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Alzheimer’s: Evidence-Based Clinical Intervention


Alzheimer’s disease (AD) is a form of dementia − an acquired progressive degradation of mental functioning that leads to a complete disintegration of the personality. Degenerative brain changes associated with AD predominantly impact the behavior and cognitive abilities of a person. However, in the later stages, the disorder also affects patients’ physical condition and appearance.

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Signs and Symptoms

According to recent statistics, AD affects 3% of the population aged 65-74, 17% of 75-84 years old people, and 32% of those older than 85 (Alzheimer’s Association, 2017). The degenerative process in the disease starts approximately 10-15 years before the first clinical symptoms are manifested. Then, the patient begins to show the symptoms of memory disorders starting with a slight decrease in the short-term and episodic memory (Weintraub, Wicklund, & Salmon, 2012).

At this stage, the individual’s intellectual capabilities can be mostly preserved, and his/her daily functionality maybe not impaired. Later, other cognitive dysfunctions and problems interfering with his/her everyday life gradually appear. The major symptoms of the progressive AD include the spatial and speech disorders which signify the involvement of the parietal lobes of the brain in the degenerative process (Weintraub et al., 2012). AD affects the patient’s verbal fluency and semantic categorization as well (Weintraub et al., 2012). It means that he/she may hear what others say, can repeat the words, but may have difficulties in understanding them.

Since in the early stages of the disease the patient can critically evaluate his/her position, the awareness of a progressive cognitive defect often becomes a cause of anxiety and depression (Bird, 2015). With the progression of AD, the person may also show the symptoms of behavioral disorders such as aggressiveness, aimless motor activity, delirium, etc. As a result, the patient’s dependence on caregivers increases over time, and he/she ultimately comes to the point of complete helplessness. At the latest stages of AD, the affected person usually has urinary incontinence, requires assistance with eating, loses major psychomotor skills including walking, and shows neurological symptoms of the brain deactivation.

Up to 6% of all AD cases are associated with early-onset (60-65 years) and “approximately 60% of early-onset AD is familial, with 13% appearing to be inherited in an autosomal dominant manner” (Bird, 2015, para. 5). It means that genetics is among the main factors for disease development. Other aggravating factors may include serious craniocerebral injuries, severe psychological shocks, episodes of depression, and low intellectual activity throughout the lifespan.

Additionally, such pathological conditions contributing to the onset of acute or chronic oxygen deficiency in the cells of the cerebral cortex as high blood pressure, atherosclerosis, increased lipid levels, diabetes mellitus, etc. may accelerate AD progression. Along with fractures and pain that may result from the patient’s impaired sense of balance and mobility, these conditions represent the primary concomitant disease states.


Genetic defects play an essential role in AD development. All family forms of the disease are of an autosomal dominant type (i.e., a pathological gene from an affected parent blocks a normal gene obtained from the healthy one). Most frequently, AD is associated with the defects in genes located on chromosomes 1, 14, and 21 (Huang, 2016). The genetic abnormalities usually lead to such morphological changes as the extracellular deposition of β-amyloid, the presence of intracellular paired helical filaments, the development of senile plaques, and the neurons’ decay (Huang, 2016). A simple visual examination of the cerebral hemispheres may reveal degenerative processes of the brain in AD.

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The pathophysiological processes leading to total atrophy of the nervous tissue “in medial temporal lobe structures…interrupting the neural network critical for episodic memory function” and resulting in the inability to process and remember information (Weintraub et al., 2012, p. 2).

Differential Diagnoses

Major Depressive Disorder (Pseudo-Dementia)

Pseudo-dementia “closely mimics” other types of dementia including AD, and, therefore, it may be a source of confusion during the diagnostics (Kang et al., 2014, p. 147). Severe depression may be associated with the symptoms of cognitive deficiency but, compared to AD, it is reversible if identified in a timely manner. Like AD, it may become a cause of impaired concentration and memory, as well as the difficulties in decision-making and thinking.

Moreover, the fact that patients with AD often show the symptoms of depression poses a significant challenge for the diagnosis of pseudo-dementia because a trial treatment with antidepressants may have no diagnostic value. However, in contrast to patients with dementia, in pseudo-dementia, memory impairment happens mainly due to the problems with motivation − the patient can name objects and calculate although his/her psychomotor processes remain slow (Kang et al., 2014).

Thyroid Disease

The impairment of the neuromuscular system similar to the symptoms observed in AD is one of the most frequent complications of hypothyroidism and thyrotoxicosis. The common signs include “depressive or anxiety disorder, memory deficits, executive inability, and even psychosis” (Stasiolek, 2015, p. A25). Moreover, researchers state that thyroid disorders can cause a reduction in the hippocampus size which is considered “a prognostic factor in dementia” (Daghighi et al., 2016, p. 354). It is observed that the lack of thyroid hormones in the organism may lead to the impairment of the oxidative processes and the consequent occurrence of memory and cognitive disorders.

Vitamin B12 Deficiency

The condition often induces various neurologic and psychiatric symptoms including impaired memory, mood disorders, anxiety, behavioral problems, depression, delirium, etc. Issac, Soundarya, Christopher, and Chandra (2015) state that cognitive decline associated with the condition is provoked by an elevated serum cholesterol level and, compared, to AD symptoms, it is reversible. Like in dementia, the signs of vitamin B12 deficiency are more likely to manifest in older adults (Issac et al., 2015). Thus, it is essential to differentiate them from AD to prevent the aggravation of the patient’s condition.


