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April 29, 2008; 70 (18) Correspondence

IMAGING β-AMYLOID BURDEN IN AGING AND DEMENTIA

G. Linazasoro
First published April 28, 2008, DOI: https://doi.org/10.1212/01.wnl.0000318046.06992.24
G. Linazasoro
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IMAGING β-AMYLOID BURDEN IN AGING AND DEMENTIA
G. Linazasoro
Neurology Apr 2008, 70 (18) 1649-1650; DOI: 10.1212/01.wnl.0000318046.06992.24

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To the Editor:

I read the article by Rowe et al.1 with interest. Diagnosing Alzheimer disease (AD) in a preclinical phase would enable early implementation of therapeutic interventions which might have long-term benefits.

PET technology by using the Pittsburgh compound (PiB) allows detection of amyloid deposits in the brain.1,2 Pathologic studies indicate that amyloid deposition is present in cortical regions of all patients with AD even before the onset of dementia.3 One application of PiB-PET may be all that is necessary to identify the neuropathologic changes of AD in clinically normal individuals prior to the development of cognitive changes. These individuals would be considered to have preclinical AD.

PET studies performed with PiB in cognitively intact subjects have shown that between 15 and 22% of them had abnormal scans.1,2 The objective is to determine who and when someone will become demented. It is and will be unclear because the proportion of subjects with cerebral amyloid deposits is, and will be, higher than the proportion of people with clinical AD.

Otherwise, it is impossible to understand pathologic observations which indicate that more than 30% of older persons over age 75 die without any clinical evidence of dementia despite showing amyloid deposits and pathologic changes characteristic of AD.3 Presumably all of them would have abnormal PiB-PET scans. Amyloid deposition is not synonymous with clinical AD unless we assume that everyone with an abnormal PiB-PET scan would develop AD.

Even in this case, many of them (70% according to pathologic data and prevalence estimates of AD) will die without dementia in the …

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