Inflammation at the Blood–Brain Barrier in Multiple Sclerosis

2013 ◽  
pp. 117-142
Author(s):  
Mark R. Mizee ◽  
Ruben van Doorn ◽  
Alexandre Prat ◽  
Helga E. de Vries
Keyword(s):  
Multiple Sclerosis ◽  
Blood Brain Barrier ◽  
Brain Barrier ◽  
Blood Brain

scholarly journals Vascular pathology in multiple sclerosis: reframing pathogenesis around the blood-brain barrier

2017 ◽  
Vol 89 (1) ◽  
pp. 42-52 ◽  
Author(s):  
Jonathan I Spencer ◽  
Jack S Bell ◽  
Gabriele C DeLuca
Keyword(s):  
Multiple Sclerosis ◽  
Immune Response ◽  
Blood Brain Barrier ◽  
Immune Cell ◽  
Neurological Diseases ◽  
Specific Immune Response ◽  
Brain Barrier ◽  
Vascular Pathology ◽  
Current Evidence ◽  
Blood Brain

Blood-brain barrier (BBB) disruption has long been recognised as an important early feature of multiple sclerosis (MS) pathology. Traditionally, this has been seen as a by-product of the myelin-specific immune response. Here, we consider whether vascular changes instead play a central role in disease pathogenesis, rather than representing a secondary effect of neuroinflammation or neurodegeneration. Importantly, this is not necessarily mutually exclusive from current hypotheses. Vascular pathology in a genetically predisposed individual, influenced by environmental factors such as pathogens, hypovitaminosis D and smoking, may be a critical initiator of a series of events including hypoxia, protein deposition and immune cell egress that allows the development of a CNS-specific immune response and the classical pathological and clinical hallmarks of disease. We review the changes that occur in BBB function and cerebral perfusion in patients with MS and highlight genetic and environmental risk factors that, in addition to modulating immune function, may also converge to act on the vasculature. Further context is provided by contrasting these changes with other neurological diseases in which there is also BBB malfunction, and highlighting current disease-modifying therapies that may also have an effect on the BBB. Indeed, in reframing current evidence in this model, the vasculature could become an important therapeutic target in MS.

BREAKDOWN OF THE BLOOD-BRAIN BARRIER PRECEDES SYMPTOMS AND OTHER MRI SIGNS OF NEW LESIONS IN MULTIPLE SCLEROSIS

Brain ◽  
1990 ◽  
Vol 113 (5) ◽  
pp. 1477-1489 ◽  
Author(s):  
A. G. KERMODE ◽  
A. J. THOMPSON ◽  
P. TOFTS ◽  
D. G. MACMANUS ◽  
B. E. KENDALL ◽  
...  
Keyword(s):  
Multiple Sclerosis ◽  
Blood Brain Barrier ◽  
Brain Barrier ◽  
Blood Brain

Disease Duration, Relapse rate and Clinical Course in Multiple Sclerosis: Relation to IgG Production within the Blood Brain Barrier

1990 ◽  
pp. 23-31
Author(s):  
Paolo Livrea ◽  
Maria Trojano ◽  
Isabella Laura Simone ◽  
Carlo Avolio ◽  
Francesca De Robertis ◽  
...  
Keyword(s):  
Multiple Sclerosis ◽  
Blood Brain Barrier ◽  
Relapse Rate ◽  
Disease Duration ◽  
Clinical Course ◽  
Brain Barrier ◽  
Blood Brain

scholarly journals Blood-brain barrier breakdown in non-enhancing multiple sclerosis lesions detected by 7-Tesla MP2RAGE ΔT1 mapping

PLoS ONE ◽  
2021 ◽  
Vol 16 (4) ◽  
pp. e0249973
Author(s):  
Seongjin Choi ◽  
Margaret Spini ◽  
Jun Hua ◽  
Daniel M. Harrison
Keyword(s):  
Multiple Sclerosis ◽  
Relaxation Time ◽  
White Matter ◽  
Blood Brain Barrier ◽  
White Matter Lesions ◽  
Brain Barrier ◽  
7 Tesla ◽  
T1 Relaxation Time ◽  
T1 Relaxation ◽  
Blood Brain

Although the blood-brain barrier (BBB) is altered in most multiple sclerosis (MS) lesions, gadolinium enhancement is seen only in acute lesions. In this study, we aimed to investigate gadolinium-induced changes in T1 relaxation time in MS lesions on 7-tesla (7T) MRI as a means to quantify BBB breakdown in non-enhancing MS lesions. Forty-seven participants with MS underwent 7T MRI of the brain with a magnitude-prepared rapid acquisition of 2 gradient echoes (MP2RAGE) sequence before and after contrast. Subtraction of pre- and post-contrast T1 maps was used to measure T1 relaxation time change (ΔT1) from gadolinium. ΔT1 values were interrogated in enhancing white matter lesions (ELs), non-enhancing white matter lesions (NELs), and normal appearing white matter (NAWM) and metrics were compared to clinical data. ΔT1 was measurable in NELs (median: -0.139 (-0.304, 0.174) seconds; p < 0.001) and was negligible in NAWM (median: -0.001 (-0.036, 0.155) seconds; p = 0.516). Median ΔT1 in NELs correlated with disability as measured by Expanded Disability Status Scale (EDSS) (rho = -0.331, p = 0.026). Multiple measures of NEL ΔT1 variability also correlated with EDSS. NEL ΔT1 values were greater and more variable in patients with progressive forms of MS and greater in those not on MS treatment. Measurement of the changes in T1 relaxation time caused by contrast on 7T MP2RAGE reveals clinically relevant evidence of BBB breakdown in NELs in MS. This data suggests that NEL ΔT1 should be evaluated further as a biomarker for disease severity and treatment effect in MS.

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