Purpose: Magnetic resonance fingerprinting (MRF) offers rapid quantitative imaging but may be subject to confounding effects (CE) if these are not included in the model-based reconstruction. This study characterizes the influence of in-plane , slice profile and diffusion effects on T and T estimation in the female breast at 1.5T.
Methods: Simulations were used to predict the influence of each CE on the accuracy of MRF and to investigate the influence of electronic noise and spiral aliasing artefacts. The experimentally observed bias in regions of fibroglandular tissue (FGT) and fatty tissue (FT) was analyzed for undersampled spiral breast MRF data of 6 healthy volunteers by performing MRF reconstruction with and without a CE.
Results: Theoretic analysis predicts T under-/T overestimation if the nominal flip angles are underestimated and inversely, T under-/T overestimation if omitting slice profile correction, and T under-/T underestimation if omitting diffusion in the signal model. Averaged over repeated signal simulations, including spiral aliasing artefacts affected precision more than accuracy. Strong in-plane effects occurred in vivo, causing T left-right inhomogeneity between both breasts. Their correction decreased the T difference from 29 to 5 ms in FGT and from 29 to 9 ms in FT. Slice profile correction affected FGT T most strongly, resulting in -22% smaller values. For the employed spoiler gradient strengths, diffusion did not affect the parameter maps, corresponding well with theoretic predictions.
Conclusion: Understanding CEs and their relative significance for an MRF sequence is important when defining an MRF signal model for accurate parameter mapping.
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http://dx.doi.org/10.1002/mrm.28545 | DOI Listing |
Background: Metabotropic glutamate receptor 5 (mGluR5) modulates excitatory glutamatergic synaptic transmission and plays an important role in learning and memory, and in the pathphysiology of Alzheimer's disease (AD). Here, we aimed to assess the alterations of mGluR5 in the hippocampus of AD patients and mouse model, and the association with amyloid pathology.
Method: Immunofluorescence staining was performed on postmortem brain tissue from 35 AD patients and 36 control patients, as well as on the brain tissue slices from 15 months-old 3×Tg and arcAβ mouse models of AD amyloidosis.
Alzheimers Dement
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Centre for Discovery Brain Sciences at the University of Edinburgh, Edinburgh, Scotland, United Kingdom.
Background: Synapse loss represents the closest correlate of cognitive decline in Alzheimer's Disease (AD). Standard microscopy, due to increased diffraction of light with tissue depth, imposes a limit on axial resolution extending to ∼ 700nm. Array tomography (AT), developed by Micheva & Smith (2007), extends this axial limit via physical sectioning of resin-embedded tissue into ribbons of 70nm contiguous sections that are serially imaged and reconstructed into 3D volumes; thus, allowing for nanometric synaptic puncta to be resolved at the mesoscale.
View Article and Find Full Text PDFAlzheimers Dement
December 2024
University of Illinois Urbana Champaign, Urbana Champaign, IL, USA.
Background: Increasing evidence shows that many lipids play important roles in the pathogenesis of Alzheimer's disease (AD), including Aβ plaque formation. Of note, the greatest genetic risk of late onset AD, apolipoprotien E4 (APOE4), plays a major role in lipid transport. However, the profile of lipids that play a role in AD is poorly understood.
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View Article and Find Full Text PDFBackground: There are no cures for Alzheimer's disease (AD), a progressive neurodegenerative disorder characterized by elevation of beta-amyloid and tau proteins besides neuronal death and causing cognitive impairment. Phosphodiesterase 5 (PDE5) is a cyclic guanosine monophosphate-degrading enzyme involved in numerous biological pathways including those relevant to memory formation. PDE5 inhibition offers the potential to attenuate AD progression by acting at the downstream level of beta-amyloid and tau elevation.
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