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Prevalence Estimates Using the 2000 Census

Liesi E. Hebert, ScD; Paul A. Scherr, ScD; Julia L. Bienias, ScD; David A. Bennett, MD; Denis A. Evans, MD

Arch Neurol. 2003;60:1119-1122.

ABSTRACT
Context  Current and future estimates of Alzheimer disease (AD) are essential for public health planning.

Objective  To provide prevalence estimates of AD for the US population from 2000 through 2050.

Design  Alzheimer disease incidence estimates from a population-based, biracial, urban study, using a stratified random sampling design, were converted to prevalence estimates and applied to US Census Bureau estimates of US population growth.

Setting  A geographically defined community of 3 adjacent neighborhoods in Chicago, Ill, applied to the US population.

Participants  Alzheimer disease incidence was measured in 3838 persons free of AD at baseline; 835 persons were evaluated for disease incidence.

Main Outcome Measure  Current and future estimates of prevalence of clinically diagnosed AD in the US population.

Results  In 2000, there were 4.5 million persons with AD in the US population. By 2050, this number will increase by almost 3-fold, to 13.2 million. Owing to the rapid growth of the oldest age groups of the US population, the number who are 85 years and older will more than quadruple to 8.0 million. The number who are 75 to 84 years old will double to 4.8 million, while the number who are 65 to 74 years old will remain fairly constant at 0.3 to 0.5 million.

Conclusion  The number of persons with AD in the US population will continue to increase unless new discoveries facilitate prevention of the disease.

INTRODUCTION

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CHANGING AGE structure of the US population markedly affects the occurrence of Alzheimer disease (AD). Because the disease has a great effect on the quality of life for affected individuals and caregivers and because it places heavy demands on the health care system, estimates of its occurrence and projections of future occurrence are essential for public health planning.

Available estimates^1-2 vary in how data from source studies are applied to the US population, and, more importantly, in how AD is ascertained by source studies. Most studies have used a 2-stage approach, with a second stage of expert clinical evaluation required to measure disease. Some studies have used a screening approach, restricting second-stage evaluation for disease to persons failing a screening cognitive test. Others have evaluated disease in random fractions of both those failing and passing such a test, usually in several strata having different probabilities of random selection.

As prevalence estimates derived from restricting disease evaluation to those failing a screening test assume perfect screening test sensitivity,³ while random sampling of all fractions of the population does not, screening approaches typically give lower AD prevalence estimates. Differences resulting from using the 2 methods have been only infrequently examined,⁴ but may be large, depending on the severity of disease a study aims to detect. Gradual development of AD from normality results in a second variation in data collection methods. Although criteria⁵ for the disease reflect good conceptual agreement, translation into an operational cutoff point along the continuum between normality and advanced disease varies. A third variation in data collection is in "blinding" examiners performing the second-stage evaluations for disease to each subject's first-stage cognitive test performance. Although we are unaware of systematic investigations of blinding, judging from its importance in trials,⁶ its effect here seems potentially great.

Analytic variation occurs in applying study estimates to the US population. One method directly applies the prevalence of AD from a study to the number of people in the United States. The alternative life-table approach estimates prevalence from incidence of AD from a study. The first approach is more direct, but the second better adjusts for survival differences and takes advantage of incidence being a more accurate measure of disease occurrence, especially in studies of groups with large cultural differences.⁷

We use incidence estimates from a population study using stratified random sampling and blinded disease evaluation in a biracial urban community. We combine them with 2000 US census and National Center for Health Statistics mortality data to estimate prevalence of AD in the US population. We then project future population disease prevalence, using US Census Bureau high, middle, and low series of population growth projections.

METHODS

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CHICAGO POPULATION STUDY

Estimates of AD incidence are from a study⁸ of a biracial (black and white), geographically defined community of 3 adjacent neighborhoods in Chicago, Ill —Morgan Park, Washington Heights, and Beverly. Of all residents older than 65 years, 79% participated. Each study data collection cycle consists of an in-home interview of all participants and clinical evaluation for AD of a stratified random sample. Alzheimer disease incidence was measured in a cohort of 3838 persons determined to be free of AD at baseline, with disease developing during an average interval of 4.1 years between the baseline cycle and cycle 2. Sampling for clinical evaluation was based on age, race, sex, and change in cognitive function from the first to the second cycle home interview of the entire cohort, with persons randomly selected for evaluation from all levels of cognitive change. All 835 persons examined received identical structured clinical evaluations by examiners blinded to population-interview cognitive testing and sampling category. Criteria for AD were those of the of the National Institute of Neurological and Communicative Disorders and Stroke–Alzheimer's Disease and Related Disorders Association Working Group for probable AD,⁵ except that persons who met these criteria and had another condition-impairing cognition were retained.

