Introduction
Presently, definitive diagnosis of AD requires histopathological demonstration of amyloid plaques and neurofibrillary tangles at autopsy. An in vivo amyloid-imaging technology that could contribute to accurate the diagnosis in early and perhaps pre-symptomatic stages of AD is under development (1, 2) Positron emission tomography (PET) is a useful tool, which can be used in diagnosis and to follow the progression of AD. Recently a new PET-tracer, PIB (11C-6-hydroxy-benzothiazol), was developed( 3 ) revealing the presence of amyloid in AD patients.
Aims
The aims of the follow-up study were:
To find changes in amyloid deposition in the AD patients after a period of 1.5–2.5 years. To evaluate changes in the glucose cerebral metabolic rate (CMRglc) measured by FDG, and the relation with the amyloid deposition.
Methods
16 patients recruited from the dept. of geriatric medicine at Karolinska Univ. Hosp. Huddinge, Stockholm and previously examined in a Siemens HR+ PET camera at Uppsala Imanet, Sweden, were examined again after 1.5–2.5 years using the same protocol as before. Regions of interest (ROI:s) covering most of the cerebral cortex were selected and various kinetic models were used for the analysis ( 4 ).
Results
A group of patients showed unchanged PIB uptake; another group, increased uptake and some patients showed lower PIB uptake at the second examination. The changes over time for the PIB uptake, revealed inter and intra-individual differences that might be coupled to differences in disease duration and progression, age, medication, or changes in the binding properties of the amyloid. Further analysis of the data and comparisons with changes in CMRglc are necessary.
