Background: In relapsing-remitting multiple sclerosis (RRMS), early disease control reduces the risk of permanent disability. The blood-brain barrier (BBB) is compromised in MS, and its permeability is a potential biomarker.
Objective: To investigate BBB permeability measured by MRI as a marker of alemtuzumab efficacy.
Methods: Patients with RRMS initiating alemtuzumab treatment were recruited prospectively. BBB permeability was assessed as the Patlak-derived influx constant (K) by dynamic contrast-enhanced MRI before and 6, 12, and 18 months after the first course of alemtuzumab. No Evidence of Disease Activity-3 (NEDA-3) status was ascertained two years after treatment initiation.
Results: Patients who maintained NEDA-3 status at two years (n = 7) had a larger decrease in K between baseline and six months (-0.029 ml/100 g/min [CI -0.005 - -0.053]) and between baseline and 12 months in normal appearing white matter (0.043 [CI 0.022 - -0.065]), than those who experienced disease activity (n = 8). ROC curve analysis of the K change between baseline and 12 months in NAWM predicted a loss of NEDA status at 2 years with 86% sensitivity and 86% specificity (AUC 0.98, p = 0.002).
Conclusion: BBB permeability predicted alemtuzumab efficacy at two years, indicating that BBB permeability is a biomarker of treatment response in RRMS.
Download full-text PDF |
Source |
---|---|
http://dx.doi.org/10.1016/j.msard.2022.103891 | DOI Listing |
Neurotherapeutics
December 2024
Department of Neurology, Johns Hopkins University School of Medicine, Baltimore, MD, United States; Neurocritical Care Division, Department of Anesthesiology and Critical Care Medicine, Johns Hopkins University School of Medicine, MD, United States; Department of Neurosurgery, Johns Hopkins University School of Medicine, Baltimore, MD, United States; Department of General Internal Medicine, Johns Hopkins University School of Medicine, Baltimore, MD, United States. Electronic address:
Brain ischemia is a major cause of neurological dysfunction and mortality worldwide. It occurs not only acutely, such as in acute ischemic stroke (AIS), but also in chronic conditions like cerebral small vessel disease (cSVD). Any other conditions resulting in brain hypoperfusion can also lead to ischemia.
View Article and Find Full Text PDFZhongguo Zhong Yao Za Zhi
September 2024
the First Affiliated Hospital of Henan University of Chinese Medicine Zhengzhou 450000, China.
This study explores the reparative effect of Qixiong Zuogui Compound Prescription(QXZG) intervention on the blood-brain barrier(BBB) in the aging brain with middle cerebral artery occlusion(MCAO) in rats mediated by bone marrow stem cells(BMSCs)-derived exosomes, as well as its anti-aging mechanism. An aging MCAO composite model was established using D-galactose-induced aging combined with line embolism. Rats were divided into young sham surgery group, aging sham surgery group, model group, exosome group, and exosome with traditional Chinese medicine(TCM) intervention group.
View Article and Find Full Text PDFJ Neuroinflammation
December 2024
Department of Molecular Cell Biology and Immunology, Amsterdam UMC location Vrije Universiteit Amsterdam, De Boelelaan 1117, Amsterdam, The Netherlands.
Microvascular brain endothelial cells tightly limit the entry of blood components and peripheral cells into the brain by forming the blood-brain barrier (BBB). The BBB is regulated by a cascade of mechanical and chemical signals including shear stress and elasticity of the adjacent endothelial basement membrane (BM). During physiological aging, but especially in neurological diseases including multiple sclerosis (MS), stroke, small vessel disease, and Alzheimer's disease (AD), the BBB is exposed to inflammation, rigidity changes of the BM, and disturbed cerebral blood flow (CBF).
View Article and Find Full Text PDFJ Nanobiotechnology
December 2024
Brain Injury Center, Department of Neurosurgery, Ren Ji Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai, 200127, China.
Traumatic brain injury (TBI) is one of the leading public health concerns in the world. Therapeutic hypothermia is routinely used in severe TBI, and pathophysiological hyperthermia, frequently observed in TBI patients, has an unclear impact on drug transport in the injured brain due to a lack of study on its effects. We investigated the effect of post-traumatic therapeutic hypothermia at 33°C and pathophysiological hyperthermia at 39°C on brain transport and cell uptake of neuroprotectants after TBI.
View Article and Find Full Text PDFMol Neurobiol
December 2024
Department of Neuroscience, School of Science and Advanced Technologies in Medicine, Hamadan University of Medical Sciences, Hamedan, Iran.
There is no acquiesced remedy for the treatment of traumatic brain injury (TBI)-associated impairment, especially cognitive decline. The first 24 h after TBI is a golden time for preventing the progress of the impairments. The present study aimed to examine the acute effects of fucoidan on neurological outcomes and memory performance and investigate its potential mechanisms in rats with TBI.
View Article and Find Full Text PDFEnter search terms and have AI summaries delivered each week - change queries or unsubscribe any time!