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European Journal of Nuclear Medicine and Molecular Imaging

Erschienen in:

01.02.2011 | Original Article

In vivo changes in microglial activation and amyloid deposits in brain regions with hypometabolism in Alzheimer’s disease

verfasst von: Masamichi Yokokura, Norio Mori, Shunsuke Yagi, Etsuji Yoshikawa, Mitsuru Kikuchi, Yujiro Yoshihara, Tomoyasu Wakuda, Genichi Sugihara, Kiyokazu Takebayashi, Shiro Suda, Yasuhide Iwata, Takatoshi Ueki, Kenji J. Tsuchiya, Katsuaki Suzuki, Kazuhiko Nakamura, Yasuomi Ouchi

Erschienen in: European Journal of Nuclear Medicine and Molecular Imaging | Ausgabe 2/2011

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Abstract

Purpose

Amyloid β protein (Aβ) is known as a pathological substance in Alzheimer’s disease (AD) and is assumed to coexist with a degree of activated microglia in the brain. However, it remains unclear whether these two events occur in parallel with characteristic hypometabolism in AD in vivo. The purpose of the present study was to clarify the in vivo relationship between Aβ accumulation and neuroinflammation in those specific brain regions in early AD.

Methods

Eleven nootropic drug-naïve AD patients underwent a series of positron emission tomography (PET) measurements with [¹¹C](R)PK11195, [¹¹C]PIB and [¹⁸F]FDG and a battery of cognitive tests within the same day. The binding potentials (BPs) of [¹¹C](R)PK11195 were directly compared with those of [¹¹C]PIB in the brain regions with reduced glucose metabolism.

Results

BPs of [¹¹C](R)PK11195 and [¹¹C]PIB were significantly higher in the parietotemporal regions of AD patients than in ten healthy controls. In AD patients, there was a negative correlation between dementia score and [¹¹C](R)PK11195 BPs, but not [¹¹C]PIB, in the limbic, precuneus and prefrontal regions. Direct comparisons showed a significant negative correlation between [¹¹C](R)PK11195 and [¹¹C]PIB BPs in the posterior cingulate cortex (PCC) (p < 0.05, corrected) that manifested the most severe reduction in [¹⁸F]FDG uptake.

Conclusion

A lack of coupling between microglial activation and amyloid deposits may indicate that Aβ accumulation shown by [¹¹C]PIB is not always the primary cause of microglial activation, but rather the negative correlation present in the PCC suggests that microglia can show higher activation during the production of Aβ in early AD.

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Titel: In vivo changes in microglial activation and amyloid deposits in brain regions with hypometabolism in Alzheimer’s disease
verfasst von: Masamichi Yokokura
Norio Mori
Shunsuke Yagi
Etsuji Yoshikawa
Mitsuru Kikuchi
Yujiro Yoshihara
Tomoyasu Wakuda
Genichi Sugihara
Kiyokazu Takebayashi
Shiro Suda
Yasuhide Iwata
Takatoshi Ueki
Kenji J. Tsuchiya
Katsuaki Suzuki
Kazuhiko Nakamura
Yasuomi Ouchi
Publikationsdatum: 01.02.2011
Verlag: Springer-Verlag
Erschienen in: European Journal of Nuclear Medicine and Molecular Imaging / Ausgabe 2/2011
Print ISSN: 1619-7070
Elektronische ISSN: 1619-7089
DOI: https://doi.org/10.1007/s00259-010-1612-0

Springer Medizin

Abstract

Purpose

Methods

Results

Conclusion

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