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Sökning: WFRF:(Lätt Jimmy) > Maly Sundgren Pia

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1.
  • Askaner, Krister, et al. (författare)
  • Differentiation of Brain Metastases due to Primary Malignancy and Glioblastomas using Dynamic Susceptibility Contrast-Enhanced MR at 3T
  • 2017
  • Konferensbidrag (refereegranskat)abstract
    • Purpose:To find out differences in cerebral blood volume (CBV) maps derived from dynamic susceptibility contrast-enhanced magnetic resonance imaging (DSCE-MRI) in glioblastomas and cerebral metastases. The main purpose was to compare CBV maps between metastases with different primary malignancies. Furthermore the metastasis group was compared with the glioblastoma group.Method:Conventional imaging and DSCE-MRI using 3T MRI system was performed in 114 patients, 38 glioblastomas and 76 metastases, 32 lung, 12 breast, 12 melanoma, 10 gastrointestinal (GI), and 10 other. CBV values were measured in the solid tumor area, peritumoral edema, area adjacent to peritumoral edema, and in normal apparent white matter in contralateral semioval center. The four subgroups of metastases were compared with one-way ANOVA to determine differences in CBV of significance. CBV values in glioblastomas and metastases were then statistically compared using paired t-test. Receiver -operating characteristic analysis was used to determine optimal cut-off values when parameters showed statistical differences.Results:There were no significantly differences in CBV between the four subgroups of metastases. CBV in the peritumoral edema significantly differentiated metastases from glioblastomas, p=0.0001. CBV cutoff value of 2.3 yielded a sensitivity, specificity, positive predictive value, and negative predictive value of 87, 87, 71, and 91% respectively. Conclusions:Differentiation of glioblastomas and metastases is possible using DSCE-MRI. No statistically significant differences regarding CBV between metastases from lung, breast, melanoma, and GI were detected.
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3.
  • Vogel, Jacob W., et al. (författare)
  • Spread of pathological tau proteins through communicating neurons in human Alzheimer's disease
  • 2020
  • Ingår i: Nature Communications. - : Springer Science and Business Media LLC. - 2041-1723. ; 11
  • Tidskriftsartikel (refereegranskat)abstract
    • Tau is a hallmark pathology of Alzheimer's disease, and animal models have suggested that tau spreads from cell to cell through neuronal connections, facilitated by β-amyloid (Aβ). We test this hypothesis in humans using an epidemic spreading model (ESM) to simulate tau spread, and compare these simulations to observed patterns measured using tau-PET in 312 individuals along Alzheimer's disease continuum. Up to 70% of the variance in the overall spatial pattern of tau can be explained by our model. Surprisingly, the ESM predicts the spatial patterns of tau irrespective of whether brain Aβ is present, but regions with greater Aβ burden show greater tau than predicted by connectivity patterns, suggesting a role of Aβ in accelerating tau spread. Altogether, our results provide evidence in humans that tau spreads through neuronal communication pathways even in normal aging, and that this process is accelerated by the presence of brain Aβ.
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