Jeroen Vreijling
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View article: Small Vessel Disease Phenotype Associated With Monoallelic <i>NOTCH3</i> Loss-of-Function Variants
Small Vessel Disease Phenotype Associated With Monoallelic <i>NOTCH3</i> Loss-of-Function Variants Open
We conclude that monoallelic NOTCH3lof variants cause a small vessel disease that (1) remains subclinical in most cases but may be exacerbated by cardiovascular risk factors and aging, and (2) is distinct from CADA…
View article: The Acute Effects of Morning Bright Light on the Human White Adipose Tissue Transcriptome: Exploratory Post Hoc Analysis
The Acute Effects of Morning Bright Light on the Human White Adipose Tissue Transcriptome: Exploratory Post Hoc Analysis Open
The circadian rhythm of the central brain clock in the suprachiasmatic nucleus (SCN) is synchronized by light. White adipose tissue (WAT) is one of the metabolic endocrine organs containing a molecular clock, and it is synchronized by the …
View article: Neurovascular Decoupling Is Associated With Lobar Intracerebral Hemorrhages and White Matter Hyperintensities
Neurovascular Decoupling Is Associated With Lobar Intracerebral Hemorrhages and White Matter Hyperintensities Open
Background Neurovascular coupling is a fundamental aspect of brain function by regulating cerebral blood flow in response to regional neuronal activity. Increasing evidence suggest neurovascular decoupling occurs early in the progression o…
View article: Defective Schwann cell lipid metabolism alters plasma membrane dynamics in Charcot-Marie-Tooth disease 1A
Defective Schwann cell lipid metabolism alters plasma membrane dynamics in Charcot-Marie-Tooth disease 1A Open
Duplication of PMP22 causes Charcot-Marie-Tooth disease type 1A (CMT1A) and is known to disrupt the lipid metabolism in myelinating Schwann cells by unknown mechanisms. By using two CMT1A mouse models overexpressing human PMP22 , we discov…
View article: The systemic inhibition of the terminal complement system reduces neuroinflammation but does not improve motor function in mouse models of CMT1A with overexpressed PMP22
The systemic inhibition of the terminal complement system reduces neuroinflammation but does not improve motor function in mouse models of CMT1A with overexpressed PMP22 Open
View article: Development, Characterization, and in vivo Validation of a Humanized C6 Monoclonal Antibody that Inhibits the Membrane Attack Complex
Development, Characterization, and in vivo Validation of a Humanized C6 Monoclonal Antibody that Inhibits the Membrane Attack Complex Open
Damage and disease of nerves activates the complement system. We demonstrated that activation of the terminal pathway of the complement system leads to the formation of the membrane attack complex (MAC) and delays regeneration in the perip…
View article: Supplementary Material for: Development, Characterization, and in vivo Validation of a Humanized C6 Monoclonal Antibody that Inhibits the Membrane Attack Complex
Supplementary Material for: Development, Characterization, and in vivo Validation of a Humanized C6 Monoclonal Antibody that Inhibits the Membrane Attack Complex Open
Damage and disease of nerves activates the complement system. We demonstrated that activation of the terminal pathway of the complement system leads to the formation of the membrane attack complex (MAC) and delays regeneration in the perip…
View article: Whole-exome Sequencing Identifies SLC52A1 and ZNF106 Variants as Novel Genetic Risk Factors for (Early) Multiple-organ Failure in Acute Pancreatitis
Whole-exome Sequencing Identifies SLC52A1 and ZNF106 Variants as Novel Genetic Risk Factors for (Early) Multiple-organ Failure in Acute Pancreatitis Open
Objective: The aim of this study was to identify genetic variants associated with early multiple organ failure (MOF) in acute pancreatitis. Summary Background Data: MOF is a life-threatening complication of acute pancreatitis, and risk fac…
View article: M. leprae components induce nerve damage by complement activation: identification of lipoarabinomannan as the dominant complement activator
M. leprae components induce nerve damage by complement activation: identification of lipoarabinomannan as the dominant complement activator Open