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• W2897282004 abstract "Autopsy studies have suggested that neuromelanin density in the locus coeruleus (LC) follows an inverted U-curve with aging. Recent studies show that atrophy in the LC occurs from Braak stage III, a disease stage when amyloid pathology is present in the neocortex. We aimed to investigate this inverted U-curve pattern by combining neuromelanin-sensitive MRI protocols with amyloid and tau PET imaging across the lifespan. In addition, we hypothesized that LC MRI signal intensity would be lower in individuals with higher levels of amyloid as compared to those with lower levels. Fifty-two clinically normal individuals underwent 3T MRI scanning (Figure 1) (22-92 years old). Of these subjects, 27 older subjects underwent Pittsburg B-compound PET (amyloid) and Flortaucipir-PET (tau). Brainstem regions of interest on the MRI (LC and pontine tegmentum as reference) were registered to each subject using high-dimensional diffeomorphic normalization transformations. Interslice variability was removed by normalizing the within-slice intensity to the reference region and LC intensity was thresholded by selecting iteratively the highest five connecting voxels. Amyloid burden was derived from a neocortical aggregate (cut-off for elevated amyloid: 1.32 DVR) and tau pathology was extracted from the entorhinal cortex (FreeSurfer-defined). Generalized additive (GAM) and (curvi-)linear regression models were performed to investigate LC intensity associations with age, APOE status, amyloid and tau. Examples of neuromelanin sensitive MRI images with age. A nonlinear age-relationship with LC signal was observed (p=0.02 polynomial, p=0.05 GAM, Figure 2). The peak in LC signal intensity occurred at ∼45 years, comparable to the age of 50 reported in autopsy studies. Individuals with elevated amyloid burden (n=9) showed a lower LC signal compared to individuals with lower amyloid levels (n=18; p=0.03, age-corrected) and a borderline difference between APOE-E4 carriers (n=7) and non-carriers (n=9) was observed (p=0.07). We observed an interaction between LC intensity and amyloid burden on entorhinal tau pathology (n=16; p=0.03, corrected for age), suggesting that lower LC intensity was associated with higher entorhinal tau when amyloid burden increases (Figure 3). Age-relationship with LC signal intensity. Note: Smooth fit from the Generalized Additive Model of age on LC MRI signal intensity. Gray area corresponds to the 95% confidence interval. Polynomial linear regression model showed similar fits. Relationship between LC signal intensity and AD biomarkers. Note: Top: boxplots show the distribution of the LC signal intensity between individuals with elevated amyloid (PIB+) or lower levels of amyloid (PIB-), and between individuals who are carrier (e4+) or non-carrier (e4-) of the APOE-E4 allele. Bottom: the relationship between LC signal intensity and entorhinal (EC) tau is dependent on amyloid pathology (depicted are the estimated marginal means, corrected for age). These preliminary findings suggest that LC changes can reflect early Alzheimer's disease pathology that is not entirely attributable to age. Further inclusion of participants across the entire lifespan is ongoing." @default.
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• W2897282004 date "2018-07-01" @default.
• W2897282004 modified "2023-10-18" @default.
• W2897282004 title "P1‐480: LOCUS COERULEUS SIGNAL INTENSITY IS ASSOCIATED WITH ENTORHINAL TAU PATHOLOGY AT HIGHER LEVELS OF AMYLOID BURDEN" @default.
• W2897282004 doi "https://doi.org/10.1016/j.jalz.2018.06.490" @default.
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