These additional symptoms are noted and progressively worsen as the disease process progresses.
Plaques of amyloid beta and tau proteins develop and deposit in the smooth muscle of the cerebral arteries, forming "tangles". These tangles contribute to the neuronal death, and are typically more concentrated in the memory areas of the brain, such as the cerebral cortex and the hippocampus (Boss & Huether, 2018).

Alzheimer's Disease
and Related Dementias

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In 2017, it was estimated that 5.5 million Americans have been diagnosed with Alzheimer’s disease, noting that Alzheimer’s is the sixth highest cause of death in America (Alzheimer's Association, 2018).

Cellular

Extracellular & Intracellular

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Alzheimer’s disease is a multi-proteinopathy, involving both extracellular amyloid-β deposits (i.e. amyloid-β plaques) and intracellular accumulation of post-translationally modified tau proteins (Murray et al., 2015)

ROS & Free Radicals

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During normal metabolism, the mitochondria are the greatest source and the target of Reactive Oxygen Series, or ROS. Mitochondrial oxidative stress has been implicated in heart disease, Alzheimer's disease, and Parkinson's disease, as well as aging itself (McCance, Grey, Rodway, 2018).

Genetics

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Alzheimer’s disease (AD) is the most prevalent neurodegenerative disease that mostly affects the aging population (Park et al., 2017)

Differentially methylated Genes

Differentially expressed Genes

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DNA methylation affects the expression level of neuronal function-related genes in AD patients (Park et al., 2017)

Pathophysiology

Progressive Cognitive Impairment

Undesirable Behaviors

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Undesirable behaviors are described as any verbal or motor activity that does not seem purposeful or appropriate to the situation, including increased motor activity and irritability (Jutkowitz, et al., 2016)

Agitation

Aggression

Unmet Needs

Cohen-Mansfield's
Unmet Needs Model

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Cohen-Mansfield’s Unmet Needs Model states that “problem behaviors of people with dementia result from unmet needs stemming from a decreased ability to communicate those needs and to provide for oneself” (Cohen-Mansfield, Dakheel-Ali, Marx, Thein, & Regier, 2015).  

Need for Toileting
Boredom
Hunger

Disease Manifestations

Pre-clinical

Forgetfullness

Emotional and/or Mood
Changes

Prodromal

Memory loss
(Increases as the
disease progresses)

Abstract thinking
Problem solving
Judgement

Inclination for Mood swings r/t
impaired cognition. Anxiety, Hosility,
Emotional labile behaviors are common.

Neuro-Genetic Disorder

References

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Alzheimer's Association. (2018). Facts and Figures. Retrieved from Alzheimer's Association: https://alz.org/alzheimers-dementia/facts-figuresBoss, B. J., & Huether, S. E. (2018). Alterations in Cognitive Systems, Cerebral Dynamics, and Motor Function. In K. L. McCance, & S. E. Huether, Pathophysiology. The Biologic Basis for Disease in Adults and Children (pp. 504-549). St. Louis: Elsevier.Cohen-Mansfield, J., Dakheel-Ali, M., Marx, M. S., Thein, K., & Regier, N. G. (2015). Which unmet needs contribute to behavior problems in persons with advanced dementia?. Psychiatry research, 228, 59-64.Jutkowitz, E., Brasure, M., Fuchs, E., Shippee, T., Kane, R. A., Fink, H. A., ... & Kane, R. L. (2016). Care‐delivery interventions to manage agitation and aggression in dementia nursing home and assisted living residents: a systematic review and meta‐analysis. Journal of the American Geriatrics Society, 64, 477-488.McCance, K. L., Grey, T. C., & Rodway, G. W. (2018). Altered Cellular and Tissue Biology. In K. L. McCance, & S. E. Huether, Pathophysiology. Biologic Basis for Disease in Adults and Children (pp. 46-104). St. Louis: Elsevier.Murray, M. E., Lowe, V. J., Graff-Radford, N. R., Liesinger, A. M., Cannon, A., Przybelski, S. A., ... & Ross, O. A. (2015). Clinicopathologic and 11C-Pittsburgh compound B implications of Thal amyloid phase across the Alzheimer’s disease spectrum. Brain, 138, 1370-1381.Park, L., Uekawa, K., Garcia-Bonilla, L., Koizumi, K., Murphy, M., Pistik, R., ... & Anrather, J. (2017). Brain perivascular macrophages initiate the neurovascular dysfunction of Alzheimer Aβ peptides. Circulation research, 121(3), 258-269.

Sporadic Late-Onset Alzheimer's Disease
does not have a specific gene association

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Sporadic Late-Onset Alzheimer's disease (AD) does not have a specific gene association; however, the cellular pathology is the same as that for gene-associated early and late-onset AD (Boss & Huether, 2018).