STATISTICAL METHODS

We used the methods of Brookmeyer et al² with the following modifications. First, we calculated separate incidence estimates for 432 groups defined by single year of age, sex, 2 racial groups, and 3 educational groups, based on a logistic model weighted for the complex sample design with terms for age, age squared, race, educational groups, and follow-up interval. We then computed a weighted average incidence across the educational groups for each age, sex, and racial group. The weights were based on the current level of education from US census data⁹; future education was obtained by aging the current population. Second, instead of using the total population death rate for each age, sex, and racial group as the probability for the disease-free segment and multiplying that by 1.44 for the diseased segment, we distributed the total number of expected deaths between the diseased group and disease-free group using an iterative algorithm to obtain the ratio of 2.14 reported previously.¹⁰ Third, for the numbers of people alive at age 65 years and age-, sex-, race-, and birth cohort–specific death rates, we used National Center for Health Statistics life tables through 1999¹¹ and US census projected life tables up to 2050.¹² For the number of people in the US, we used the 2000 US census¹³ and the US Census Bureau estimates of US population growth through 2050.¹² We repeated the estimation for the year 2000, using different model specifications to examine sensitivity to variations in the logistic model.

We estimated the sample-weighted proportion of persons in each disease severity category by age group, using prevalence data from the baseline cycle of the Chicago study. Severity was classified by score on the Mini-Mental State Examination (MMSE)¹⁴ as mild (18), moderate (10-17),^10-17 or severe (9).

RESULTS

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CURRENT NUMBER OF PERSONS WITH AD

In 2000, we estimate there were 4.5 million people in the United States with AD. A fairly small number, 0.3 million (7%), were between the ages of 65 and 74 years, 2.4 million (53%) were between the ages of 75 and 84 years, and 1.8 million (40%) were 85 years of age and older. The estimate was insensitive to variations in statistical method; specifically, excluding a term for black race (not significant), including a term for sex (not significant), modeling educational level linearly by year, modeling educational level in different groups, and modeling age as a single linear term produced results within 0.5 million of the 4.5 million estimate.

In the Chicago population study, with most affected persons still living in the community, 48% of prevalent cases of AD were classified as mild, 31% as moderate, and 21% as severe. Prevalence of disease and proportion of severe disease increased with age (Figure 1). Among persons aged 65 to 74 years, 17% of these cases were severe compared with 20% among persons aged between 75 and 84 years and 28% among persons 85 years and older.

View larger version (27K): [in this window] [in a new window] Figure 1. Prevalence of severe (Mini-Mental State Examination score, 9), moderate (Mini-Mental State Examination score, 10-17), and mild (Mini-Mental State Examination score, 18) Alzheimer disease, in each of 3 age groups, in the community population providing data for these estimates.

FUTURE NUMBER OF PERSONS WITH AD

Both the number of persons with AD in the US population and their age distribution will change substantially over the next 50 years (Table 1). Prevalence is expected to increase almost 3-fold to 13.2 million persons in 2050 (Table 1 and Figure 2). To indicate the uncertainty in these future estimates, we bracket the estimates derived from the middle-series US Census Bureau estimates of population growth with estimates derived from the high- and low-series estimates of population growth. For 2010, the estimate derived from the middle series is 5.1 million persons with AD and is bracketed by an estimate derived from the low series of 5.1 million persons and an estimate derived from the high series of 5.3 million persons. By 2050, the uncertainty increases substantially. The estimate of 13.2 million persons with AD derived from the middle series is bracketed by a figure of 11.3 million derived from the low series and 16.0 million derived from the high series.

