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Vol. 60 No. 8, August 2003 TABLE OF CONTENTS
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Alzheimer Disease in the US Population

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 estimates1-2 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.



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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.


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Current and Projected Number of Persons With Alzheimer Disease (in Millions) Older Than 65 Years in the US Population by 3 Age Subgroups*



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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.



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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 studies16-19 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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1. Evans DA. Estimated prevalence of Alzheimer's disease in the United States. Milbank Q. 1990;68:267-289. FULL TEXT | WEB OF SCIENCE | PUBMED
2. Brookmeyer R, Gray S, Kawas C. Projections of Alzheimer's disease in the United States and the public health impact of delaying disease onset. Am J Public Health. 1998;88:1337-1342. WEB OF SCIENCE | PUBMED
3. Rogan WJ, Gladen B. Estimating prevalence from the results of a screening test. Am J Epidemiol. 1978;107:71-76. FREE FULL TEXT
4. Albert M, Smith LA, Scherr PA, Taylor JO, Evans DA, Funtenstein HH. Use of brief cognitive tests to identify individuals in the community with clinically-diagnosed Alzheimer's disease. Int J Neurosci. 1991;57:167-178. WEB OF SCIENCE | PUBMED
5. McKhann G, Drachman D, Folstein M, Katzman R, Price D, Stadlan EM. Clinical diagnosis of Alzheimer's disease: Report of the NINCDS-ADRDA Work Group under the auspices of Department of Health and Human Services Task Force on Alzheimer's Disease. Neurology. 1984;34:939-944. FREE FULL TEXT
6. Hennekins CH, Buring JE. Epidemiology in Medicine. Boston, Mass: Little Brown & Co; 1987:192-194.
7. Hendrie HC, Ogunniyi A, Hall KS, et al. Incidence of dementia and Alzheimer disease in 2 communities: Yoruba residing in Ibadan, Nigeria, and African Americans residing in Indianapolis, Indiana. JAMA. 2001;285:739-747. FREE FULL TEXT
8. Evans DA, Bennett DA, Wilson RS, et al. Incidence Alzheimer disease in a biracial urban community: relation to apolipoprotein E allele status. Arch Neurol. 2003;60:185-189. FREE FULL TEXT
9. Continuous Measurement Office, Demographic Surveys Division, US Census Bureau. Census 2000 Supplementary PUMS: Educational Attainment. Available at: http://www.census.gov/acs/www/Products/PUMS/PUMS2.htm, 2002. Accessed March 10, 2003.
10. Hebert LE, Scherr PA, McCann JJ, Beckett LA, Evans DA. Is the risk of developing Alzheimer's disease greater for women than for men? Am J Epidemiol. 2001;153:132-136. FREE FULL TEXT
11. National Center for Health Statistics. US life tables 1965-1999. Hyattsville, MD. Also available at: http://www.CDC.gov/nchs/data/nvsr/nvsr50/nvsr50_06.pdf. Accessed March 10, 2003.
12. Population Projections Program, Population Division, US Census Bureau. Population and life tables, population projections of the United States by age, race, sex, Hispanic origin and nativity: 1999 to 2100. Available at: http://www.census.gov/population/projections/nation/detail. Accessed March 10, 2003.
13. US Census Bureau. Census 2000 Summary File 1 (Sf 1) 100-percent data, Tables pctl2 and pctl2b. Available at: http://www.factfinder.census.gov, 2002. Accessed March 10, 2003.
14. Folstein MF, Folstein SE, McHugh PR. "Mini-mental state": a practical method for grading the cognitive state of patients for the clinician. J Psychiatr Res. 1975;12:189-198. FULL TEXT | WEB OF SCIENCE | PUBMED
15. Brookmeyer R, Gray S. Methods for projecting the incidence and prevalence of chronic diseases in aging populations: application to Alzheimer's disease. Stat Med. 2000;19:1481-1493. FULL TEXT | WEB OF SCIENCE | PUBMED
16. Kawas C, Gray S, Brookmeyer R, Fozard J, Zonderman A. Age-specific incidence rates of Alzheimer's disease: the Baltimore Longitudinal Study of Aging. Neurology. 2000;54:2072-2077. FREE FULL TEXT
17. Kokmen E, Chandra V, Schoenberg BS. Trends in incidence of dementing illness in Rochester, Minnesota, in three quinqennial periods, 1960-1974. Neurology. 1988;38:975-980. FREE FULL TEXT
18. Bachman DL, Wolf PA, Linn RT, et al. Incidence of dementia and probable Alzheimer's disease in a general population: the Framingham Study. Neurology. 1993;43:515-519. FREE FULL TEXT
19. Hebert LE, Scherr PA, Beckett LA, et al. Age-specific incidence of Alzheimer's disease in a community population. JAMA. 1995;273:1354-1359. FREE FULL TEXT


