Publications by authors named "E Herranz"
Article Synopsis
- C-PBR28 PET imaging and paramagnetic rim lesions (PRL) are both potential markers for assessing chronic inflammation in multiple sclerosis (MS), but there's no agreed-upon best option between them.
- In a study with 30 MS patients, less than half of the non-PRL white matter lesions were found to be active according to C-PBR28 PET imaging, and both marker types showed similar levels of microstructural integrity but were distinct in their correlation with disability measures.
- C-PBR28 PET proved to be more effective in identifying active lesions compared to PRL assessments, with the volume of whole active lesions being the strongest predictor of neurological impairment as measured by the Expanded Disability Status Scale.
Compartmentalized meningeal inflammation is thought to represent one of the key players in the pathogenesis of cortical demyelination in multiple sclerosis. PET targeting the 18 kDa mitochondrial translocator protein (TSPO) is a molecular-specific approach to quantifying immune cell-mediated density in the cortico-meningeal tissue compartment in vivo. This study aimed to characterize cortical and meningeal TSPO expression in a heterogeneous cohort of multiple sclerosis cases using in vivo simultaneous MR-PET with 11C-PBR28, a second-generation TSPO radioligand, and ex vivo immunohistochemistry.
View Article and Find Full Text PDFBackground: Paramagnetic rim white matter (WM) lesions (PRL) are thought to be a main driver of non-relapsing multiple sclerosis (MS) progression. It is unknown whether cerebrospinal fluid (CSF)-soluble factors diffusing from the ventricles contribute to PRL formation.
Objective: To investigate the distribution of PRL and non-rim brain WM lesions as a function of distance from ventricular CSF, their relationship with cortical lesions, the contribution of lesion phenotype, and localization to neurological disability.
Axonal degeneration is a central pathological feature of multiple sclerosis and is closely associated with irreversible clinical disability. Current noninvasive methods to detect axonal damage in vivo are limited in their specificity and clinical applicability, and by the lack of proper validation. We aimed to validate an MRI framework based on multicompartment modeling of the diffusion signal (AxCaliber) in rats in the presence of axonal pathology, achieved through injection of a neurotoxin damaging the neuronal terminal of axons.
View Article and Find Full Text PDFBackground: The in vivo relation between microglia activation and demyelination in multiple sclerosis is still unclear.
Objective: We combined C-PBR28 positron emission tomography and rapid estimation of myelin for diagnostic imaging (REMyDI) to characterize the relation between these pathological processes in a heterogeneous MS cohort.
Methods: C-PBR28 standardized uptake values normalized by a pseudo-reference region (SUVR) were used to measure activated microglia.