View this table: [in this window] [in a new window] Current and Projected Number of Persons With Alzheimer Disease (in Millions) Older Than 65 Years in the US Population by 3 Age Subgroups*

View larger version (21K): [in this window] [in a new window] Figure 2. Projected number of persons in US population with Alzheimer disease using the 2000 US Census Bureau middle-series estimates of population growth, bounded by high- and low-series estimates.

As rapid growth of the oldest age groups of the US population continues, the age distribution of AD will change (Table 1 and Figure 3). The number of persons aged 75 to 84 years with the disease will double to 4.8 million by the year 2050. The number of persons older than 85 years with AD, however, will more than quadruple to 8.0 million. The number of persons aged between 65 and 74 years with the disease will remain fairly constant at 0.3 to 0.5 million.

View larger version (22K): [in this window] [in a new window] Figure 3. Projected number of persons in US population with Alzheimer disease by age groups, 65 to 74 years old, 75 to 84 years old, and 85 years and older, using the 2000 US Census Bureau middle-series estimate of population growth.

Projected decline in death rates among persons older than 65 years in the US population to about half their current annual values by 2050¹¹ will, first, increase the number and proportion of persons who survive to the oldest ages where AD is most frequent, and, second, result in increased survival of persons with AD, and thus increased prevalence. We applied an estimate of the current ratio in survival of 1:2.14 to persons without the illness⁹ and assumed it will remain constant.

COMMENT

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These estimates suggest that prevalence of AD in the US population will substantially increase, as older age groups increase in size. Further, the age distribution of the disease will change, as much of this increase will be attributable to the number of persons older than 85 years with AD.

COMPARABILITY TO ESTIMATES FROM OTHER STUDIES

Our estimate of AD prevalence in the year 2000 closely agrees with a projection from the earlier East Boston Study,¹ despite a different statistical method. The number of affected persons projected in 2050 is 35% higher than estimated from the East Boston Study because our methods assumes that projected increases in survival over the next 50 years will affect both persons with and without AD, with the ratio of survival among unaffected persons to survival among affected persons remaining constant at its present level.

Another study² provided lower estimates, especially for the absolute number of persons affected by AD in future years. These differences appear due more to differences in the studies providing estimates of current AD occurrence rather than to fairly small differences in how these estimates of AD occurrence were applied to US Census Bureau estimates of population growth.¹⁵ Both this study and the earlier one suggest marked growth in numbers of persons affected by AD. The estimates from the prior study used 4 different source studies^16-19 to estimate AD occurrence. One was the incidence phase of the East Boston Study,¹⁹ which used stratified random sampling to ascertain disease. The other 3 studies, however, used methods that gave lower estimates, especially in the oldest age groups. One¹⁷ used only medical records to identify cases; another¹⁸ eliminated the low-scoring 10% of persons from the dementia-free cohort and used a restrictive protocol to detect incident disease. Another¹⁶ examined a highly educated volunteer cohort that was likely healthier than the total population. Because the older subgroups of the US population will experience the greatest growth, these lower estimates of disease in the oldest aged groups result in large differences in projected AD prevalence in future years.

STRENGTHS AND LIMITATIONS OF THE STUDY

Strengths of this study include an estimation of population prevalence from source study incidence and a source study of a single population of black and white Americans that used random sampling for detailed evaluation from all strata of cognitive test performance and examiners blinded to prior cognitive test results. Weaknesses include a limited proportion of persons of Hispanic origin in this source study. While use of a single, rigorously designed study of AD is a strength, no single community is likely to exactly represent the entire country. The average educational level in the study community was fairly similar to that of the US current educational levels of persons older than 25 years suggesting that there will be little increase in the average educational level of people older than 65 years in the next 50 years. The effect of race on AD occurrence is unclear. We assumed the risk of death for persons with AD compared with that of unaffected persons will remain constant. Life expectancy with AD has a substantial effect on projected prevalence of the disease and is subject to such influences as improvements in care.

CONCLUSIONS

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These estimates of a substantial increase in AD prevalence assume that the age-, race-, and education-specific risk of disease will remain constant over the next 50 years. The large public health challenge is to make these projections obsolete and irrelevant by discovering routes to the prevention of the illness through better understanding of its underlying biology and by discovery of modifiable risk factors.

