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Source: Peron EP, Slattum PW, Powers KE, Hobgood SE. Alzheimer disease. In: DiPiro JT, Talbert RL, Yee GC, Matzke GR, Wells BG, Posey L, eds. Pharmacotherapy: A Pathophysiologic Approach. 10th ed. New York, NY: McGraw-Hill; 2017. http://accesspharmacy.mhmedical.com/content.aspx?bookid=1861§ionid=146062470. Accessed January 20, 2017.
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Exact pathophysiology of Alzheimer disease (AD) not entirely known, and no cure exists.
Intracellular neurofibrillary tangles, extracellular neuritic plaques, degeneration of neurons and synapses, cortical atrophy.
β-Amyloid protein aggregation leading to plaque formation, hyperphosphorylation of tau protein, inflammatory processes, vasculature injury, depletion of neurotrophin and neurotransmitters.
Loss of cholinergic activity and serotonergic neurons.
Increased activity of monoamine oxidase type B
Abnormal glutamate pathways of cortex and limbic structures.
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Affects approximately 5.3 million Americans.
Number of AD patients is projected to be 13.8 million by 2050.
Most cases present in persons over age 65 years, but 4% occur in younger persons.
AD is the fifth leading cause of death in persons age 65 years and older in the United States.
Most common form of dementing illness, and the prevalence of AD increases with each decade of life.
AD accounts for 60% of cases in persons over the age of 65 years.
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CLINICAL PRESENTATION
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MEANS OF CONFIRMATION AND DIAGNOSIS
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