The now outdated practice of giving Alzheimer disease and senile dementia the status of separate diseases is attributable to the relatively young age (51 years) of the patient originally studied by Alois Alzheimer in 1907. Such a division is no longer tenable as, except for their age of onset, they are clinically and pathologically indistinguishable. It is probably useful to consider as related but separable, the several heredofamilial forms of Alzheimer disease discussed below.
Although Alzheimer disease has been described at every period of adult life, the majority of patients are in their sixties or older; a relatively small number have been in their late fifties or younger. It is one of the most frequent mental illnesses, making up a large proportion of persons in assisted living and skilled nursing facilities. The incidence of clinically diagnosed Alzheimer disease is similar throughout the world, and it increases with age, approximating 3 new cases yearly per 100,000 persons younger than age 60 years and a staggering 125 new cases per 100,000 of those older than age 60 years. The prevalence of the disease per 100,000 population is near 300 in the group aged 60 to 69 years; it is 3,200 in the 70to 79-year-old group and 10,800 in those older than age 80. In the year 2015, there were estimated to be more than 30 million persons with Alzheimer disease in the world. (It should be borne in mind that these are not pathologically proven cases and, while probably correct as an approximation, are likely combined with other diseases.) Prevalence rates, which depend also on overall mortality, are approximately 3 times higher in women, although the incidence of new cases is only slightly disproportionate in women. However, there is a suggestion that incidence rates for dementia in general are declining (see Satizabal et al) and it is likely that most of the cases are due to Alzheimer disease. The survival of patients with Alzheimer disease is reduced to half the expected rate, mainly because of respiratory and cardiovascular causes and inanition, but also for other reasons that are not entirely clear.
Several putative epidemiologic risk factors for Alzheimer disease proposed in the past, such as birth order, mother’s age at birth, and a family history of Down syndrome seem marginal at best and in some instances, may be a result of selection bias. Depression and possibly head injuries seem to confer a somewhat increased risk later in life. Whether low educational attainment is a risk factor for the development of Alzheimer disease or, conversely, whether cognitively demanding occupations or higher intelligence protects against dementia is still under discussion. Provocative data indicating that inherent intellectual endowment (cognitive reserve) is important were presented in Chap. 20 (Katzman; Cobb et al). Finally, associations between diabetes or hyperglycemia and dementia, in general, have emerged from epidemiologic studies, for example, one reported by Crane and coworkers, but the ostensible mechanism by which this confers risk (if it is even valid) has not been established. In their report, a higher than average glucose level over the preceding 5 years conferred a slightly increased risk of dementia but not necessarily of Alzheimer disease.