Alzheimer's Disease PDF

10/24/23, 3:14 PM Realizeit for Student Alzheimer Disease AD is the sixth leading cause of death in the United States. For adults 65 years of age and older it is the fifth leading cause of death. AD is a progressive, irreversible, degenerative neurologic disease that begins insidiously and is char...

10/24/23, 3:14 PM Realizeit for Student Alzheimer Disease AD is the sixth leading cause of death in the United States. For adults 65 years of age and older it is the fifth leading cause of death. AD is a progressive, irreversible, degenerative neurologic disease that begins insidiously and is characterized by gradual losses of cognitive function and disturbances in behavior and affect. AD can occur in people as young as 40 years of age but is less common before 65 years of age. Although the prevalence of AD increases dramatically with increasing age, affecting as many as half of those 85 years and older, AD is not a normal part of aging. Without a cure or any preventive measures, it is estimated that 13.8 million Americans will have this disease by 2050 (Alzheimer’s Association, 2019). There are numerous theories about the cause of age-related cognitive decline. Although the greatest risk factor for AD is increasing age, many environmental, dietary, and inflammatory factors also may determine whether a person suffers from this cognitive disease. AD is a complex brain disorder caused by a combination of various factors that may include genetics, neurotransmitter changes, vascular abnormalities, stress hormones, circadian changes, head trauma, and the presence of seizure disorders. AD can be classified into two types: familial or early-onset AD and sporadic or late-onset AD. Familial AD is rare, accounting for less than 2% of all cases, and is frequently associated with genetic mutations. It can occur in middle-aged adults. If family members have at least two other relatives with AD, then there is a familial component, which may include both environmental triggers and genetic determinants (NIH, 2017). Pathophysiology The pathogenesis of AD is uncertain but the disease includes specific neuropathologic and biochemical changes that interfere with neurotransmission. These changes consist of neurofibrillary tangles (tangled masses of nonfunctioning neurons) and senile or neuritic plaques (deposits of amyloid protein, part of a larger protein called amyloid precursor protein in the brain). The neuronal damage occurs primarily in the cerebral cortex and results in decreased brain size. Similar changes are found in the normal brain tissue of nonsymptomatic older adults, although to a lesser extent. Cells that use the neurotransmitter acetylcholine are principally affected by AD. At the biochemical level, the enzyme active in producing acetylcholine, which is specifically involved in memory processing, is decreased. Scientists have been studying complex neurodegenerative diseases such as AD and have focused on two key issues: whether a gene might influence a person’s overall risk of developing the disease, and whether a gene might influence some particular aspect of a person’s risk, such as the age at which the disease begins (age at onset). There are genetic differences in early- and late-onset forms of AD (NIH, 2017). Researchers are investigating what predisposes people to develop the plaques and https://herzing.realizeithome.com/RealizeitApp/Student.aspx?Token=0Dn26kXyU%2f6F5gOCz4%2f2IUFUzXhwrkmByRPKGm7XOkO3V8uhfXYXOmPZGy%2b… 1/2 10/24/23, 3:14 PM Realizeit for Student neurofibrillary tangles that can be seen at autopsy in the brains of patients with AD. Understanding the complex ways in which aging as well as genetic and nongenetic factors affect brain cells over time, eventually leading to AD, continues to increase. Clinical Manifestations In the early stages of AD, forgetfulness and subtle memory loss occur. Patients may experience small difficulties in work or social activities but have adequate cognitive function to compensate for the loss and continue to function independently. With further progression of AD, the deficits can no longer be concealed. Forgetfulness is manifested in many daily actions; patients may lose their ability to recognize familiar faces, places, and objects and they may become lost in a familiar environment. They may repeat the same stories or ask the same question repeatedly. Trying to reason with people with AD and using reality orientation (a person’s ability to recognize who and where they are in a time continuum) only increase their anxiety without increasing function. Conversation becomes difficult, and word-finding difficulties occur. The ability to formulate concepts and think abstractly disappears—for example, a patient can interpret a proverb only in concrete terms. Patients are often unable to recognize the consequences of their actions and, therefore, exhibit impulsive behavior—for example, on a hot day a patient may decide to wade in the city fountain fully clothed. Patients have difficulty with everyday activities, such as operating simple appliances and handling money. Personality changes are also usually evident. Patients may become depressed, suspicious, paranoid, hostile, and even combative. Progression of the disease intensifies the symptoms: Speaking skills deteriorate to nonsense syllables, agitation and physical activity increase, and patients may wander at night. Eventually, assistance is needed for most ADLs, including eating and toileting, because dysphagia and incontinence develop. The terminal stage, in which patients are usually immobile and require total care, may last months or years. Occasionally, patients may recognize family members or caregivers. Death occurs as a result of complications such as pneumonia, malnutrition, or dehydration. https://herzing.realizeithome.com/RealizeitApp/Student.aspx?Token=0Dn26kXyU%2f6F5gOCz4%2f2IUFUzXhwrkmByRPKGm7XOkO3V8uhfXYXOmPZGy%2b… 2/2