. Brain stimulation activities (puzzles, dancing, music, singing)
  5. Integration into the Alzheimer's Association or other support groups.
  6. Regular sleep and stress management (Cummings, Isaacson, Schmitt, & Velting, 2015).

Clinical Guidelines

The American Academy of Neurology and the American Psychiatric Association have published the most comprehensive guidelines on Alzheimer’s disease management in 2003 and 2007 (Geldmacher & Kerwin, 2013). Other investigations were conducted by the National Institute on Aging and the Alzheimer’s Association workgroup and other institutions (McKhann et al., 2011). The evidence-based approach includes cognitive assessment during the initial and annual wellness visits for the primary detection of dementia.

Guidelines recommend early detection of dementia at the stage of mild impairments with cognitive assessment at the core of the evaluation. Approved pharmacological interventions are the intake of acetylcholinesterase inhibitors (Donepezil, Rivastigmine, Galantamine) and the N-methyl-d-aspartate receptor antagonist (Memantine). There is no evidence as to when to stop taking these medications. The caregiver should initiate social activities and health promotion programs for the client (Geldmacher & Kerwin, 2013).

A protocol for the Nurse Practitioner includes twelve visits to the client for twelve months. During the first two visits, the nurse evaluates how the patient/family adjusts to the news about dementia and explains cognitive impairments that may emerge with time. A complete review of medications is conducted at this stage. Starting from the first visit, the cognitive condition and psychological picture should be studied. Nonpharmacological interventions are added to every meeting if necessary (Fortinsky et al., 2014).

Treatment Outcomes

Patients with Alzheimer's disease compose a heterogeneous group, so it is usually difficult to predict the outcomes. In general, better results are shown by men, who take higher doses of acetylcholinesterase inhibitors with nonsteroidal anti-inflammatory drugs, and with absent Apolipoprotein E4 allele (Wattmo, Wallin, Londos, & Minthon, 2011). Males also have a better response to the treatment, which might be explained by hormonal background. It also needs to be mentioned that aged patients respond to treatment better than young ones, albeit they have a better knowledge of their impairment. The same study shows that patients with higher education develop the disease with milder symptoms, but their decline is faster on the follow-up (Wattmo et al., 2011). It is assumed that a greater burden of pathology is needed to damage individuals with high cognitive abilities.

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Expected outcomes of treatment are targeted at supporting the social engagement of the client. Depression and secondary conditions among the patients should be controlled; the dietary patterns and physical activity need to be corrected and supported on each level continuously. Because Alzheimer's disease is an incurable chronic condition, the life of such patients directly depends on supportive and symptomatic care. The patient should never be retained from medical attention. For example, 40% of these patients experience weight loss, so it is the responsibility of the caregiver to recognize malnourishment on time (Cummings et al., 2015).


Alzheimer's disease is a devastating medical condition with an increasing prevalence. The etiology and pathophysiology of the condition are poorly investigated. The clinical course of Alzheimer's disease is disappointing and management options are currently limited. Intensive scientific research is being conducted in this area. Although certain success in the understanding of its mechanisms has been achieved, while new therapeutic options are under investigation, the health care is generally palliative.

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