AD is the most common type of dementia, affecting approximately 4.5 million Americans in the year 2000. Various classifications of dementia include dementia of the Alzheimer's type, vascular dementia, and dementia due to HIV disease, head trauma, Parkinson's disease, Huntington's disease, Pick's disease, or Creutzfeldt-Jakob disease. This chapter will address only dementia of the Alzheimer's type.
The prevalence of AD increases with age, and it is most prevalent in persons aged 65 years and older. In the year 2000, it was estimated that there were 4.5 million people with AD in the United States. Of those affected, 7% were 65 to 74 years of age, 53% were between 75 and 84 years of age, and 40% were persons over 85 years of age. It is projected that by the year 2050, there will be a threefold increase in prevalence yielding potentially 13.4 million AD patients due to a population increase in persons over 65 years of age. It is projected that three out of five individuals greater than or equal to 85 years of age will have AD. Additionally, the cost to society due to rising Medicare spending for AD is projected to increase from $62 billion in 2000 to over $1 trillion in 2050. Furthermore, the costs associated with nursing home care alone are projected to increase from $19 billion in 2000 to $118 billion in 2050 (Fig. 35—1)4,5 The severity of AD also correlates with increasing age and is classified as mild, moderate, or severe. Other risk factors associated with AD besides age include family history, female gender, and vascular risk factors such as diabetes, hypertension, heart disease, and current smoking.6,7 However, it is unknown how other factors such as environment contribute and interact with the genetic predisposition for AD.
The mean survival time of persons with AD is reported to be approximately 6 years from the onset of symptoms until death. However, age at diagnosis, severity of AD, and other medical conditions affect survival time.8 Although AD does not directly cause death, it is associated with an increase in various risk factors which often contribute to death such as senility, sepsis, stroke, pneumonia, dehydration, and decubitus ulcers.
The exact etiology of AD is unknown; however, it has been suggested that genetic factors may contribute to errors in protein synthesis resulting in the formation of abnormal proteins involved in the pathogenesis of AD.9 Early onset, which is defined as AD prior to age 60, accounts for approximately 1% of all AD. This type is usually familial and follows an autosomal dominant pattern in approximately 50% of cases of early-onset AD. Mutations in three genes, presenilin 1 on chromosome 14, amyloid precursor protein (APP) on chromosome 21, and presenilin 2 on chromosome 1, lead to an increase in the accumulation of amyloid beta (Aft) in the brain, resulting in oxidative stress, neuronal destruction, and the clinical syndrome of AD.10,11
The genetic basis for the more common late-onset AD appears more complex. Genetic susceptibility is more sporadic and it may be more dependent on environmental factors.9 The apolipoprotein E (apo E) gene on chromosome 19 has been identified as a strong risk factor for late-onset AD. There are three variants of apo E; however, carriers of two or more of the apo E4 allele have an earlier onset of AD (approximately 6 years earlier) compared with noncarriers.9 Only 50% of AD patients have the apo E4 allele, thus indicating it is only a susceptibility marker.
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