Background: Associations between cognition and brain markers of amyloid, tau, and neurodegeneration are poorly understood in the oldest-old (>90 years) compared to younger populations. Prior work suggests that the link between neuropathology and cognition may become weaker in advanced old age, reducing the applicability of accepted biomarker cascade models of Alzheimer's disease progression. Addressing this question in the oldest-old is challenging, partly due to limited data and methodological challenges of neuroimaging analysis.
View Article and Find Full Text PDFBackground: Cerebrovascular disease features as the most common comorbidity in older individuals with dementia. White matter (WM) injury identified through white matter hyperintensities (WMH) on FLAIR represents evident late-stage pathophysiological manifestations of CVD. This study aims to assess the role of baseline microstructural WM integrity, using free water (FW), a measure from diffusion tensor imaging (DTI), in predicting WMH growth dynamic.
View Article and Find Full Text PDFObjective: To evaluate the main outcomes of disease activity and their association with other measures of activity, damage, and quality of life in patients with idiopathic inflammatory myopathy (IIM) according to time since diagnosis and positivity to antisynthetase autoantibodies (ASAs).
Methods: Cross-sectional multicenter study within the Spanish Myo-Spain registry. Cases were classified as incident (≤ 12 months since diagnosis) and prevalent.
Antiepileptics and antidepressants are frequently prescribed for chronic pain, but their efficacy and potential adverse effects raise concerns, including dependency issues. Increased prescriptions, sometimes fraudulent, prompted reclassification of antiepileptics in some countries. Our aim is to comprehend opinions, perceptions, beliefs, and attitudes towards co-analgesics from online discussions on X (formerly known as Twitter), offering insights closer to reality than conventional surveys.
View Article and Find Full Text PDFThe oncogenic Epstein-Barr virus (EBV) can drive tumorigenesis with disrupted host immunity, causing malignancies including post-transplant lymphoproliferative disorders (PTLDs). PTLD can also arise in the absence of EBV, but the biological differences underlying EBV(+) and EBV(-) B cell PTLD and the associated host-EBV-tumor interactions remain poorly understood. Here, we reveal the core differences between EBV(+) and EBV(-) PTLD, characterized by increased expression of genes related to immune processes or DNA interactions, respectively, and the augmented ability of EBV(+) PTLD B cells to modulate the tumor microenvironment through elaboration of monocyte-attracting cytokines/chemokines.
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