A5053882105- Alzheimer's disease research and treatments
- Neuroinflammation and Neurodegeneration Mechanisms
- Tryptophan and brain disorders
- Dementia and Cognitive Impairment Research
- Complement system in diseases
- Clusterin in disease pathology
- S100 Proteins and Annexins
- Inflammatory mediators and NSAID effects
- Drug Transport and Resistance Mechanisms
- Amyloidosis: Diagnosis, Treatment, Outcomes
- Monoclonal and Polyclonal Antibodies Research
- Nuclear Receptors and Signaling
- Neurological Disease Mechanisms and Treatments
- Barrier Structure and Function Studies
- Prion Diseases and Protein Misfolding
- Blood groups and transfusion
- Animal Genetics and Reproduction
- Adenosine and Purinergic Signaling
- Computational Drug Discovery Methods
- Bioinformatics and Genomic Networks
- Cholinesterase and Neurodegenerative Diseases
- Cholesterol and Lipid Metabolism
- Neuropeptides and Animal Physiology
- Immune Response and Inflammation
- Parkinson's Disease Mechanisms and Treatments
Amsterdam Neuroscience
2005-2023
Amsterdam University Medical Centers
2018-2023
Vrije Universiteit Amsterdam
2006-2023
GGZ inGeest
2018
Amsterdam UMC Location Vrije Universiteit Amsterdam
2007-2016
Univé (Netherlands)
2013
Amsterdam University of Applied Sciences
2011
University Medical Center
2010
University Hospital and Clinics
2010
Amsterdam UMC Location University of Amsterdam
2002-2007
Complement activation is known to occur in white matter multiple sclerosis (MS) lesions. It thought mediate oligodendrocyte/myelin damage and be a marker of pathologic heterogeneity among individuals. Less about complement deposition the gray MS. The aim this study was characterize presence distribution products cortical MS Immunohistochemical staining performed on cryostat sections from brains 22 patients 5 nonneurologic control obtained at autopsy. Deposition C1q, C3d, C5b-9 (membrane...
Abstract Intracerebral accumulation of amyloid‐β (Aβ) leading to Aβ plaque formation, is the main hallmark Alzheimer's disease and might be caused by defective Aβ‐clearance. We previously found primary human astrocytes microglia able bind ingest Aβ1‐42 in vitro , which appeared limited fibril formation. now confirm that astrocytic Aβ‐uptake depends on size and/or composition Aβ‐aggregates as preferably take up oligomeric over fibrillar Aβ. Upon exposure either fluorescence‐labelled oligomers...
Synucleinopathies such as Parkinson's disease (PD) are hallmarked by α-synuclein (α-syn) pathology and neuroinflammation. This neuroinflammation involves activated microglia with increased secretion of interleukin-1β (IL-1β). The main driver IL-1β from is the NLRP3 inflammasome. A critical link between microglial inflammasome activation progression both α-syn dopaminergic neurodegeneration has been identified in various PD models vivo. α-Syn known to activate murine models, but its...
Parkinson's disease (PD) is characterized by the loss of nigral dopaminergic neurons leading to impaired striatal dopamine signaling, α-synuclein- (α-syn-) rich inclusions, and neuroinflammation. Degenerating are surrounded activated microglia with increased secretion interleukin-1β (IL-1β), driven largely NLRP3 inflammasome. A critical role for microglial inflammasome activation in progression both neurodegeneration α-syn pathology has been demonstrated parkinsonism mouse models. Fibrillar...
Defective clearance of the amyloid‐β peptide (Aβ) from brain is considered a strong promoter in Alzheimer's disease (AD) pathogenesis. Astrocytes and microglia are important mediators Aβ aggregation state presence amyloid associated proteins (AAPs), such as Apolipoproteins E J (ApoE ApoJ), may influence by these cells. Here we set out to investigate whether astrocytes differ uptake efficiency oligomers (Aβ oligo ) fibrils fib ), and/or AAPs affect cells vitro . Adult human primary...
Background: HDL-cholesterol transporter Apolipoprotein A1 (ApoA1) holds neuroprotective properties, such as inhibition of amyloid-β aggregation. Low plasma ApoA1 concentrations are associated with Alzheimer’s disease (AD). Little is known about levels in the pre-dementia stages AD. Objective: To investigate associations between cerebrospinal fluid (CSF) and clinical progression toward AD non-demented elderly. Methods: From Amsterdam Dementia Cohort, we included 429 elderly subjective...
Regular use of non-steroidal anti-inflammatory drugs (NSAIDs) seems to reduce the progression several diseases, including colon cancer, lung breast cancer and Alzheimer disease (AD). Several studies have shown that NSAIDs can modulate cell cycle progression, especially in G0/G1 phase. The main target most is enzyme cyclo-oxygenase (COX), which occurs 2 isoforms, COX-1 COX-2. In AD non-demented control brain, COX-2 expressed neuronal cells. this study expression COX-2, cyclin D1, E was...