. PET imaging of fibrillar amyloid in brain more sensitive diagnostic marker than CSF Aß42?. Human Amyloid Imaging 2010 Meeting Abstracts. 2010 April 9;


There is a rapid increasing knowledge of the molecular pathogenesis of Alzheimer’s disease (AD). Early diagnostic markers are needed for identifying subjects at risk for developing AD as well as for outcome measures in clinical trials of new disease modifying drugs. Amyloid (Aß) imaging offers possibilities to further understand the influence of amyloid deposition on functional changes during development of clinical AD. High amyloid PIB retention is observed in prodromal AD. The CSF biomarkers Aß42, tau and ptau have in large, multicentre studies shown high predictive value as clinical diagnostic tools in AD.

A cohort of patients (age range 51-83 years), who underwent routine clinical assessment for cognitive problems at the Department of Geriatric Medicine, Karolinska University Hospital Huddinge (including MRI, CSF biomarkers and neuropsychology testing) and diagnosed as mild cognitive impairment (MCI) and mild AD, also underwent PET scans with 11C-PIB and 18F-FDG. A comparison was made been the percentage of patients who showed high PIB retention (PIB+) compared to those who showed pathological CSF Aß42, tau and ptau levels, respectively.

When the patients underwent PIB PET scans, 82% of the AD and MCI patients showed high amyloid load in the brain (PIB+). Forty-six% of the patients showed pathological low Aß42 values, 63% high tau values and 81% high levels of ptau in CSF. We and others have previously reported a reverse correlation between brain PIB retention and Aß42 levels in CSF. Although this relationship was noticed, we observed patients with high PIB retention (PIB+), normal Aß42 levels but elevated CSF ptau levels. It is important to further study the time course of brain fibrillar Aß levels and CSF biomarkers in prodromal AD to obtain a deeper insight into the disease mechanisms. In these ongoing studies, we now also include PET tracers for studies of activated astrocytes as a component of inflammatory processes.


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  1. Toronto: HAI Amyloid Imaging Conference Abstracts