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Validity of Estimated Dietary Eicosapentaenoic Acid and Docosahexaenoic Acid Intakes Determined by Interviewer-Administered Food Frequency Questionnaire Among Older Adults With Mild-to-Moderate Cognitive Impairment or Dementia
Arsenault et al.
Am J Epidemiol 2009;170:95-103.
ABSTRACT | FULL TEXT  

Long-term effects of the concomitant use of memantine with cholinesterase inhibition in Alzheimer disease
Lopez et al.
J. Neurol. Neurosurg. Psychiatry 2009;80:600-607.
ABSTRACT | FULL TEXT  

Review: Donepezil in Severe Alzheimer's Disease
Winblad
AM J ALZHEIMERS DIS OTHER DEMEN 2009;24:185-192.
ABSTRACT  

Treatment of Alzheimer's disease in the long-term-care setting
Smith
Am J Health Syst Pharm 2009;66:899-907.
ABSTRACT | FULL TEXT  

Psychiatric symptoms of dementia: Treatable, but no silver bullet
SCHWAB et al.
Cleveland Clinic Journal of Medicine 2009;76:167-174.
ABSTRACT | FULL TEXT  

The Association of Transient Ischemic Attack Symptoms With Memory Impairment Among Elderly Participants of the Third US National Health and Nutrition Examination Survey
Takahashi et al.
J Geriatr Psychiatry Neurol 2009;22:46-51.
ABSTRACT  

The Metabolic Syndrome and Development of Cognitive Impairment Among Older Women
Yaffe et al.
Arch Neurol 2009;66:324-328.
ABSTRACT | FULL TEXT  

Nicotinic Acetylcholine Receptor Signalling: Roles in Alzheimer's Disease and Amyloid Neuroprotection
Buckingham et al.
Pharmacol. Rev. 2009;61:39-61.
ABSTRACT | FULL TEXT  

Surrogate consent for dementia research: A national survey of older Americans
Kim et al.
Neurology 2009;72:149-155.
ABSTRACT | FULL TEXT  

Alzheimer disease: Time to improve its diagnosis and treatment
SALLOWAY and CORREIA
Cleveland Clinic Journal of Medicine 2009;76:49-58.
ABSTRACT | FULL TEXT  

100 Years After Alzheimer: Contemporary Neurology Practice Assessment of Referrals for Dementia
Chow et al.
AM J ALZHEIMERS DIS OTHER DEMEN 2009;23:516-527.
ABSTRACT  

A systematic review of the use of contingent valuation in Alzheimer's disease research
Oremus and Tarride
Dementia 2008;7:461-480.
ABSTRACT  

Dementia of the Alzheimer Type
Jalbert et al.
Epidemiol Rev 2008;30:15-34.
ABSTRACT | FULL TEXT  

Functional Rescue of Degenerating Photoreceptors in Mice Homozygous for a Hypomorphic cGMP Phosphodiesterase 6 b Allele (Pde6bH620Q)
Davis et al.
IOVS 2008;49:5067-5076.
ABSTRACT | FULL TEXT  

Frequent Amyloid Deposition Without Significant Cognitive Impairment Among the Elderly
Aizenstein et al.
Arch Neurol 2008;65:1509-1517.
ABSTRACT | FULL TEXT  

