WK10Assgn Raney W
Alzheimer’s Disease
Wendy Raney
Walden University
NURS 6501, N-19, Advanced Pathophysiology
May 10, 2015
Alzheimer’s Disease (AD)
Alzheimer’s disease is an irreversible and progressive disease of the brain that gradually destroys thinking and memory skills. The disease eventually leads to the inability to carry out simple activities of daily living.
Pathophysiology
There are 3 forms of AD: early-onset, early-onset familial, and lateonset
Early-onset familial AD is linked to mutations of 3 genes on chromosome 21: abnormal amyloid precursor protein 14 (APP14), abnormal presenilin 1 (PSEN1), abnormal presenilin 2 (PSEN2)
Late-onset AD is possibly related to a link between chromosome 19 and apolipoprotein E gene-allele 4 (APOE4)
(Huether & McCance, 2012)
Pathophysiology Continued
Abnormal deposits of proteins lead to the formation of neuritic plaques and tau tangles throughout the brain. Neurons that were once healthy begin to work less efficiently. As the disease progresses, the neurons lose their capability of functioning and communicating with one another, leading to neuron death.
With the progression of AD the damage spreads to the hippocampus, a brain structure. The hippocampus is vital for forming memories.
As more and more neurons die, regions of the brain that are affected begin to shrink. By the end stage of Alzheimer’s disease, brain tissue has shrank drastically and damage is widespread.
(Huether & McCance, 2012)
Epidemiology
Late-onset AD, most common disease of aging
AD is the most prevalent cause of dementia and accounts for over
50% of cases
Symptoms of AD typically appear after the age of 65
Slowly Progressive disease that advances over a period of 5-10 years
(McPhee & Hammer, 2012)
Clinical Presentation
Progressive mental deterioration
Memory failure
Mood changes
Disorientation
Confusion
Lack of concentration
Hallucinosis
Dyspraxia
(Huether & McCance, 2012)
Diagnosis
A
Wendy Raney
Walden University
NURS 6501, N-19, Advanced Pathophysiology
May 10, 2015
Alzheimer’s Disease (AD)
Alzheimer’s disease is an irreversible and progressive disease of the brain that gradually destroys thinking and memory skills. The disease eventually leads to the inability to carry out simple activities of daily living.
Pathophysiology
There are 3 forms of AD: early-onset, early-onset familial, and lateonset
Early-onset familial AD is linked to mutations of 3 genes on chromosome 21: abnormal amyloid precursor protein 14 (APP14), abnormal presenilin 1 (PSEN1), abnormal presenilin 2 (PSEN2)
Late-onset AD is possibly related to a link between chromosome 19 and apolipoprotein E gene-allele 4 (APOE4)
(Huether & McCance, 2012)
Pathophysiology Continued
Abnormal deposits of proteins lead to the formation of neuritic plaques and tau tangles throughout the brain. Neurons that were once healthy begin to work less efficiently. As the disease progresses, the neurons lose their capability of functioning and communicating with one another, leading to neuron death.
With the progression of AD the damage spreads to the hippocampus, a brain structure. The hippocampus is vital for forming memories.
As more and more neurons die, regions of the brain that are affected begin to shrink. By the end stage of Alzheimer’s disease, brain tissue has shrank drastically and damage is widespread.
(Huether & McCance, 2012)
Epidemiology
Late-onset AD, most common disease of aging
AD is the most prevalent cause of dementia and accounts for over
50% of cases
Symptoms of AD typically appear after the age of 65
Slowly Progressive disease that advances over a period of 5-10 years
(McPhee & Hammer, 2012)
Clinical Presentation
Progressive mental deterioration
Memory failure
Mood changes
Disorientation
Confusion
Lack of concentration
Hallucinosis
Dyspraxia
(Huether & McCance, 2012)
Diagnosis
A
References: Huether, S. E., & McCance, K. L. (2012). Understanding pathophysiology (Laureate custom ed.). St. Louis, MO: Mosby. McPhee, S. J., & Hammer, G. D. (2012). Pathophysiology of disease: An introduction to clinical medicine (Laureate Education, Inc., custom ed.). New York, NY: McGraw-Hill Medical.