AUTHOR INFORMATION

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Corresponding author and reprints: Denis A. Evans, MD, Rush-Presbyterian–St Luke's Medical Center, Suite 675, 1645 W Jackson Blvd, Chicago, IL 60612 (e-mail: Denis_Evans{at}rsh.net).

Accepted for publication April 22, 2003.

Author contributions: Study concept and design (Drs Hebert, Scherr, Bennett, and Evans); acquisition of data (Drs Hebert, Scherr, Bennett, and Evans); analysis and interpretation of data (Drs Hebert, Scherr, Bienias, Bennett, and Evans); drafting of the manuscript (Drs Hebert, Bienias, and Evans); critical revision of the manuscript for important intellectual content (Drs Hebert, Scherr, Bienias, Bennett, and Evans); statistical expertise (Drs Hebert, Scherr, and Bienias); obtained funding (Dr Evans); administrative, technical, and material support (Drs Hebert, Bennett, and Evans); study supervision (Drs Bennett and Evans).

This study was supported by grants R01-AG 11101 and P30-AG 10161 from the National Institute on Aging, National Institutes of Health, Bethesda, Md; and by a grant from the Alzheimer's Association, Chicago, Ill.

From the Rush Institute on Healthy Aging (Drs Hebert, Bienias, Bennett, and Evans), the Rush Alzheimer's Disease Center (Drs Bennett and Evans), Rush-Presbyterian– St Luke's Medical Center, Chicago, Ill; and the National Center for Chronic Disease Prevention and Health Promotion, Centers for Disease Control and Prevention, Atlanta, Ga (Dr Scherr).

REFERENCES

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Estimated Prevalence of People With Cognitive Impairment: Results From Nationally Representative Community and Institutional Surveys
Bernstein and Remsburg
Gerontologist 2007;47:350-354.
ABSTRACT | FULL TEXT  

Spousal dementia caregiving in the context of late-life remarriage
Sherman and Boss
Dementia 2007;6:245-270.
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Patient's Rating of Cognitive Ability: Using the AD8, a Brief Informant Interview, as a Self-rating Tool to Detect Dementia
Galvin et al.
Arch Neurol 2007;64:725-730.
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Invited Commentary: Lipoproteins and Dementia--Is It the Apolipoprotein A-I?
Scarmeas
Am J Epidemiol 2007;165:993-997.
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Presenilin-1 C410Y Alzheimer Disease Plaques Contain Synaptic Proteins
Haleem et al.
AM J ALZHEIMERS DIS OTHER DEMEN 2007;22:137-144.
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Conceptualizing Alzheimer's Disease as a Terminal Medical Illness
Wolf-Klein et al.
AM J HOSP PALLIAT CARE 2007;24:77-82.
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How common are the "common" neurologic disorders?
Hirtz et al.
Neurology 2007;68:326-337.
ABSTRACT | FULL TEXT  

Sensory Gating in Patients With Alzheimer's Disease and Their Biological Children
Ally et al.
AM J ALZHEIMERS DIS OTHER DEMEN 2007;21:439-447.
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Qualitative Estimates of Medial Temporal Atrophy as a Predictor of Progression From Mild Cognitive Impairment to Dementia
DeCarli et al.
Arch Neurol 2007;64:108-115.
ABSTRACT | FULL TEXT  

Behavior-Based Interventions to Enhance Cognitive Functioning and Independence in Older Adults
Shumaker et al.
JAMA 2006;296:2852-2854.
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Body mass index in older persons is associated with Alzheimer disease pathology
Buchman et al.
Neurology 2006;67:1949-1954.
ABSTRACT | FULL TEXT  

Low Folate and the Risk of Cognitive and Functional Deficits in the Very Old: The Monzino 80-plus Study
Tettamanti et al.
J. Am. Coll. Nutr. 2006;25:502-508.
ABSTRACT | FULL TEXT  

Making Sense of Mild Cognitive Impairment: A Qualitative Exploration of the Patient's Experience
Lingler et al.
Gerontologist 2006;46:791-800.
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Delta-aminolevulinic acid dehydratase polymorphism and the relation between low level lead exposure and the Mini-Mental Status Examination in older men: the Normative Aging Study
Weuve et al.
Occup. Environ. Med. 2006;63:746-753.
ABSTRACT | FULL TEXT  

