Alzheimer’s presents changes in the brain referred to as neuritic plaques and neurofibrillary tangles. The neuritic plaques are formed when amyloid precursor proteins are not processed, resulting in toxic amyloid beta proteins, forming to make plaques. Neurofibrillary tangles are formed from the tau protein, a microtubule-binding protein, detaching from neurons to form tangles. Both plaques and tangles contribute to the death of neurons, resulting in the hallmark features of Alzheimer’s disease (McCance & Huether, 2014). These plaques and tangles begin in the entorhinal cortex, and exhibit some of the initial signs of Alzheimer’s disease. The entorhinal cortex is part of the temporal lobe and is involved in memory and the connection of
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It is as this time a cerebral biopsy can confirm the pathological processes of Alzheimer’s disease with the observation of plaques, tangles, and brain atrophy. The clinical assessments completed in patient history, ongoing change in symptoms, cognitive testing, diagnostic laboratory rule-out, and the patients qualifying for Amyloid PET imagining, are simply a diagnosis from clinical findings (McCance & Huether, 2013).
Genetic Contributions
Alzheimer 's Dementia has two classifications: early-onset or late-onset type. Researchers have not identified genes that contribute to late-onset Alzheimer 's Dementia (National Institute on Aging [NIA], 2014). While researchers believe that extrinsic factors such as lifestyle and environment are driving forces in late-onset Alzheimer 's, research uncovered that early-onset Alzheimer 's is primarily genetic in nature (NIA, 2014). …show more content…
Cholinesterase inhibitors are used to treat mild to moderate disease. Medications used to block glutamine receptors are used for moderate to severe disease. Medications that block glutamine work to block glutamine receptors, specifically noncompetitive N-methyl-D-asparate (NMDA) receptors (McCance & Huether, 2014). A popular drug on the market is Namenda. Namenda is an NMDA receptor antagonist (Frandsen & Pennington, 2014). According to Frandsen and Pennington persistent activation of NMDA receptors increases effects of Alzheimer 's Dementia
It is as this time a cerebral biopsy can confirm the pathological processes of Alzheimer’s disease with the observation of plaques, tangles, and brain atrophy. The clinical assessments completed in patient history, ongoing change in symptoms, cognitive testing, diagnostic laboratory rule-out, and the patients qualifying for Amyloid PET imagining, are simply a diagnosis from clinical findings (McCance & Huether, 2013).
Genetic Contributions
Alzheimer 's Dementia has two classifications: early-onset or late-onset type. Researchers have not identified genes that contribute to late-onset Alzheimer 's Dementia (National Institute on Aging [NIA], 2014). While researchers believe that extrinsic factors such as lifestyle and environment are driving forces in late-onset Alzheimer 's, research uncovered that early-onset Alzheimer 's is primarily genetic in nature (NIA, 2014). …show more content…
Cholinesterase inhibitors are used to treat mild to moderate disease. Medications used to block glutamine receptors are used for moderate to severe disease. Medications that block glutamine work to block glutamine receptors, specifically noncompetitive N-methyl-D-asparate (NMDA) receptors (McCance & Huether, 2014). A popular drug on the market is Namenda. Namenda is an NMDA receptor antagonist (Frandsen & Pennington, 2014). According to Frandsen and Pennington persistent activation of NMDA receptors increases effects of Alzheimer 's Dementia