History
Although Alzheimer’s disease only recently “has exploded into public and scientific consciousness” (Rabins 1988), it doubtlessly has a long history under such rubrics as “senility,” “hardening of the arteries,” and “dementia,” to name but a few.
Certainly senility and dementia are conditions that have been recognized for millennia. The Assyrians, Greeks, and Romans all knew and described them. Peter V. Rabins (1988) credits J. E. D. Esquirol, however, for the first modern description, in 1838, of what seems to have been Alzheimer’s disease. Esquirol wrote of a “senile dementia” that increases with age (Beach 1987). Seven years later, Wilhelm Griesinger published a textbook on mental disease that clearly recognized the condition of “presenile dementia” caused by brain atrophy found at autopsy. Neither of these reports, however, seems to have had much influence on investigators at the time (Wisniewski 1989).It was during the latter half of the nineteenth century that public as well as scientific concern for problems of the elderly increased considerably. With that concern came the birth of the field of geriatrics and increasing attention paid to dementia in the elderly (Beach 1987). Much of the effort during these decades focused on whether it was an inevitable product of aging, or rather an actual disease. Emil Kraepelin, one of the founders of modern psychiatry, pointed out the difficulty in separating normal senility from senile dementia. In applying the new technique of silver staining, Alzheimer, his student, identified a new neuropathological marker of dementia in the brain of a patient who had died at age 55 after a 4-year illness. This marker was the neurofibrillary tangle, which he speculated was the marker of a dead cell. Alzheimer thus made the first correlation between clinical characteristics of dementia in a patient and pathological lesions in the brain.
Kraepe- Iin later named the illness Alzheimer’s disease in honor of his former pupil.The question then became one of determining if this disease was the same as senile dementia. It revolved around the ancient problem of what pathological changes can be attributed to aging as opposed to other causes. Kraepelin had emphasized the presenile nature of Alzheimer’s disease, yet because of its similarity to senile dementia some investigators suggested that Alzheimer’s disease might be caused by “a premature onset of the aging process” (Beach 1987). Also confusing the picture was the nineteenth-century notion which extended also into the twentieth century: that cerebral arteriosclerosis might be the cause of senile dementia. By the late 1920s, there had been a sufficient accumulation of case descriptions of dementia among the elderly that statistical analysis could be brought to bear on the problem. It was found that most of the cases did in fact occur between the ages of 50 and 60, sustaining the notion of its presenile nature. In 1955 Martin Roth showed that mental changes could be triggered by a variety of both “functional” and “organic” diseases, and by the 1960s two major groups of researchers were at work on Alzheimer’s disease. One, headed by Robert Terry, was based at Albert Einstein University, and the other, headed by Bernard Tomlinson, Gary Blessed, and Roth, was located at Newcastle-upon-Tyne. From their work and from other studies, it became apparent, among other things, that the changes in the brain found in cases of presenile dementia were the same as those in senile dementia (Katzman 1986; Vannoy and Greene 1989).
The discovery broadened the definition of Alzheimer’s disease and thereby increased enormously the number of individuals viewed as victims of it. It also created major semantic problems. Previously the presenile nature of Alzheimer’s disease was a defining factor. Now the illness shown to be a major affliction of the elderly population was called senile dementia of the Alzheimer type (SDAT), which psychiatrists call “primary degenerative dementia.” Senile dementia (SD) has been used to mean either SDAT or Alzheimer’s disease (AD), but it may also refer to other forms of dementia in the elderly (Reisberg 1983). In addition, Alzheimer’s disease and senile dementia were often lumped together as senility or as cerebral arteriosclerosis.
This latter concept proved to be so tenacious that even as late as the middle 1970s it was called “probably the most common medical misdiagnosis” of the cause of mental deterioration in the elderly (Beach 1987).In the early 1980s, Alzheimer’s disease was defined as an “age-associated cognitive decline of gradual onset and course, accompanied by Alzheimer-type neuropathologic brain changes” with “no distinction with respect to age of onset” (Reisberg 1983), and was thought to be responsible for 50 percent or more of all dementias (Vannoy and Greene 1989).
This definition is essentially the working one as we enter the last decade of the twentieth century. Experts at a 1990 conference on the illness believe that Alzheimer’s disease is being diagnosed correctly in about 80 percent of cases, even though such diagnoses can be confirmed only after death, and even though the etiology and epidemiology of the disease remain obscure.
It may well be determined that Alzheimer’s disease is not a single disease but, rather, many different diseases with multiple causes ranging from genetics to exogenous toxins. The extent to which age and aging will rank among those causes remains a subject of debate. Reports of the condition among individuals in their 30s have been used to support the contention that the disease is unrelated to aging. On the other hand, there is a rising prevalence with age, such that by age 85 and over, some 20 percent or more are demented. If, of course, Alzheimer’s disease is a specific disease or diseases (as opposed to an inevitable product of the aging process for some 5 to 7 percent of the population over age 65), then, of course, there is hope for a cure.
The question, however, of why Alzheimer’s disease has been called the disease of this century - one that has only recently burst upon the developed world in epidemic proportions - is certainly bound up with advancing age for many and with the demographic changes that this has wrought. In 1900, there were only 3 million Americans aged 65 or older.
Today there are 27 million, and it has been estimated that in the year 2030 there will be 50 million. Given the fact that an individual who lives to be 80 has an almost 1:4 chance of developing Alzheimer’s disease or a related disorder, estimates suggest that the number of these victims will increase from some 2.5 million in the late 1980s to about 4 million by the turn of the century. As the 1990s began, it was further estimated that fully half of all nursing home patients in the United States are Alzheimer victims.The implications of the growing number of these victims for health care delivery systems are staggering. In 1967 a White House conference on aging resulted in the creation of the National Institute on Aging, which greatly facilitated research on Alzheimer’s disease. In 1983, a Task Force on Alzheimer’s Disease was created by the Department of Health and Human Services, which has emphasized the need for increased research and increased research funding, and in 1987 the journal Alzheimer’s Disease and Associated Disorders — An International Journal was founded to report such research. As more and more resources are brought to bear, the outlook for breakthroughs in understanding the causes of Alzheimer’s disease and treating it are more optimistic than in former times. But at the time of writing, it remains a devastating disease whose etiology is unknown.
JosephA. Kwentus