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      Amyloid imaging in cognitively normal individuals, at-risk populations and preclinical Alzheimer's disease

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          Recent developments of PET amyloid ligands have made it possible to visualize the presence of Aβ deposition in the brain of living participants and to assess the consequences especially in individuals with no objective sign of cognitive deficits. The present review will focus on amyloid imaging in cognitively normal elderly, asymptomatic at-risk populations, and individuals with subjective cognitive decline. It will cover the prevalence of amyloid-positive cases amongst cognitively normal elderly, the influence of risk factors for AD, the relationships to cognition, atrophy and prognosis, longitudinal amyloid imaging and ethical aspects related to amyloid imaging in cognitively normal individuals. Almost ten years of research have led to a few consensual and relatively consistent findings: some cognitively normal elderly have Aβ deposition in their brain, the prevalence of amyloid-positive cases increases in at-risk populations, the prognosis for these individuals is worse than for those with no Aβ deposition, and significant increase in Aβ deposition over time is detectable in cognitively normal elderly. More inconsistent findings are still under debate; these include the relationship between Aβ deposition and cognition and brain volume, the sequence and cause-to-effect relations between the different AD biomarkers, and the individual outcome associated with an amyloid positive versus negative scan. Preclinical amyloid imaging also raises important ethical issues. While amyloid imaging is definitely useful to understand the role of Aβ in early stages, to define at-risk populations for research or for clinical trial, and to assess the effects of anti-amyloid treatments, we are not ready yet to translate research results into clinical practice and policy. More researches are needed to determine which information to disclose from an individual amyloid imaging scan, the way of disclosing such information and the impact on individuals and on society.


          • Ten to thirty percent of cognitively normal elderly have Aβ deposition in their brain
          • The prognosis for these individuals is worse than for those with no Aβ deposition
          • Significant increase in Aβ deposition over time is detectable in normal elderly
          • Aβ deposition is poorly related to cognitive performance and brain volume
          • The individual outcome associated with an amyloid positive scan is unclear

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          Most cited references 131

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          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.

          Clinical criteria for the diagnosis of Alzheimer's disease include insidious onset and progressive impairment of memory and other cognitive functions. There are no motor, sensory, or coordination deficits early in the disease. The diagnosis cannot be determined by laboratory tests. These tests are important primarily in identifying other possible causes of dementia that must be excluded before the diagnosis of Alzheimer's disease may be made with confidence. Neuropsychological tests provide confirmatory evidence of the diagnosis of dementia and help to assess the course and response to therapy. The criteria proposed are intended to serve as a guide for the diagnosis of probable, possible, and definite Alzheimer's disease; these criteria will be revised as more definitive information become available.
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            The amyloid hypothesis of Alzheimer's disease: progress and problems on the road to therapeutics.

             D. Selkoe,  John Hardy (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.
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              Hypothetical model of dynamic biomarkers of the Alzheimer's pathological cascade.

              Currently available evidence strongly supports the position that the initiating event in Alzheimer's disease (AD) is related to abnormal processing of beta-amyloid (Abeta) peptide, ultimately leading to formation of Abeta plaques in the brain. This process occurs while individuals are still cognitively normal. Biomarkers of brain beta-amyloidosis are reductions in CSF Abeta(42) and increased amyloid PET tracer retention. After a lag period, which varies from patient to patient, neuronal dysfunction and neurodegeneration become the dominant pathological processes. Biomarkers of neuronal injury and neurodegeneration are increased CSF tau and structural MRI measures of cerebral atrophy. Neurodegeneration is accompanied by synaptic dysfunction, which is indicated by decreased fluorodeoxyglucose uptake on PET. We propose a model that relates disease stage to AD biomarkers in which Abeta biomarkers become abnormal first, before neurodegenerative biomarkers and cognitive symptoms, and neurodegenerative biomarkers become abnormal later, and correlate with clinical symptom severity. Copyright 2010 Elsevier Ltd. All rights reserved.

                Author and article information

                Neuroimage (Amst)
                Neuroimage (Amst)
                NeuroImage : Clinical
                5 March 2013
                5 March 2013
                : 2
                : 356-365
                [a ]INSERM, U1077 Caen, France
                [b ]Université de Caen Basse-Normandie, UMR-S1077, Caen, France
                [c ]Ecole Pratique des Hautes Etudes, UMR-S1077, Caen, France
                [d ]CHU de Caen, U1077 Caen, France
                [e ]CHU de Caen, Service de Neurologie, Caen, France
                [f ]Laboratory for Cognitive Neurology, Department of Neurosciences, University of Leuven, Belgium
                [g ]Neurology Department, University Hospitals Leuven, Belgium
                [h ]Alzheimer Research Centre KU Leuven, Leuven Institute of Neuroscience and Disease, University of Leuven, Belgium
                Author notes
                [* ]Corresponding author at: Unité de Recherche U1077, Centre Cyceron, Bd H. Becquerel, BP 5229, 14074 Caen Cedex, France. Tel.: + 33 2 31 47 01 73; fax: + 33 2 31 47 02 75. chetelat@
                © 2013 The Authors

                This is an open-access article distributed under the terms of the Creative Commons Attribution-NonCommercial-ShareAlike License, which permits non-commercial use, distribution, and reproduction in any medium, provided the original author and source are credited.

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