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- W2896567296 abstract "Neuroinflammation may be a primary contributor to Alzheimer's disease (AD) or a nonspecific response to neurodegeneration. 11C-PBR28 is a second generation PET radioligand for the 18 kDa translocator protein (TSPO), which is overexpressed by activated microglia and correlates with severity and progression of AD. We sought to determine if TSPO binding differed between cognitively impaired patients with biomarker evidence of AD and impaired patients without evidence of amyloidopathy. Twenty-one patients meeting clinical criteria for amnestic mild cognitive impairment or mild AD who had AD-pattern of neurodegeneration on MRI underwent florbetaben PET. An age-matched group of amyloid-negative cognitive controls (n = 15) was also included. 11C-PBR28 PET images were acquired 60-90 min post-injection. Standardized uptake value ratios were calculated using cerebellar gray-matter as a “pseudo-reference” region. Among impaired patients, 15 were amyloid-positive and 7 were amyloid-negative. Using a region-of-interest approach, 11C-PBR28 binding in amyloid-positive patients was greater than in amyloid-negative controls in middle and inferior temporal gyrus, medial temporal cortex, posterior cingulate gyrus, superior parietal lobule and inferior parietal lobule (p < 0.02). 11C-PBR28 binding in amyloid-positive patients was greater than amyloid-negative patients in posterior cingulate (p = 0.01) and superior parietal lobule (p = 0.04). Using a statistical parametric mapping (SPM) approach, clusters of significantly increased 11C-PBR28 binding were found in amyloid-positive patients than in amyloid-negative controls in precuneus and posterior cingulate. SPM analysis also showed greater binding in amyloid-positive patients than amyloid-negative patients in left lateral temporal cortex. No difference in 11C-PBR28 binding was seen between amyloid-negative patients and controls in any region using either region-of-interest or SPM analysis. Among patients meeting clinical criteria for amnestic MCI or mild AD, those who are amyloid-positive on PET have greater TSPO binding than those who are amyloid-negative, despite evidence of neurodegeneration in both groups. These results suggest that microglial activation in AD is not simply a response to neurodegeneration, but a response to cerebral β-amyloidosis. Neuroinflammation may therefore play a stronger role in AD than in non-AD neurodegenerative diseases that cause memory impairment." @default.
- W2896567296 created "2018-10-26" @default.
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- W2896567296 date "2018-07-01" @default.
- W2896567296 modified "2023-10-12" @default.
- W2896567296 title "IC‐P‐181: TRANSLOCATOR PROTEIN BINDING IS ELEVATED IN CLINICAL ALZHEIMER'S DISEASE BUT NOT IN IMPAIRED PATIENTS WITH SUSPECTED NON‐AD PATHOPHYSIOLOGY" @default.
- W2896567296 doi "https://doi.org/10.1016/j.jalz.2018.06.2248" @default.
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