Epidemiology of Alzheimers Disease and Dementia Advances and Challenges

ROBERT KATZMAN

INTRODUCTION

A defining event of the twentieth century was the dramatic increase in life expectancy at birth—an increase of over 50%, from under age 50 in 1900 to over age 76 in 2000. With the consequent aging of our populations, age-associated diseases have come to the forefront. Of these, Alzheimer's disease (AD) and related dementing disorders are the most age-dependent. It is anomalous that of all of the risk factors for AD, the biological basis of age is the least understood.

During the past two decades the extent of the public health impact of AD and related dementias has been defined. Jorm et al. demonstrated the consistency of the exponential rise of dementia with age in a quantitative integration of 27 prevalence studies dating back to 1945 (Jorm et al., 1987). Prevalence doubles with each five years of age, as shown by the regression line in Figure 2.1. In this figure, the log of age-specific dementia prevalence is plotted against age. The age-specific prevalence rates obtained in the Jorm meta-analysis, the Eurodem meta-analysis of six later prevalence studies (Hofman et al., 1991) and the Canadian Study of Health and Aging (1994)— whose subjects included 9008 community subjects and 1255 institutional residents in nine provinces—are similar, as shown in Figure 2.1. Katzman and Fox (1999), using the United Nations 1998 population projections (middle series) and prevalence rates based upon the Canadian Study of Health and Aging, adjusted for the changing structure in the age distribution of populations over time, projected that the number of cases of dementia in the developed world would rise from 13.5 million in 2000, to 21.2 million in 2025, and 36.7 million in 2050. Most of the increase is attributable to the aging of the population that will occur in the next 50 years. This extraordinary increase would be mitigated if we learned how to delay the onset of AD. Khatchaturian

Alzheimer's Disease: Advances in Etiology, Pathogenesis and Therapeutics. Edited by K. Iqbal, S. S. Sisodia & B. Winblad. © 2001 John Wiley & Sons, Ltd.

Figure 2.1. Prevalence of age-specific dementia (as log prevalence of age-defined population) plotted against age. The regression line is based upon the meta-analyses of Jorm (Jorm et al., 1987) and Eurodem (Hofman et al., 1991) and the nine-province Canadian study (Canadian Study of Health and Aging, 1994). Additional data points include East Boston (Evans et al., 1989) and Shanghai (Zhang et al., l990); the oldest old in the Canadian study (Ebly et al., 1994); Gothenburg (Skoog et al., 1993); Munich (Fichter et al., 1995); Seattle Japanese Americans (Graves et al., 1999); and Cache County, Utah (Breitner et al., 1999). Pertinent to less developed countries are a comparison of African Americans in Indianapolis and residents of Ibadan, Nigeria (Hendrie et al., 1994), and data from three communities in India: Ballabgarh (Chandra et al., 1998), Kerala (Brenner, 1999), and Madras (Rajkumar et al., 1997)

Figure 2.1. Prevalence of age-specific dementia (as log prevalence of age-defined population) plotted against age. The regression line is based upon the meta-analyses of Jorm (Jorm et al., 1987) and Eurodem (Hofman et al., 1991) and the nine-province Canadian study (Canadian Study of Health and Aging, 1994). Additional data points include East Boston (Evans et al., 1989) and Shanghai (Zhang et al., l990); the oldest old in the Canadian study (Ebly et al., 1994); Gothenburg (Skoog et al., 1993); Munich (Fichter et al., 1995); Seattle Japanese Americans (Graves et al., 1999); and Cache County, Utah (Breitner et al., 1999). Pertinent to less developed countries are a comparison of African Americans in Indianapolis and residents of Ibadan, Nigeria (Hendrie et al., 1994), and data from three communities in India: Ballabgarh (Chandra et al., 1998), Kerala (Brenner, 1999), and Madras (Rajkumar et al., 1997)

(1992) pointed out that if dementia prevalence doubles with every five years of age, then prevalence would be halved by delaying the onset of AD by five years. This has become a major research objective.

In the projection of dementia prevalence in the developed world, we used the Canadian prevalence rates since this is the largest population-based study that contains significant numbers of subjects over age 90, the age group that will increase in numbers most rapidly in the next 50 years. What happens to the exponential increase in dementia at advanced ages has been a matter of controversy. Hagnell et al. in 1981, on the basis of data from the Lundby study, suggested that the risk of dementia might decrease after age 85. Unfortunately this does not appear to be true. As shown in Figure 2.1, evidence from recent studies with significant numbers of subjects over the age of 90 [Canada (Ebly et al., 1994), Munich (Fichter et al., 1995), Seattle Japanese Americans (Graves et al., 1996a) and Stockholm (Fratiglioni et al., 1997)] indicates that the exponential increase of the prevalence of dementia continues well past 85, apparently up to age 95. As the prevalence of dementia may exceed 50% after age 95, there must then be a plateau, since there certainly are centenarians with intact cognitive functions. Determining what happens at very advanced ages will be a major objective for future epidemiological studies.

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