8.02.2004

Dr. Robert Heller, our Medical Advisor noticed the following article in Diagnostic Imaging which which I wanted to bring to your attention.


Patients in an early stage of Alzheimer's disease can benefit from disease-modifying treatments. Surrogate imaging markers of early AD pathology are needed for testing potential preventive therapies.

Mayo Clinic researchers suggest that FDG-PET distinguishes between patients with amnestic mild cognitive impairment (aMCI) and those with AD.

Dr. Kejal Kantarci and colleagues in Rochester, MN, used FDG-PET to image nine patients with AD, six with aMCI, and 12 healthy controls. FDG uptake was extracted using a 3D stereotactic surface projection technique (3D-SSP). The 3D-SSP maps of each group were compared against one another pixel by pixel.

Compared with normals, people with aMCI had decreased FDG uptake in the frontal pole, orbitofrontal cortices, and frontal, temporal, and parietal association cortices. Compared with normals, subjects with AD had decreased glucose uptake in the frontal and temporal lobes, parietal association cortex, posterior cingulate cortex, and precuneus.

FDG uptake in the primary sensory and motor cortices and in the occipital lobes were similar for all three groups.

An ROC curve analysis showed that FDG uptake in the right temporal lobe was the most accurate marker to differentiate patients with aMCI from normals, with 69% sensitivity and 80% specificity.

The same region distinguished patients with AD from normals with 91% and 85% sensitivity and specificity, respectively. Patients with AD showed the most significant decrease in FDG uptake in the temporal and parietal lobes, with a very high level of accuracy.

FDG uptake in all regions of interest in aMCI patients confirmed that MCI is a transitional stage between normal and AD, Kantarci said.

Using region of interest analysis, researchers unexpectedly found a decrease in FDG uptake in the medial temporal lobe of AD patients, while it remained normal in aMCI. This finding contradicts many structural MR studies showing hippocampal atrophy in MCI, she said. Previous FDG-PET studies also showed decreased FDG uptake in the medial temporal lobe.

One explanation Kantarci offered dealt with a flaw in the ROI analysis. Because of PET's low resolution, images could have included pixels from outside the medial temporal lobe structures, which might have affected the average FDG uptake. In aMCI, structures adjacent to the medial temporal lobe may have normal FDG uptake, and including them in the ROI may mask decreased glucose metabolism in the medial temporal lobe.

In AD, however, pixels adjacent to the medial temporal lobe may have decreased FDG uptake due to the extent of the pathologic temporal lobe involvement in AD. Therefore, medial temporal lobe uptake may be measured lower than normal in AD but not in aMCI.

"We will be using MR coregistration to trace the medial temporal region of interest as a result of this issue," Kantarci said.



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