Home > Journals > The Quarterly Journal of Nuclear Medicine and Molecular Imaging > Past Issues > The Quarterly Journal of Nuclear Medicine and Molecular imaging 2011 June;55(3) > The Quarterly Journal of Nuclear Medicine and Molecular imaging 2011 June;55(3):225-36

CURRENT ISSUE
 

JOURNAL TOOLS

eTOC
To subscribe PROMO
Submit an article
Recommend to your librarian
 

ARTICLE TOOLS

Reprints
Permissions

 

REVIEWS  CLINICAL OUTCOMES OF AMYLOID IMAGIN IN CROSS SECTIONAL AND LONGITUDINAL STUDIES 

The Quarterly Journal of Nuclear Medicine and Molecular imaging 2011 June;55(3):225-36

Copyright © 2011 EDIZIONI MINERVA MEDICA

language: English

Alzheimer’s disease: genetic basis and amyloid imaging as endophenotype

Berti V., Nacmias B., Bagnoli S., Sorbi S.

1 Unit of Nuclear Medicine, Department of Clinical Pathophysiology, University of Florence, Florence, Italy; 2 Department of Psychiatric and Neurological Sciences, University of Florence, Florence, Italy


PDF


To date, all known Alzheimer’s disease genes influence amyloid β (Aβ). Imaging of Aβ deposition in the human brain using positron emission tomography (PET) tracers as [11C]Pittsburgh Compound B ([11C]PiB) or [18F]FDDNP offers the possibility of using cortical tracer binding as a quantitative endophenotype for genetic studies of late-onset Alzheimer’s disease (AD). In this review we investigate the association between cerebral Aβ burden, as measured by amyloid PET imaging, and different genetic risk factors involved in AD. Through a look at the major genetic risk factors for both early-onset familial and late-onset sporadic forms of AD, we discuss the possible role of amyloid PET imaging as an endophenotype in AD. Several PET studies confirmed the high heritability of amyloid load estimated by PET imaging and its association with the major genetic risk factors for early and late onset AD, suggesting that cerebral binding of these amyloid tracers could represent an useful trait for large-scale genetic studies of AD.

top of page