3D comparison of hippocampal atrophy in amnestic mild cognitive impairment and Alzheimer's disease
Apostolova et al.
Brain 2006;129:2867-2873.
ABSTRACT | FULL TEXT  

Relation between body mass index and cognitive function in healthy middle-aged men and women.
Cournot et al.
Neurology 2006;67:1208-1214.
ABSTRACT | FULL TEXT  

Alzheimer's disease: Psychopathology, medical management and dental implications.
Friedlander et al.
Journal of the American Dental Association 2006;137:1240-1251.
ABSTRACT | FULL TEXT  

Correlates and outcomes of dementia among dialysis patients: the Dialysis Outcomes and Practice Patterns Study
Kurella et al.
Nephrol Dial Transplant 2006;21:2543-2548.
ABSTRACT | FULL TEXT  

Information and service needs of persons with Alzheimer's disease and their family caregivers living in rural communities.
Edelman et al.
AM J ALZHEIMERS DIS OTHER DEMEN 2006;21:226-233.
ABSTRACT  

Developing more flexible approaches to respite for people living with dementia and their carers.
Shanley
AM J ALZHEIMERS DIS OTHER DEMEN 2006;21:234-241.
ABSTRACT  

Exploring the association of glyceraldehyde-3-phosphate dehydrogenase gene and Alzheimer disease.
Lin et al.
Neurology 2006;67:64-68.
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Galantamine With Adjunctive Memantine: Combined Effects on Brain Nicotinic Acetylcholine Receptors and N-methyl-D-aspartate Receptors May Improve Alzheimer's Disease Symptomatology
Scharre
J Clin Pharmacol 2006;46:6S-7S.
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Pharmacology of Acetylcholinesterase Inhibitors and N-methyl-D-aspartate Receptors for Combination Therapy in the Treatment of Alzheimer's Disease
Geerts and Grossberg
J Clin Pharmacol 2006;46:8S-16S.
ABSTRACT | FULL TEXT  

Reductions in levels of the Alzheimer's amyloid {beta} peptide after oral administration of ginsenosides
Chen et al.
FASEB J. 2006;20:1269-1271.
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Coronary artery disease is associated with Alzheimer disease neuropathology in APOE4 carriers
Beeri et al.
Neurology 2006;66:1399-1404.
ABSTRACT | FULL TEXT  

Managing patients with Alzheimer's disease
Corey-Bloom et al.
PN 2006;6:78-89.
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Cognitive leisure activities, but not watching TV, for future brain benefits
Rundek and Bennett
Neurology 2006;66:794-795.
FULL TEXT  

Recognition and treatment of Alzheimer's disease: A case-based review
Marseille and Silverman
AM J ALZHEIMERS DIS OTHER DEMEN 2006;21:119-125.
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The Cost-Effectiveness of Noninstitutional Long-Term Care Services: Review and Synthesis of the Most Recent Evidence
Grabowski
Med Care Res Rev 2006;63:3-28.
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The Value of Telephone Support Groups Among Ethnically Diverse Caregivers of Persons With Dementia
Bank et al.
Gerontologist 2006;46:134-138.
ABSTRACT | FULL TEXT  

Can We Escape Stroke and Alzheimer Disease?
Kurth and Logroscino
Stroke 2006;37:279-280.
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Temporal Profile of Amyloid-beta (Abeta) Oligomerization in an in Vivo Model of Alzheimer Disease: A LINK BETWEEN Abeta AND TAU PATHOLOGY
Oddo et al.
J. Biol. Chem. 2006;281:1599-1604.
ABSTRACT | FULL TEXT  

Mens Sana in Corpore Sano
Podewils and Guallar
ANN INTERN MED 2006;144:135-136.
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Cholinesterase Inhibitor Use and Age in the General Population
Lucca et al.
Arch Neurol 2006;63:154-155.
FULL TEXT  

Children of Alzheimer Patients: An Overview
Jarvik and Blazer
J Geriatr Psychiatry Neurol 2005;18:181-186.
 

Longitudinal Models of Growth and Survival Applied to the Early Detection of Alzheimer's Disease
McArdle et al.
J Geriatr Psychiatry Neurol 2005;18:234-241.
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