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      The Public Health Impact of Alzheimer's Disease, 2000–2050: Potential Implication of Treatment Advances

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          Abstract

          Recent developments in basic research suggest that therapeutic breakthroughs may occur in Alzheimer's disease treatment over the coming decades. To model the potential magnitude and nature of the effect of these advances, historical data from congestive heart failure and Parkinson's disease were used. Projections indicate that therapies which delay disease onset will markedly reduce overall disease prevalence, whereas therapies to treat existing disease will alter the proportion of cases that are mild as opposed to moderate/severe. The public health impact of such changes would likely involve both the amount and type of health services needed. Particularly likely to arise are new forms of outpatient services, such as disease-specific clinics and centers. None of our models predicts less than a threefold rise in the total number of persons with Alzheimer's disease between 2000 and 2050. Therefore, Alzheimer's care is likely to remain a major public health problem during the coming decades.

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          Most cited references 36

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          A new clinical scale for the staging of dementia

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            Immunization with amyloid-beta attenuates Alzheimer-disease-like pathology in the PDAPP mouse.

            Amyloid-beta peptide (Abeta) seems to have a central role in the neuropathology of Alzheimer's disease (AD). Familial forms of the disease have been linked to mutations in the amyloid precursor protein (APP) and the presenilin genes. Disease-linked mutations in these genes result in increased production of the 42-amino-acid form of the peptide (Abeta42), which is the predominant form found in the amyloid plaques of Alzheimer's disease. The PDAPP transgenic mouse, which overexpresses mutant human APP (in which the amino acid at position 717 is phenylalanine instead of the normal valine), progressively develops many of the neuropathological hallmarks of Alzheimer's disease in an age- and brain-region-dependent manner. In the present study, transgenic animals were immunized with Abeta42, either before the onset of AD-type neuropathologies (at 6 weeks of age) or at an older age (11 months), when amyloid-beta deposition and several of the subsequent neuropathological changes were well established. We report that immunization of the young animals essentially prevented the development of beta-amyloid-plaque formation, neuritic dystrophy and astrogliosis. Treatment of the older animals also markedly reduced the extent and progression of these AD-like neuropathologies. Our results raise the possibility that immunization with amyloid-beta may be effective in preventing and treating Alzheimer's disease.
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              Practice parameter: early detection of dementia: mild cognitive impairment (an evidence-based review). Report of the Quality Standards Subcommittee of the American Academy of Neurology.

              The goal of this project was to determine whether screening different groups of elderly individuals in a general or specialty practice would be beneficial in detecting dementia. Epidemiologic studies of aging and dementia have demonstrated that the use of research criteria for the classification of dementia has yielded three groups of subjects: those who are demented, those who are not demented, and a third group of individuals who cannot be classified as normal or demented but who are cognitively (usually memory) impaired. The authors conducted computerized literature searches and generated a set of abstracts based on text and index words selected to reflect the key issues to be addressed. Articles were abstracted to determine whether there were sufficient data to recommend the screening of asymptomatic individuals. Other research studies were evaluated to determine whether there was value in identifying individuals who were memory-impaired beyond what one would expect for age but who were not demented. Finally, screening instruments and evaluation techniques for the identification of cognitive impairment were reviewed. There were insufficient data to make any recommendations regarding cognitive screening of asymptomatic individuals. Persons with memory impairment who were not demented were characterized in the literature as having mild cognitive impairment. These subjects were at increased risk for developing dementia or AD when compared with similarly aged individuals in the general population. There were sufficient data to recommend the evaluation and clinical monitoring of persons with mild cognitive impairment due to their increased risk for developing dementia (Guideline). Screening instruments, e.g., Mini-Mental State Examination, were found to be useful to the clinician for assessing the degree of cognitive impairment (Guideline), as were neuropsychologic batteries (Guideline), brief focused cognitive instruments (Option), and certain structured informant interviews (Option). Increasing attention is being paid to persons with mild cognitive impairment for whom treatment options are being evaluated that may alter the rate of progression to dementia.
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                Author and article information

                Journal
                Annual Review of Public Health
                Annu. Rev. Public Health
                Annual Reviews
                0163-7525
                1545-2093
                May 2002
                May 2002
                : 23
                : 1
                : 213-231
                Affiliations
                [1 ]Cecil G. Sheps Center for Health Services Research, e-mail:
                [2 ]Department of Family Medicine,
                [3 ]School of Social Work,
                [4 ]Department of Biostatistics,
                [5 ]Program on Aging, University of North Carolina at Chapel Hill, Chapel Hill, North Carolina 27599;
                Article
                10.1146/annurev.publhealth.23.100901.140525
                11910061
                © 2002

                Neurology, Health & Social care, Clinical Psychology & Psychiatry, Public health

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