Amyloid deposition after cerebral hypoperfusion: Evidenced on [18F]AV-45 positron emission tomography
Amyloid deposition after cerebral hypoperfusion: Evidenced on [18F]AV-45 positron emission tomography
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DOI:
10.1016/j.jns.2012.04.014
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发表时间:
2012-08-15
影响因子:
4.4
通讯作者:
Lee, Tsong-Hai
中科院分区:
文献类型:
--
作者:
Huang, Kuo-Lun;Lin, Kun-Ju;Lee, Tsong-Hai
Animal studies have shown that cerebral hypoperfusion may be associated with amyloid plaque accumulation. Amyloid plaque is known to be associated with dementia and [F-18]AV-45 is a positron emission tomography (PET) ligand that binds to extracelluar plaques. We hypothesized that demented patients with cerebral hypoperfusion may have increased [F-18]AV-45 uptake.Five demented patients with cerebral hypoperfusion due to unilateral carotid artery stenosis (CAS) were examined with [F-18]AV-45 PET, and the results were compared with six elderly controls. The standard uptake value ratio (SUVR) of each region of interest (ROI) was created using whole cerebellum as the reference region. All subjects underwent magnetic resonance imaging (MRI) for obtaining structural information.Patients with dementia and unilateral CAS had a higher global [F-18]AV-45 SUVR (1.34 +/- 0.06) as compared with controls (1.10 +/- 0.04, p = 0.0043), especially over the frontal, temporal, precuneus, anterior cingulate and occipital regions. The statistical distribution maps revealed a significantly increased [F-18]AV-45 SUVR in the medial frontal, caudate, thalamus, posterior cingulate, occipital and middle and superior temporal regions ipsilateral to the side of CAS (p