Caroline Van Cauwenberghe

ORCID: 0000-0002-3438-6031
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About
Contact & Profiles
Research Areas
  • Alzheimer's disease research and treatments
  • Neuroinflammation and Neurodegeneration Mechanisms
  • Bioinformatics and Genomic Networks
  • Genetic Associations and Epidemiology
  • Extracellular vesicles in disease
  • Complement system in diseases
  • Mitochondrial Function and Pathology
  • Lexicography and Language Studies
  • Folate and B Vitamins Research
  • Genetics and Neurodevelopmental Disorders
  • Parkinson's Disease Mechanisms and Treatments
  • Autoimmune and Inflammatory Disorders Research
  • Trace Elements in Health
  • Lysosomal Storage Disorders Research
  • Drug Transport and Resistance Mechanisms
  • Amyotrophic Lateral Sclerosis Research
  • Tryptophan and brain disorders
  • Machine Learning in Bioinformatics
  • Biological Research and Disease Studies
  • Dementia and Cognitive Impairment Research
  • Helicobacter pylori-related gastroenterology studies
  • Genomics and Rare Diseases
  • Diet and metabolism studies
  • Clusterin in disease pathology
  • Phytochemical Studies and Bioactivities

Ghent University
2016-2021

VIB-UGent Center for Inflammation Research
2016-2021

VIB-UAntwerp Center for Molecular Neurology
2009-2016

University of Antwerp
2009-2016

Antwerp University Hospital
2016

KU Leuven
2016

University Medical Center Groningen
2016

University of Groningen
2016

Ghent University Hospital
2016

Two multicentre genome-wide association (GWA) studies provided substantial evidence, implicating the complement receptor 1 gene (CR1) in Alzheimer disease (AD) genetic etiology. CR1 encodes a large transmembrane with crucial role immune cascade. We performed follow-up of GWA Flanders-Belgian cohort (n=1883), and investigated effect single-nucleotide polymorphisms (SNPs) located locus on AD risk cerebrospinal fluid (CSF) biomarker levels. obtained significant (P(adj)<0.03; odds ratio...

10.1038/mp.2011.24 article EN cc-by-nc-nd Molecular Psychiatry 2011-03-15

Recently, several genome-wide association studies (GWASs) have led to the discovery of nine new loci genetic susceptibility in Alzheimer's disease (AD). However, landscape AD is far away be complete and addition single-SNP (single-nucleotide polymorphism) analyses as performed conventional GWAS, complementary strategies need applied overcome limitations inherent this type approaches. We a haplotype (GWHA) study EADI1 (n=2025 cases 5328 controls) by applying sliding-windows approach. After...

10.1038/mp.2012.14 article EN cc-by-nc-sa Molecular Psychiatry 2012-03-20

Abstract Introduction The ability to identify individuals at increased genetic risk for Alzheimer's disease (AD) may streamline biomarker and drug trials aid clinical personal decision making. Methods We evaluated the discriminative of a score (GRS) covering 22 published loci AD in 1162 Flanders‐Belgian patients 1019 controls assessed correlations with family history, onset age, cerebrospinal fluid (CSF) biomarkers (Aβ 1–42 , T‐Tau, P‐Tau 181P ). Results A GRS including all single nucleotide...

10.1016/j.jalz.2015.02.013 article EN cc-by-nc-nd Alzheimer s & Dementia 2015-06-15

Research Article22 February 2018Open Access Transparent process Counteracting the effects of TNF receptor-1 has therapeutic potential in Alzheimer's disease Sophie Steeland VIB Center for Inflammation Research, Ghent, Belgium Department Biomedical Molecular Biology, Ghent University, Search more papers by this author Nina Gorlé Charysse Vandendriessche Sriram Balusu Marjana Brkic Neurobiology, Institute Biological University Belgrade, Republic Serbia Caroline Van Cauwenberghe Griet Imschoot...

10.15252/emmm.201708300 article EN cc-by EMBO Molecular Medicine 2018-02-22

Increasing evidence indicates that extracellular vesicles (EVs) play an important role in the pathogenesis of Alzheimer's disease (AD). We previously reported blood-cerebrospinal fluid (CSF) interface, formed by choroid plexus epithelial (CPE) cells, releases increased amount EVs into CSF response to peripheral inflammation. Here, we studied importance CP-mediated EV release AD pathogenesis. observed levels young transgenic APP/PS1 mice which correlated with high amyloid beta (Aβ) at this...

