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• W1996110977 abstract "Several immunopathological studies have shown that amyloid–β proteins within senile plaques are associated with activated microglia. In particular at the early stages of Alzheimer's disease (AD) an inflammatory response, associated with activated microglia, might be present. Consequently, the level of microglial activation might even be higher in MCI than in AD patients. Activated microglial cells express the peripheral type benzodiazepine receptor, which can be visualized using the PET ligand [11C](R)–PK11195. The objective of this study was to investigate whether and to what extent microglial activation, as measured using [11C](R)–PK11195 and PET, occurs in MCI converting to AD. 13 MCI patients (meeting Petersen criteria), 20 probable AD patients (meeting NINCDS–ADRDA criteria) and 21 age–matched healthy controls were included. Patients were screened extensively; clinical follow–up was a minimum of 2 years. 3D dynamic PET scans were acquired after a bolus injection of 370 MBq (R)–[11C]PK11195. Time activity curves of (R)–[11C]PK11195 concentrations were estimated in several brain regions using both a standard template and manually defined regions of interest. The simplified reference tissue model, with the cerebellum as reference tissue, was used to fit the data. The primary outcome measure was Binding Potential (BP). In addition, SPM analysis of Ichise BP images was performed. Increased [11C](R)–PK11195 binding in AD was found in medial inferior frontal lobe, medial inferior temporal lobe, entorhinal cortex, posterior cingulate cortex and occipital lobe. In MCI the medial temporal lobe and, more specifically, the entorhinal cortex showed increased binding. However, BP did not allow for differentiation between converters or non–converters. SPM analysis showed increased binding in lateral temporal and occipital lobes in both MCI and AD. The distribution of increased [11C](R)–PK11195 binding in MCI and AD agrees with areas known to be affected pathologically in AD and supports the theory that inflammation might be an early phenomenon in the etiology of AD. Although this ligand might lack sensitivity for diagnostic purposes in individual patients, it could be useful for addressing changes in [11C](R)–PK11195 binding (e.g., due to therapy) at a group level." @default.
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• W1996110977 date "2006-07-01" @default.
• W1996110977 modified "2023-09-27" @default.
• W1996110977 title "O1-03-01: Microglial activation in patients with mild cognitive impairment and Alzheimer's disease: A study using [11 C](R )-PK11195 and PET" @default.
• W1996110977 doi "https://doi.org/10.1016/j.jalz.2006.05.044" @default.
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