Reference health
Vascular pathology in multiple sclerosis: reframing pathogenesis around the blood-brain barrier
60/60 checkable references clean · checked 2026-07-23
Every reference with a DOI in the deposited reference list resolved to a known work in Crossref or DataCite at the dated check, and none carried a retraction, withdrawal, or removal notice.
The 60 checked references that resolve
resolves10.1016/j.bbadis.2010.06.017
Disruption of central nervous system barriers in multiple sclerosis
resolves10.1093/brain/awv203
Permeability of the blood–brain barrier predicts conversion from optic neuritis to multiple sclerosis
resolves10.1016/j.nbd.2014.09.016
Focal disturbances in the blood–brain barrier are associated with formation of neuroinflammatory lesions
resolves10.1002/ana.410430616
Magnetization transfer changes in the normal appering white matter precede the appearance of enhancing lesions in patients with multiple sclerosis
resolves10.1016/j.nbd.2005.06.012
Blood–brain barrier alterations in both focal and diffuse abnormalities on postmortem MRI in multiple sclerosis
resolves10.1111/j.1365-2990.2006.00781.x
Persistent endothelial abnormalities and blood–brain barrier leak in primary and secondary progressive multiple sclerosis
resolves10.1016/j.nbd.2006.08.005
Extensive extracellular matrix depositions in active multiple sclerosis lesions
resolves10.1084/jem.20051342
Dystroglycan is selectively cleaved at the parenchymal basement membrane at sites of leukocyte extravasation in experimental autoimmune encephalomyelitis
resolves10.1007/s11547-013-0357-9
Dilated Virchow–Robin spaces and multiple sclerosis: 3 T magnetic resonance study
resolves10.1093/brain/awr182
Meningeal inflammation is widespread and linked to cortical pathology in multiple sclerosis
resolves10.1093/brain/awp070
The relation between inflammation and neurodegeneration in multiple sclerosis brains
resolves10.1002/ana.24997
Fibrin(ogen) and neurodegeneration in the progressive multiple sclerosis cortex
resolves10.1136/jnnp-2013-305612
Reduced grey matter perfusion without volume loss in early relapsing-remitting multiple sclerosis
resolves10.1093/jnen/62.1.25
Preferential Loss of Myelin-Associated Glycoprotein Reflects Hypoxia-Like White Matter Damage in Stroke and Inflammatory Brain Diseases
resolves10.1093/brain/awh457
Tissue preconditioning may explain concentric lesions in Baló's type of multiple sclerosis
resolves10.1097/00004647-199805000-00007
Oligodendrocytes and Microglia Are Selectively Vulnerable to Combined Hypoxia and Hypoglycemia Injury
<i>in Vitro</i>
resolves10.1002/ana.24006
Neurological deficits caused by tissue hypoxia in neuroinflammatory disease
resolves10.1093/brain/awv398
The topograpy of demyelination and neurodegeneration in the multiple sclerosis brain
resolves10.1212/WNL.0b013e3181d6b125
Vascular comorbidity is associated with more rapid disability progression in multiple sclerosis
resolves10.1159/000320245
Risk of Arterial Cardiovascular Diseases in Patients with Multiple Sclerosis: A Population-Based Cohort Study
resolves10.1073/pnas.1222560110
Cerebral hypoperfusion in multiple sclerosis is reversible and mediated by endothelin-1
resolves10.1038/nrneurol.2016.187
Interactions between genetic, lifestyle and environmental risk factors for multiple sclerosis
resolves10.1177/1352458516635873
Genetic overlap between multiple sclerosis and several cardiovascular disease risk factors
resolves10.1093/nar/gkw943
DisGeNET: a comprehensive platform integrating information on human disease-associated genes and variants
resolves10.1111/nan.12020
Review: The role of vitamin <scp>D</scp> in nervous system health and disease
resolves10.1016/j.ijcard.2016.12.053
Vitamin D and cardiovascular disease: From atherosclerosis to myocardial infarction and stroke
resolves10.1371/journal.pone.0122821
Vitamin D Prevents Hypoxia/Reoxygenation-Induced Blood-Brain Barrier Disruption via Vitamin D Receptor-Mediated NF-kB Signaling Pathways
resolves10.1177/0271678X16671147
Intranasal administration of vitamin D attenuates blood–brain barrier disruption through endogenous upregulation of osteopontin and activation of CD44/P-gp glycosylation signaling after subarachnoid hemorrhage in rats
resolves10.1186/s12987-015-0022-x
Pathobiology of tobacco smoking and neurovascular disorders: untied strings and alternative products
resolves10.1111/bpa.12460
Age‐related small vessel disease: a potential contributor to neurodegeneration in multiple sclerosis
resolves10.1016/j.brainres.2009.06.033
Tobacco smoke: A critical etiological factor for vascular impairment at the blood–brain barrier
resolves10.1016/j.jns.2006.11.021
Elevation of matrix metalloproteinases (MMPs) in multiple sclerosis and impact of immunomodulators
resolves10.1136/jnnp-2015-312600
Back on the scent: the olfactory system in CNS demyelinating diseases
resolves10.1016/j.jneuroim.2010.08.003
Epstein-Barr virus infection of human brain microvessel endothelial cells: A novel role in multiple sclerosis
resolves10.1016/j.toxicon.2017.02.019
Clostridium perfringens epsilon toxin induces permanent neuronal degeneration and behavioral changes
resolves10.1093/brain/124.8.1544
Bacterial peptidoglycan and immune reactivity in the central nervous system in multiple sclerosis
resolves10.1038/srep37344
Brain microbiota disruption within inflammatory demyelinating lesions in multiple sclerosis
resolves10.1007/s00401-017-1682-1
Pathogenic implications of cerebrospinal fluid barrier pathology in neuromyelitis optica
resolves10.1038/mp.2013.110
Neuropsychiatric disease relevance of circulating anti-NMDA receptor autoantibodies depends on blood–brain barrier integrity
resolves10.1136/jcp.46.1.37
Intramural platelet deposition in cerebral vasculopathy of systemic lupus erythematosus.
resolves10.1038/nrn3114
Neurovascular pathways to neurodegeneration in Alzheimer's disease and other disorders
resolves10.1007/s40263-015-0239-x
Statin Treatment in Multiple Sclerosis: A Systematic Review and Meta-Analysis
resolves10.1038/ncomms2230
Fibrinogen-induced perivascular microglial clustering is required for the development of axonal damage in neuroinflammation
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