An open-access portal tracking research advances and datasets across Alzheimer’s disease, Parkinson’s disease, and ALS. Aggregating scientific findings and open repositories from Alzforum, bioRxiv, OpenNeuro, DANDI, and Agora.
Subcellular MERFISH and single-nucleus RNA sequencing across human post-mortem white matter lesions map complement C1q signaling and interferon-responsive oligodendrocyte states at paramagnetic lesion rims.
Prospective multi-center validation across 1,420 MS patients demonstrating that elevated serum GFAP paired with paramagnetic rim lesions (PRLs) predicts 24-week confirmed PIRA independent of acute gadolinium-enhancing relapses.
Multiple sclerosis (MS) is a complex, multifactorial neurodegenerative disease with an aetiology that is still partially elusive. Several risk factors are associated with MS development including genetic predisposition and various environmental stressors; however, recently, viral infections have gained significant attention as a crucial environmental trigger. Despite the well-established link between Epstein-Barr virus (EBV) and MS susceptibility, a single-pathogen model fails to clearly characterise the molecular cascades driving the disease, suggesting that the transition from infection to autoimmune response involves more than one viral agent. In this review we examine the speculation that the interactions among different neurotropic viruses could serve a collective causative role in MS, which is under-researched in the literature at present. We summarise contradictory evidence on the role of different viral agents, including the Herpesviridae family (Human Cytomegalovirus, EBV, Herpes Simplex Viruses HSV-1 and HSV-2, and Varicella Zoster Virus), Paramyxoviridae family (Measles Virus and Rubella Virus), Influenza virus, SARS-CoV-2, and Human Endogenous Retroviruses (HERVs). Through interplay within shared molecular pathways, immune modulation, and activation of latent infections, these viruses may collectively influence the inflammatory and demyelinating processes that characterise MS. This review evaluates the etiological role of viral interplay in MS through the cumulative and interactive effects of these pathogens. The available epidemiological, immunological, and experimental data converge on the concept that viral co-exposures act synergistically to shape MS susceptibility in genetically predisposed individuals. Characterising these viral interactions presents a new research direction for the identification of novel biomarkers and the development of preventative strategies through the targeted control of viral networks.
Research article from Europe PMC.
Research article from Europe PMC.
High-resolution structural MRI, T2*-weighted phase/QSM, and multi-shell diffusion tensor imaging (DTI) dataset with manual expert lesion masks for white matter lesions, paramagnetic rim lesions (PRLs), and central vein sign (CVS) assessment.
Background and objectivesSensitive, minimally invasive biomarkers that reflect functional decline in multiple sclerosis (MS) are still lacking. Untargeted metabolomic profiling allows unbiased discovery of circulating biomarkers and dysregulated biological pathways underlying MS onset and progression. We aimed to identify candidate circulating metabolite signatures correlated with clinical, imaging, and patient-reported outcomes in MS and to characterize the underlying metabolic pathways.MethodsWe conducted a cross-sectional analysis of untargeted circulating metabolomic profiles from 541 samples of 323 people with multiple sclerosis (PwMS), including both relapsing-remitting and progressive forms, detecting 332 metabolites. Associations between metabolite levels and outcomes, including clinical disability (Expanded Disability Status Scale), functional tests (walking speed, manual dexterity, and processing speed), Neuro-QoL patient-reported domains, optical coherence tomography-derived retinal layer thicknesses, and MRI-derived measures, were assessed using linear mixed-effects models adjusted for age, sex, race, treatment status, and MS subtype. To identify clusters of metabolites jointly linked to outcomes, we applied Hierarchical All-Against-All Association Analysis and weighted correlation network analysis. Pathway enrichment was also performed using Fast Gene Set Enrichment Analysis on ranked effect sizes based on the RaMP database, excluding pathways with fewer than 3 metabolites.ResultsWe identified multiple metabolites consistently associated with MS severity across clinical, patient-reported, and imaging domains. Metabolites such as p-cresol sulfate, p-cresol glucuronide, phenylacetylglutamine, and carnitine-derived species were linked to greater disease severity, whereas tryptophan betaine, ergothioneine, N-acetylcarnosine, and indolepropionate were associated with more favorable outcomes. Pathway analyses highlighted amino acid transport and metabolism, a
Purpose: Multiple sclerosis (MS) is a neurodegenerative and demyelinating disease of the central nervous system. Recent evidence suggests that localized gray matter atrophy in MS may be involved in distributed functional brain networks. However, the dynamic trajectory of functional network alteratio...
The skull bone marrow axis has recently emerged as an important source of immune cells during neuroinflammation, including in the experimental autoimmune encephalomyelitis (EAE) , the mouse model of multiple sclerosis. The cribriform plate bone marrow (cpBM), is a portion of the ethmoid bone of the ...
What is already known on this topicO_LIPrenatal and perinatal factors have been linked to offspring MS risk, but evidence has focused mainly on maternal complications or birth outcomes. C_LIO_LIMaternal BMI has been associated with other immune-mediated diseases in offspring, but large-scale evidenc...
BackgroundQuantitative susceptibility mapping (QSM) exhibits phase cancellation between paramagnetic (e.g. iron) and diamagnetic (e.g. myelin/protein) sources, obscuring microstructural lesion heterogeneity in multiple sclerosis (MS). We evaluated whether biophysical{chi} -separation identifies clin...
Vascular dementia (VaD) is a prevalent and devastating neurocognitive disorder characterized by profound white matter damage, yet the precise cellular mechanisms linking cerebrovascular stress to demyelination remain poorly understood. Here, we characterize the impact of a chronic cardiometabolic st...
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