● Confusion about the location of familiar places (getting lost begins to occur). ● Taking longer to accomplish normal daily tasks and may need prompting.
● Loss of impulse control (e.g., sloppy table manners, undressing at inappropriate times or places, use of profanity). ● Perceptual-motor problems (e.g., trouble with self-care skills or chores, such as setting the table). In the severe stage of AD, plaques and tangles are widespread throughout the brain, and areas of the brain have atrophied significantly. At this stage, individuals with AD generally cannot recognize family and loved ones or communicate in any meaningful way, and the sense of self seems to vanish; these individuals are completely dependent on others for care. Multiorgan system complications of immobility abound. Other signs and symptoms of the severe stage can include: ● Accelerating weight loss. ● Dysphagia. ● Seizures. ● Groaning, moaning, or grunting. ● Increased sleeping. ● Lack of bladder and bowel control. During the final stage, patients may be in bed much or all of the time. AD can be the primary cause of death (i.e., brain function can no longer support the living being), but more often, individuals with AD die from a secondary illness or event, likely related to immobility and/or decreased function caused by AD. Common causes of death include aspiration pneumonia, sepsis (from urinary tract infection or decubitus ulcer), and malnutrition (related to dysphagia). Individuals with AD are likely to spend the final stages of the disease in a nursing home; an estimated 75% of people with AD will be admitted into a nursing home by age 80 years, compared to 4% of the general population (Alzheimer’s Association, 2018a).
● Trouble handling money and paying bills. ● Poor judgment leading to bad decisions. ● Loss of spontaneity and sense of initiative. ● Mood and personality changes. ● Increased anxiety. ● Beginning to abandon hobbies and interests.
By the moderate stage of AD, the damage has spread to the areas of the cerebral cortex that control language, reasoning, sensory processing, and conscious thought. Affected regions continue to atrophy, and signs and symptoms become more pronounced and widespread. Behavior problems such as wandering and agitation can occur. More intensive supervision and care of the person – which can be difficult for many spouses and families – become necessary. The signs and symptoms of moderate-stage AD can include: ● Increasing memory loss and confusion. ● Shortened attention span. ● Problems recognizing friends and family members. ● Difficulty with language. ● Problems with reading, writing, and working with numbers. ● Difficulty organizing thoughts and thinking logically. ● Inability to learn new things or to cope with new or unexpected situations. ● Restlessness, agitation, anxiety, tearfulness, and wandering – especially in the late afternoon or at night (sundowning). ● Repetitive statements or movements. ● Hallucinations, delusions, suspiciousness or paranoia, and irritability.
ETIOLOGY OF ALZHEIMER’S DISEASE
The exact cause of AD is not known; however, it is clear that the disease develops because of a complex series of events that take place in the brain over a long period of time. Current research into the causes of AD focuses on a variety of factors, including genetics, neurotransmitters, beta-amyloid, tau, and neurofibrillary tangles. The discovery that early-onset AD may run in families led to the identification of mutations on chromosome 14 (presenilin-1 gene), chromosome 1 (presenilin-2 gene), and chromosome 21 (amyloid precursor protein gene), all of which cause abnormal proteins to be produced. Even if only one of these genes contains a mutation, an individual will almost inevitably develop early-onset AD. Genetic research into late-onset AD has identified a region on chromosome 19 that may be involved in the development of the disease. The protein apolipoprotein E (ApoE) is associated with beta- amyloid plaques. The gene that produces ApoE is located in a region of chromosome 19 that was pinpointed by geneticists, suggesting that one form of this gene (ApoE-4) is a risk factor for late-onset AD; however, even inheriting ApoE-4 from both parents does not translate to definitive development of AD and
some individuals with AD may not have inherited ApoE-4 from either parent. Understanding the genetics and implications in the changes in protein structures is a major focus of AD research. Scientists are hopeful that discoveries in these areas will inform new ways to diagnose, treat, or even prevent AD. Neurotransmitter depletion is also implicated in the disease process and represents another area of study. Acetylcholine is a neurotransmitter that is consistently deficient in patients with AD; the deficiency is associated with memory loss and loss of capacity for attentiveness. Other neurotransmitters that are reduced in patients with AD include serotonin, gamma- aminobutyric acid (GABA), somatostatin, and norepinephrine. Current drug therapies focus on these neurotransmitter depletions. Growth factors are important for regulating many cellular processes; their depletion, especially the depletion of brain-derived neurotrophic factor (BDNF), which is neuroprotective in nature, appears to be implicated in the pathology of AD.
RISK FACTORS FOR ALZHEIMER’S DISEASE
AD is a multifactorial disease with a long list of risk factors. The major risk factors include the following: ● Age: Age is the most strongly established risk factor for AD. The older a person gets, the greater the risk for the disease. The risk doubles every 5 years after age 65. It is relevant to mention that early-onset AD (prior to age 65) accounts for about 5% of AD cases and is usually diagnosed in individuals in their 40s and 50s. ● Genetics: As mentioned previously, for early-onset AD, mutations have been identified on chromosomes 14, 1, and 21; for late-onset AD, chromosome 19 has been identified as a source for gene ApoE-4, which is associated with an increased risk of AD. ● Vascular disease: Impaired blood flow to the brain is the cause of vascular dementia and is contributory to AD.
Systemic vascular problems that contribute to heart disease, such as atherosclerosis and hypertension, may be implicated in AD. ● Metabolic conditions: Diabetes and obesity have been associated with increased risk of AD. ● Years of education: Lower educational levels are associated with a greater likelihood of AD. Speculation regarding the role of education includes an increased cognitive reserve to compensate for brain changes that could lead to dementia among those with higher levels of education, as well as decreased access to medical care among persons with lower educational attainment, which is inexorably linked with socioeconomic status. ● Ethnicity: Although the majority of older Americans with dementia are Caucasian, research suggests that older African
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Book Code: PTNY3622B
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