10.1186/s40478-021-01245-z article EN cc-by Acta Neuropathologica Communications 2021-08-23

Abstract Alzheimer’s disease (AD) is a chronic neurodegenerative characterized by the accumulation of amyloid β (Aβ) and neurofibrillary tangles. The last decade, it became increasingly clear that neuroinflammation plays key role in both initiation progression AD. Moreover, also presence peripheral inflammation has been extensively documented. However, still ambiguous whether this observed cause or consequence AD pathogenesis. Recently, studied using precursor protein (APP) overexpression...

10.1186/s40478-021-01253-z article EN cc-by Acta Neuropathologica Communications 2021-10-07

Patients with Estrogen Receptor α-positive (ER+) Inflammatory Breast Cancer (IBC) are less responsive to endocrine therapy compared ER+ non-IBC (nIBC) patients. The study of IBC samples might reveal biomarkers for resistant breast cancer.Gene expression profiles from 201 patients were explored genes that discriminated between and nIBC. Classifier applied onto clinically annotated data 947 cancer validated RT-qPCR 231 treated first-line tamoxifen. Relationships metastasis-free survival (MFS)...

10.1016/j.molonc.2015.02.006 article EN other-oa Molecular Oncology 2015-03-04

The clusterin (CLU) gene has been identified as an important risk locus for Alzheimer's disease (AD). Although the actual risk-increasing polymorphisms at this remain to be identified, we previously observed increased frequency of rare non-synonymous mutations and small insertion-deletions CLU in AD patients, which specifically clustered β-chain domain CLU. Nonetheless pathogenic nature these variants remained unclear. Here report a novel mutation (p.I360N) Belgian Alzheimer patient have...

10.1186/s13024-015-0024-9 article EN cc-by Molecular Neurodegeneration 2015-07-15

<h3>Objective:</h3> To generate a clinical and pathologic phenotype of patients carrying rare loss-of-function mutations in <i>ABCA7</i>, identified Belgian Alzheimer patient cohort an autosomal dominant family. <h3>Methods:</h3> We performed retrospective review available data records, medical results CSF analyses neuroimaging studies, neuropathology data. <h3>Results:</h3> The mean onset age the mutation carriers (n = 22) was 73.4 ± 8.4 years with wide range 36 (54–90) years, which...

10.1212/wnl.0000000000002628 article EN cc-by-nc-nd Neurology 2016-04-02

Niemann–Pick type C (NPC) disease is a rare neurovisceral lipid storage with progressive neurodegeneration, leading to premature death. The caused by loss-of-function mutations either in the NPC1 or NPC2 gene which results accumulation late endosomes and lysosomes. involved mechanisms are still incompletely understood, making design of rational treatment very difficult. Since characterized peripheral inflammation neuroinflammation it shown that extracellular vesicles (EVs) obtained from...

10.3390/biomedicines9121864 article EN cc-by Biomedicines 2021-12-08

Niemann-Pick type C (NPC) disease, sometimes called childhood Alzheimer's, is a rare neurovisceral lipid storage disease with progressive neurodegeneration leading to premature death. The caused by loss-of-function mutations in the Npc1 or Npc2 gene which both result into accumulation late endosomes and lysosomes. Since presents broad heterogenous clinical spectrum, involved mechanisms are still incompletely understood this hampers finding an effective treatment. As NPC patients, who carry...

10.3389/fncel.2021.757482 article EN cc-by Frontiers in Cellular Neuroscience 2021-10-15

Human lymphoblast cells from a female and male patient diagnosed with Alzheimer's disease (AD) different genotypes of functional copy number variation (CNV) in the AD risk gene CR1 were used to generate integration-free induced pluripotent stem (iPSCs) employing episomal plasmids expressing OCT4, SOX2, NANOG, LIN28, c-MYC L-MYC. The iPSCs retained CNV, comparative transcriptome analyses human embryonic cell line H1 revealed Pearson correlation 0.956 for AD1-CR10 0.908 AD1-CR14.

10.1016/j.scr.2016.10.003 article EN cc-by-nc-nd Stem Cell Research 2016-10-20
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