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      Alzheimer’s Disease: A Journey from Amyloid Peptides and Oxidative Stress, to Biomarker Technologies and Disease Prevention Strategies—Gains from AIBL and DIAN Cohort Studies

      review-article
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      , ,
      Journal of Alzheimer's Disease
      IOS Press
      , Alzheimer’s disease, amyloid, apolipoprotein E, biomarker, dementia, early diagnosis, preclinical

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          There is no author summary for this article yet. Authors can add summaries to their articles on ScienceOpen to make them more accessible to a non-specialist audience.

          Abstract

          Worldwide there are over 46 million people living with dementia, and this number is expected to double every 20 years reaching about 131 million by 2050. The cost to the community and government health systems, as well as the stress on families and carers is incalculable. Over three decades of research into this disease have been undertaken by several research groups in Australia, including work by our original research group in Western Australia which was involved in the discovery and sequencing of the amyloid-β peptide (also known as Aβ or A4 peptide) extracted from cerebral amyloid plaques. This review discusses the journey from the discovery of the Aβ peptide in Alzheimer’s disease (AD) brain to the establishment of pre-clinical AD using PET amyloid tracers, a method now serving as the gold standard for developing peripheral diagnostic approaches in the blood and the eye. The latter developments for early diagnosis have been largely achieved through the establishment of the Australian Imaging Biomarker and Lifestyle research group that has followed 1,100 Australians for 11 years. AIBL has also been instrumental in providing insight into the role of the major genetic risk factor apolipoprotein E ɛ4, as well as better understanding the role of lifestyle factors particularly diet, physical activity and sleep to cognitive decline and the accumulation of cerebral Aβ.

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          Most cited references174

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          Gene dose of apolipoprotein E type 4 allele and the risk of Alzheimer's disease in late onset families.

          The apolipoprotein E type 4 allele (APOE-epsilon 4) is genetically associated with the common late onset familial and sporadic forms of Alzheimer's disease (AD). Risk for AD increased from 20% to 90% and mean age at onset decreased from 84 to 68 years with increasing number of APOE-epsilon 4 alleles in 42 families with late onset AD. Thus APOE-epsilon 4 gene dose is a major risk factor for late onset AD and, in these families, homozygosity for APOE-epsilon 4 was virtually sufficient to cause AD by age 80.
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            Exercise interventions for cognitive function in adults older than 50: a systematic review with meta-analysis

            Physical exercise is seen as a promising intervention to prevent or delay cognitive decline in individuals aged 50 years and older, yet the evidence from reviews is not conclusive.
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              Apolipoprotein E: high-avidity binding to beta-amyloid and increased frequency of type 4 allele in late-onset familial Alzheimer disease.

              Apolipoprotein E is immunochemically localized to the senile plaques, vascular amyloid, and neurofibrillary tangles of Alzheimer disease. In vitro, apolipoprotein E in cerebrospinal fluid binds to synthetic beta A4 peptide (the primary constituent of the senile plaque) with high avidity. Amino acids 12-28 of the beta A4 peptide are required. The gene for apolipoprotein E is located on chromosome 19q13.2, within the region previously associated with linkage of late-onset familial Alzheimer disease. Analysis of apolipoprotein E alleles in Alzheimer disease and controls demonstrated that there was a highly significant association of apolipoprotein E type 4 allele (APOE-epsilon 4) and late-onset familial Alzheimer disease. The allele frequency of the APOE-epsilon 4 in 30 random affected patients, each from a different Alzheimer disease family, was 0.50 +/- 0.06; the allele frequency of APOE-epsilon 4 in 91 age-matched unrelated controls was 0.16 +/- 0.03 (Z = 2.44, P = 0.014). A functional role of the apolipoprotein E-E4 isoform in the pathogenesis of late-onset familial Alzheimer disease is suggested.
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                Author and article information

                Journal
                J Alzheimers Dis
                J. Alzheimers Dis
                JAD
                Journal of Alzheimer's Disease
                IOS Press (Nieuwe Hemweg 6B, 1013 BG Amsterdam, The Netherlands )
                1387-2877
                1875-8908
                13 March 2018
                2018
                : 62
                : 3 , Special 20th Anniversary Issue
                : 965-992
                Affiliations
                [a ]Centre of Excellence for Alzheimer’s Disease Research and Care, School of Medical and Health Sciences, Edith Cowan University , Joondalup, WA, Australia
                [b ]Australian Alzheimer’s Research Foundation, Ralph and Patricia Sarich Neuroscience Research Institute , Nedlands, WA, Australia
                [c ]Department of Biomedical Sciences, Macquarie University , Sydney, NSW, Australia
                [d ]School of Psychiatry and Clinical Neurosciences, University of Western Australia , Perth WA, Australia
                [e ]KaRa Institute of Neurological Diseases , Sydney NSW, Australia
                [f ]School of Biomedical Sciences, Faculty of Health Sciences, Curtin Health Innovation Research Institute, Curtin University of Technology , Bentley, WA, Australia
                [g ]School of Psychology and Exercise Science, Murdoch University , Perth, WA, Australia
                [h ]CSIRO Australian e-Health Research Centre/Health and Biosecurity , Perth, WA, Australia
                [i ]Anglicare, Sydney, NSW, Australia
                [j ]School of Medical Sciences, University of New South Wales , Kensington, NSW, Australia
                [k ]CSIRO Health and Biosecurity, Australian E-Health Research Centre , Brisbane, Australia
                [l ]Department of Neurology, Icahn School of Medicine at Mount Sinai , New York, NY, USA
                [m ]University of North Texas Health Science Centre , Fort Worth, TX, USA
                [n ]Department of Nuclear Medicine and Centre for PET, Austin Health, Heidelberg, Australia
                [o ]Florey Institute of Neuroscience and Mental Health , Parkville, VIC, Australia
                [p ]Cooperative Research Centre for Mental Health , Carlton, VIC, Australia
                [q ]Department of Psychiatry, The University of Melbourne , Parkville, VIC, Australia
                [r ]National Ageing Research Institute , Parkville, VIC, Australia
                [s ]University of Melbourne Academic Unit for Psychiatry of Old Age , St George’s Hospital, Kew, VIC, Australia
                [t ]Collaborative Genomics Group, Centre of Excellence for Alzheimer’s Disease Research and Care, School of Medical Sciences, Edith Cowan University , Joondalup, WA, Australia
                [u ]eHealth, CSIRO Health and Biosecurity, Parkville, VIC, Australia
                [v ]Tanz Centre for Research in Neurodegenerative Diseases, University of Toronto , ON, Canada
                [w ]Lee Kong Chian School of Medicine, Nanyang Technological University , Singapore
                Author notes
                [* ]Correspondence to: Professor Ralph N. Martins, School of Medical and Health Sciences, Edith Cowan University, 270 Joondalup Drive, Joondalup, Western Australia, 6027 Australia. Tel.: +61 8 9347 4200; Fax: +61 8 9347 4299; E-mail: ralph.n.martins@ 123456gmail.com .
                Article
                JAD171145
                10.3233/JAD-171145
                5870031
                29562546
                765e4764-2488-4ec2-92f6-6b4419bab66d
                © 2018 – IOS Press and the authors. All rights reserved

                This is an open access article distributed under the terms of the Creative Commons Attribution Non-Commercial (CC BY-NC 4.0) License, which permits unrestricted non-commercial use, distribution, and reproduction in any medium, provided the original work is properly cited.

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                Categories
                Review

                ,alzheimer’s disease,amyloid,apolipoprotein e,biomarker,dementia,early diagnosis,preclinical

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