IntroductionAlzheimer’s disease (AD) is the most common cause of dementia in older persons, usually begins with impairment of learning and recent memory and it is a slowly progressive disease (Hammer & McPhee, 2014). Approximately 5.2 million Americans have AD and expected to increase in the future (Huether & McCance, 2017).
Pathophysiology of Alzheimer’s disease (AD)AD is portrayed by extracellular neuritic plaques in the cerebral cortex and in the mass of meningeal and cerebral blood vessels. These plaques contain a thick center of amyloid materials that are encompassed by dystrophic neurites (axons, dendrites), receptive astrocytes and microglia. Other pathological alterations in the brain or structural changed include the formation of intraneuronal neurofibrillary tangles, neuronal and synaptic loss, reactive astrocytosis, and microglial proliferation. The creation neurofibrillary tangle contributes to neuronal death (Hammer & McPhee, 2014). The death and destruction of the nerve cells, therefore, causes failure of the memory, changes in personality, problems with daily activities and other issues related with the disease (Curran & Wattis, 2012).
Pathophysiological changes two body systemsAD progresses from short-term memory deficits culminating in total loss of cognitive and executive functions. The individual becomes progressively more forgetful over time, particularly forgetting recent events. Memory loss increases as the disease progresses, the