Browsing by Author "Emir, Uzay"

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    Feasibility and comparison of 3D modified rosette ultra-short echo time (PETALUTE) with conventional weighted acquisition in 31P-MRSI
    (Springer Nature, 2025-02-22) Bozymski, Brian; Shen, Xin; Özen, Ali; Chiew, Mark; Thomas, M. Albert; Clarke, William T.; Sawiak, Stephen; Dydak, Ulrike; Emir, Uzay; Radiology and Imaging Sciences, School of Medicine
    Phosphorus-31 magnetic resonance spectroscopic imaging (31P-MRSI) provides valuable non-invasivein vivoinformation on tissue metabolism but is burdened by poor sensitivity and prolonged scan duration. Ultra-short echo time (UTE) acquisitions minimize signal loss when probing signals with relatively short spin-spin relaxation time (T2), while also preventing first-order dephasing. Here, a three-dimensional (3D) UTE sequence with a rosette k-space trajectory (PETALUTE) is applied to 31P-MRSI at 3T. Conventional weighted MRSI employs highly regular Cartesian k-space sampling, susceptible to substantial artifacts when accelerated via undersampling. In contrast, this novel sequence's "petal-like" pattern offers incoherent sampling more suitable for compressed sensing (CS). These results showcase the competitive performance of PETALUTE against conventional weighted 31P-MRSI with simulation, phantom, and in vivo leg muscle comparisons.
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    Lead Acetate Exposure and Cerebral Amyloid Accumulation: Mechanistic Evaluations in APP/PS1 Mice
    (EHP, 2024) Gu, Huiying; Liu, Luqing L.; Wu, Alanna; Yu, Yongqi; Emir, Uzay; Sawiak, Stephen J.; Territo, Paul R.; Farlow, Matin R.; Zheng, Wei; Du, Yansheng; Neurology, School of Medicine
    Background: The role of environmental factors in Alzheimer’s disease (AD) pathogenesis remains elusive. Mounting evidence suggests that acute and past exposure to the environmental toxicant lead (Pb) is associated with longitudinal decline in cognitive function, brain atrophy, and greater brain β-amyloid (A⁢β) deposition. However, the nature of Pb-induced amyloid deposition and how it contributes to AD development remain unclear. Objectives: This study investigates the role of Pb in the pathogenesis of cerebral amyloid angiopathy (CAA) and whether plasminogen activator inhibitor-1 (PAI-1) contributes to this process in the APP/PS1 mouse model. Methods: Female APP/PS1 mice at 8 wk of age were administered either 50mg/kg Pb-acetate (PbAc) (i.e., 27mg Pb/kg) or an equivalent molar concentration of sodium acetate (NaAc) via oral gavage once daily for 8 wk. Amyloid deposition and vascular amyloid were determined by immunostaining. In addition, A⁢β perivascular drainage, vascular binding assay, and microglial endocytosis were examined to determine underlying mechanisms. Furthermore, magnetic resonance imaging demyelination imaging was performed in vivo measure the level of demyelination. Finally, Y-maze and Morris water maze tests were assessed to evaluate the cognitive function of mice. Results: APP/PS1 mice (an AD mice model) exposed to PbAc demonstrated more vascular amyloid deposition less neocortical myelination, and lower cognitive function, as well as greater vascular binding to A⁢β⁢40, higher A⁢β⁢40/A⁢β⁢42 ratios, strikingly lower A⁢β⁢40 levels in the perivascular drainage, and microglial endocytosis. Importantly, exposure to a specific PAI-1 inhibitor, tiplaxtinin, which previously was reported to lower CAA pathology in mice, resulted in less CAA-related outcomes following PbAc exposure. Discussion: Our findings suggest that PbAc induced CAA/AD pathogenesis via the PAI-1 signaling in the APP/PS1 mouse model, and the inhibition of PAI-1 could be a potential therapeutic target for PbAc-mediated CAA/AD disorders.