Publicaties
Evidence of amyloid-β cerebral amyloid angiopathy transmission through neurosurgery KU Leuven
TUDCA, a Bile Acid, Attenuates Amyloid Precursor Protein Processing and Amyloid-β Deposition in APP/PS1 Mice KU Leuven
Plasma amyloid β 42/40 ratios as biomarkers for amyloid β cerebral deposition in cognitively normal individuals Vrije Universiteit Brussel
Introduction Plasma amyloid β (Aβ) peptides have been previously studied as candidate biomarkers to increase recruitment efficiency in secondary prevention clinical trials for Alzheimer's disease. Methods Free and total Aβ42/40 plasma ratios (FP42/40 and TP42/40, respectively) were determined using ABtest assays in cognitively normal subjects from the Australian Imaging, Biomarker and Lifestyle Flagship Study. This population was followed-up ...
Adeno-associated virus gene therapy with cholesterol 24-hydroxylase reduces the amyloid pathology before or after the onset of amyloid plaques in mouse models of Alzheimer's disease Universiteit Antwerpen
The Role of Amyloid PET in Diagnosing Possible Transmissible Cerebral Amyloid Angiopathy in Young Adults with a History of Neurosurgery: A Case Series KU Leuven
Cerebral amyloid angiopathy: pathogenetic mechanisms and link to dense amyloid plaques Universiteit Antwerpen
Heterotypic Amyloid ß interactions facilitate amyloid assembly and modify amyloid structure. Vlaams Instituut voor Biotechnologie KU Leuven
Altered cerebrospinal fluid levels of amyloid β and amyloid precursor-like protein 1 peptides in Down's syndrome Vrije Universiteit Brussel Universiteit Antwerpen
Down's syndrome (DS) patients develop early Alzheimer's disease pathology with abundant cortical amyloid plaques, likely due to overproduction of the amyloid precursor protein (APP), which subsequently leads to amyloid β (Aβ) aggregation. This is reflected in cerebrospinal fluid (CSF) levels of the 42-amino acid long Aβ peptide (Aβ1-42), which are increased in young DS patients and decreases with age. However, it is unclear whether DS also ...
Early pathologic amyloid induces hypersynchrony of BOLD resting-state networks in transgenic mice and provides an early therapeutic window before amyloid plaque deposition Vrije Universiteit Brussel KU Leuven Universiteit Antwerpen Universiteit Gent
INTRODUCTION: In Alzheimer's disease (AD), pathologic amyloid-beta (Aβ) is synaptotoxic and impairs neuronal function at the microscale, influencing brain networks at the macroscale before Aβ deposition. The latter can be detected noninvasively, in vivo, using resting-state functional MRI (rsfMRI), a technique used to assess brain functional connectivity (FC).
METHODS: RsfMRI was performed longitudinally in TG2576 and PDAPP mice, ...