NR 507 Week 7 Discussion.
Alzheimer’s disease is the leading cause of severe cognitive dysfunction in older adults, (McCance, K.L. & Huether, S.E., 2019). It is a progressive disease that starts off with mild memory loss and possibly leading to loss of the ability to carry on a conversation and respond to the environment. At first, Alzheimer’s disease typically destroys neurons and their connections in parts of the brain involved in memory, including the entorhinal cortex and hippocampus. It later affects areas in the cerebral cortex responsible for language, reasoning, and social behavior. It is believed that Alzheimer’s disease has two pathologic hallmarks: extracellular beta-amyloid deposits, and intracellular neurofibrillary tangles, (Ricciarelli, R., & Fedele, E., 2017). The buildup of beta-amyloid deposition and neurofibrillary tangles leads to the loss of synapses and neurons. The abnormal levels of beta-amyloid protein clumps together to form plaques that collect between neurons and disrupt cell function. Neurofibrillary tangles are abnormal accumulations of a protein called tau that collect inside neurons and these chemical changes cause tau to detach from microtubules and stick to other tau molecules, (Ricciarelli, R., & Fedele, E., 2017). These tangles block the neuron’s transport system, which harms the synaptic communication between neurons.
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