Role of the Neuropathology of Alzheimer Disease in Dementia in the Oldest-Old
Haroutunian et al.
Arch Neurol 2008;65:1211-1217.
ABSTRACT | FULL TEXT  

Transitioning Dementia Residents from Assisted Living to Memory Care Units: A Pilot Study
Kelsey et al.
AM J ALZHEIMERS DIS OTHER DEMEN 2008;23:355-362.
ABSTRACT  

An Educational Intervention to Support Caregivers of Elders With Dementia
Devor and Renvall
AM J ALZHEIMERS DIS OTHER DEMEN 2008;23:233-241.
ABSTRACT  

Young Adult Attitudes About Alzheimer's Disease
Lundquist and Ready
AM J ALZHEIMERS DIS OTHER DEMEN 2008;23:267-273.
ABSTRACT  

History of depression, depressive symptoms, and medial temporal lobe atrophy and the risk of Alzheimer disease
Geerlings et al.
Neurology 2008;70:1258-1264.
ABSTRACT | FULL TEXT  

Altered neuronal gene expression in brain regions differentially affected by Alzheimer's disease: a reference data set
Liang et al.
Physiol. Genomics 2008;33:240-256.
ABSTRACT | FULL TEXT  

Prevalence of Cognitive Impairment without Dementia in the United States
Plassman et al.
ANN INTERN MED 2008;148:427-434.
ABSTRACT | FULL TEXT  

Conjugal Alzheimer Disease: Risk in Children When Both Parents Have Alzheimer Disease
Jayadev et al.
Arch Neurol 2008;65:373-378.
ABSTRACT | FULL TEXT  

Measuring perceived stigma in persons with progressive neurological disease: Alzheimer's dementia and Parkinson's disease
Burgener and Berger
Dementia 2008;7:31-53.
ABSTRACT  

Telephone-Delivered Psychosocial Intervention Reduces Burden in Dementia Caregivers.
Tremont et al.
Dementia 2008;7:503-520.
ABSTRACT  

A 93-Year-Old Man With Advanced Dementia and Eating Problems
Mitchell
JAMA 2007;298:2527-2536.
ABSTRACT | FULL TEXT  

Oxidative DNA damage in mild cognitive impairment and late-stage Alzheimer's disease
Lovell and Markesbery
Nucleic Acids Res 2007;35:7497-7504.
ABSTRACT | FULL TEXT  

Cognitive-Behavioral Profiles of Neurodegenerative Dementias: Beyond Alzheimer's Disease
Levy and Chelune
J Geriatr Psychiatry Neurol 2007;20:227-238.
ABSTRACT  

Rivastigmine-induced dystonia
Pavlis et al.
Am J Health Syst Pharm 2007;64:2468-2470.
ABSTRACT | FULL TEXT  

Grief and Personal Growth Experience of Spouses and Adult-Child Caregivers of Individuals With Alzheimer's Disease and Related Dementias
Ott et al.
The Gerontologist 2007;47:798-809.
ABSTRACT | FULL TEXT  

Survival of Ethnic Chinese With Alzheimer's Disease: A 5-Year Longitudinal Study in Taiwan
Tsai et al.
J Geriatr Psychiatry Neurol 2007;20:172-177.
ABSTRACT  

Deletion of tumor necrosis factor death receptor inhibits amyloid {beta} generation and prevents learning and memory deficits in Alzheimer's mice
He et al.
JCB 2007;178:829-841.
ABSTRACT | FULL TEXT  

Accelerating Amyloid-beta Fibrillization Reduces Oligomer Levels and Functional Deficits in Alzheimer Disease Mouse Models
Cheng et al.
J. Biol. Chem. 2007;282:23818-23828.
ABSTRACT | FULL TEXT  

Dementia and Comorbidities: An Overview of Diagnosis and Management
Swanson and Carnahan
Journal of Pharmacy Practice 2007;20:296-317.
ABSTRACT  

Donepezil preserves cognition and global function in patients with severe Alzheimer disease
Black et al.
Neurology 2007;69:459-469.
ABSTRACT | FULL TEXT  




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