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      Autosomal-dominant Alzheimer's disease: a review and proposal for the prevention of Alzheimer's disease

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          Autosomal-dominant Alzheimer's disease has provided significant understanding of the pathophysiology of Alzheimer's disease. The present review summarizes clinical, pathological, imaging, biochemical, and molecular studies of autosomal-dominant Alzheimer's disease, highlighting the similarities and differences between the dominantly inherited form of Alzheimer's disease and the more common sporadic form of Alzheimer's disease. Current developments in autosomal-dominant Alzheimer's disease are presented, including the international Dominantly Inherited Alzheimer Network and this network's initiative for clinical trials. Clinical trials in autosomal-dominant Alzheimer's disease may test the amyloid hypothesis, determine the timing of treatment, and lead the way to Alzheimer's disease prevention.

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          The amyloid hypothesis of Alzheimer's disease: progress and problems on the road to therapeutics.

          John Hardy, Dennis J Selkoe (2002)
          It has been more than 10 years since it was first proposed that the neurodegeneration in Alzheimer's disease (AD) may be caused by deposition of amyloid beta-peptide (Abeta) in plaques in brain tissue. According to the amyloid hypothesis, accumulation of Abeta in the brain is the primary influence driving AD pathogenesis. The rest of the disease process, including formation of neurofibrillary tangles containing tau protein, is proposed to result from an imbalance between Abeta production and Abeta clearance.
          Article 0 comments Cited 1306 times – based on 0 reviews     Review now
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            Global prevalence of dementia: a Delphi consensus study.

            Cleusa P Ferri, Martin Prince, Carol Brayne … (2005)
            100 years after the first description, Alzheimer's disease is one of the most disabling and burdensome health conditions worldwide. We used the Delphi consensus method to determine dementia prevalence for each world region. 12 international experts were provided with a systematic review of published studies on dementia and were asked to provide prevalence estimates for every WHO world region, for men and women combined, in 5-year age bands from 60 to 84 years, and for those aged 85 years and older. UN population estimates and projections were used to estimate numbers of people with dementia in 2001, 2020, and 2040. We estimated incidence rates from prevalence, remission, and mortality. Evidence from well-planned, representative epidemiological surveys is scarce in many regions. We estimate that 24.3 million people have dementia today, with 4.6 million new cases of dementia every year (one new case every 7 seconds). The number of people affected will double every 20 years to 81.1 million by 2040. Most people with dementia live in developing countries (60% in 2001, rising to 71% by 2040). Rates of increase are not uniform; numbers in developed countries are forecast to increase by 100% between 2001 and 2040, but by more than 300% in India, China, and their south Asian and western Pacific neighbours. We believe that the detailed estimates in this paper constitute the best currently available basis for policymaking, planning, and allocation of health and welfare resources.
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              Segregation of a missense mutation in the amyloid precursor protein gene with familial Alzheimer's disease.

              A Goate, M C Chartier-Harlin, M Mullan … (1991)
              A locus segregating with familial Alzheimer's disease (AD) has been mapped to chromosome 21, close to the amyloid precursor protein (APP) gene. Recombinants between the APP gene and the AD locus have been reported which seemed to exclude it as the site of the mutation causing familial AD. But recent genetic analysis of a large number of AD families has demonstrated that the disease is heterogeneous. Families with late-onset AD do not show linkage to chromosome 21 markers. Some families with early-onset AD show linkage to chromosome 21 markers, but some do not. This has led to the suggestion that there is non-allelic genetic heterogeneity even within early onset familial AD. To avoid the problems that heterogeneity poses for genetic analysis, we have examined the cosegregation of AD and markers along the long arm of chromosome 21 in a single family with AD confirmed by autopsy. Here we demonstrate that in this kindred, which shows linkage to chromosome 21 markers, there is a point mutation in the APP gene. This mutation causes an amino-acid substitution (Val----Ile) close to the carboxy terminus of the beta-amyloid peptide. Screening other cases of familial AD revealed a second unrelated family in which this variant occurs. This suggests that some cases of AD could be caused by mutations in the APP gene.
              Article 0 comments Cited 314 times – based on 0 reviews     Review now
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                Author and article information

                Journal
                Journal ID (nlm-ta): Alzheimers Res Ther
                Title: Alzheimer's Research & Therapy
                Publisher: BioMed Central
                ISSN (Electronic): 1758-9193
                Publication date Collection: 2011
                Publication date (Electronic): 6 January 2011
                Publication date PMC-release: 6 July 2011
                Volume: 3
                Issue: 1
                Page: 1
                Affiliations
                [1 ]Department of Neurology, Washington University School of Medicine, 660 S. Euclid, Campus Box 8111, St Louis, MO 63110, USA
                [2 ]Department of Neurosciences, University of California San Diego, Gilman Drive, La Jolla, CA 92093, USA
                [3 ]Department for Molecular and Developmental Genetics, Flanders Institute for Biotechnology (VIB), Leuven, Belgium
                [4 ]Center for Human Genetics, K.U. Leuven, Herestraat 49, 3000 Leuven, Belgium
                [5 ]Dementia Research Centre, UCL Institute of Neurology, University College London, London WC1N 3BG, UK
                [6 ]Center for Neurologic Diseases, Brigham and Women's Hospital, Harvard Medical School, Boston, MA 02115, USA
                [7 ]Mary S. Easton Center for Alzheimer's Disease Research, Department of Neurology, David Geffen School of Medicine at UCLA, Los Angeles, CA 90095, USA
                [8 ]Department of Neurology, Memory and Aging Program, Butler Hospital, 345 Blackstone Boulevard, Providence, Rhode Island 02906-4800, USA
                [9 ]Department of Clinical Neurosciences and Psychiatry, Brown Medical School, USA
                [10 ]Center for Alzheimer Research and Treatment, Brigham and Women's Hospital, Alzheimer's Disease Research Center, Massachusetts General Hospital, Harvard Medical School, Boston, MA 02115, USA
                [11 ]JSW LifeSciences GmbH, Parkring 12, A-8074 Grambach, Austria
                [12 ]Division of Biostatistics, Washington University, St Louis, MO 63110, USA
                Article
                Publisher ID: alzrt59
                DOI: 10.1186/alzrt59
                PMC ID: 3109410
                PubMed ID: 21211070
                SO-VID: b926c315-8e03-48b8-acdc-c28e3b1a5382
                Copyright © Copyright ©2011 BioMed Central Ltd
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                ScienceOpen disciplines: Neurology
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                ScienceOpen disciplines: Neurology

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