AD progression is rather an irreversible process, yet researchers suggest that dietary interventions and cognitive-behavioral therapies implemented at the early stages of the disease development can significantly slow down the manifestation of adverse neuropsychological symptoms. Schelke et al. (2016) suggest designing preventive nutritional and lifestyle interventions based on the individual patient’s biomarkers.

The researchers reveal that AD development may be accelerated by various metabolic dysfunctions mediated via abnormal lipid and glucose conditions which mediate the production of essential amino acids in the brain and define the peptide balance. The recommended intervention should thus focus on the control of insulin resistance and plasma glucose level (e.g., Mediterranean-style diet); cholesterol and lipid level (e.g., intake of omega-3 fatty acids); and oxidative stress (e.g., intake of vitamins B, E, and C) (Schelke et al., 2016).

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The vitamin supplementation and the overall better nutritional control proved to have positive effects on many elderly patients including reduced hippocampal atrophy, memory improvement, normalization of cholesterol level, etc. Additionally, Smith (2015) states that patients who underwent a course of dietary omega-3 and vitamin supplementation show a significant decrease in the manifestation of depressive symptoms.

Many depressed patients with AD undergo pharmacologic interventions. However, the evidence needed to prove the efficiency of antidepressants remains insufficient up to date. For instance, it is observed that elderly patients with dementia who were prescribed with “at least one prescription for an antidepressant had an increased risk of all-cause mortality” (Pellegrino, Peters, Lyketsos, & Marano, 2013, p. 384). Thus, behavioral and cognitive interventions are regarded as safer and potentially more beneficial for them.

For example, Innes and Selfe (2014) recommend meditation − “an intentional and self-regulated focusing of attention, whose purpose is to relax and calm the mind and body,” − as a cost-efficient self-performed treatment of all major AD symptoms including depression, stress, cortical thinning, glucose intolerance, and many more (p. 40). Meditation is proven to improve both physiological and psychological conditions of patients with neurocognitive disorders in multiple studies. Innes and Selfe (2014) assume that the core alleviating meditation mechanisms are the stimulation of the vagus nerve and the development of the sense of well-being that fosters the nervous system balance and improves most of the systematic responses in the body.


By addressing the primary risk factors for AD, it will be possible to slow down and alleviate the adverse symptoms in patients significantly. One of the main potential benefits of behavioral and nutritional interventions reviewed in the previous paragraph is the reduction of medical comorbidities considered to be the accelerators in AD progression, i.e., hypertension, diabetes, dyslipidemia, and so on. The immediate results of the proposed interventions may include the enhancement in multiple spheres of the individual’s life: psycho-social, intellectual, physical. However, it is important to consider that the non-pharmacologic treatment will be more appropriate and effective as a preventive measure or an early intervention of AD.


Alzheimer’s Association. (2017). Alzheimer’s disease facts and figures. Web.

Bird, T. (2015). Alzheimer disease overview. Web.

Daghighi, M.-H., Poureisa, M., Ahmadi, P., Reshadatjoo, M., Golestani, S., Naghavi-Behzad, M., & Karkon-Shayan, F. (2016). Serum thyroid-stimulating hormone level and relation with size of hippocampus in patients with mild cognitive disorders. Nigerian Medical Journal: Journal of the Nigeria Medical Association, 57(6), 353-356.

Huang, J. (2016). Alzheimer disease (Alzheimer’s disease). Web.

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Innes, K. E., & Selfe, T. K. (2014). Meditation as a therapeutic intervention for adults at risk for Alzheimer’s disease – Potential benefits and underlying mechanisms. Frontiers in Psychiatry, 5, 40.

Issac, T. G., Soundarya, S., Christopher, R., & Chandra, S. R. (2015). Vitamin B12 deficiency: An important reversible co-morbidity in neuropsychiatric manifestations. Indian Journal of Psychological Medicine, 37(1), 26–29.

Kang, H., Zhao, F., You, L., Giorgetta, C., D, V., Sarkhel, S., & Prakash, R. (2014). Pseudo-dementia: A neuropsychological review. Annals of Indian Academy of Neurology, 17(2), 147-154.

Pellegrino, L. D., Peters, M. E., Lyketsos, C. G., & Marano, C. M. (2013). Depression in cognitive impairment. Current Psychiatry Reports, 15(9), 384.

Schelke, M. W., Hackett, K., Chen, J. L., Shih, C., Shum, J., Montgomery, M. E.,… Isaacson, R. S. (2016). Nutritional interventions for Alzheimer’s prevention: A clinical precision medicine approach. Annals of the New York Academy of Sciences, 1367(1), 50-56.

Smith, G. S. (2015). Handbook of depression in Alzheimer’s disease. Washington, DC: IOS Press.

Stasiolek, M. (2015). Neurological symptoms and signs in thyroid disease. Thyroid Research, 8(Suppl 1), A25.

Weintraub, S., Wicklund, A. H., & Salmon, D. P. (2012). The neuropsychological profile of Alzheimer disease. Cold Spring Harbor Perspectives in Medicine, 2(4), 1-18.

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