A5014287588- Alzheimer's disease research and treatments
- Parkinson's Disease Mechanisms and Treatments
- Dementia and Cognitive Impairment Research
- Prion Diseases and Protein Misfolding
- Neuroinflammation and Neurodegeneration Mechanisms
- Neurological diseases and metabolism
- Intracerebral and Subarachnoid Hemorrhage Research
- Amyotrophic Lateral Sclerosis Research
- Advanced Neuroimaging Techniques and Applications
- Neurological disorders and treatments
- Endoplasmic Reticulum Stress and Disease
- Tryptophan and brain disorders
- Trace Elements in Health
- Cerebrovascular and genetic disorders
- S100 Proteins and Annexins
- Nuclear Receptors and Signaling
- Functional Brain Connectivity Studies
- Amyloidosis: Diagnosis, Treatment, Outcomes
- Genetic Neurodegenerative Diseases
- Cerebrospinal fluid and hydrocephalus
- Neurological Disease Mechanisms and Treatments
- Neurological Disorders and Treatments
- Neuroscience and Neuropharmacology Research
- Acute Ischemic Stroke Management
- Glioma Diagnosis and Treatment
Amsterdam UMC Location Vrije Universiteit Amsterdam
2014-2025
Amsterdam Neuroscience
2016-2025
Vrije Universiteit Amsterdam
2008-2025
Amsterdam University Medical Centers
2018-2025
Netherlands Institute for Neuroscience
2000-2024
Netherlands Metabolomics Centre
2024
Biomedical Primate Research Centre
2024
Leiden University Medical Center
2024
Royal Netherlands Academy of Arts and Sciences
2024
University Medical Center Utrecht
2012-2022
Nomenclature and nosology for neuropathologic subtypes of frontotemporal lobar degeneration : an update
A 'frontal variant of Alzheimer's disease' has been described in patients with predominant behavioural or dysexecutive deficits caused by disease pathology. The description this rare phenotype limited to case reports and small series, many clinical, neuroimaging neuropathological characteristics are not well understood. In retrospective study, we included 55 a behavioural-predominant presentation (behavioural disease) diagnosis high-likelihood (n = 17) and/or biomarker evidence pathology...
Large genomic reference data sets reveal a spectrum of pathogenicity in the prion protein gene and provide genetic validation for therapeutic strategy disease.
We used primary cultures of cortical neurons to examine the relationship between beta-amyloid toxicity and hyperphosphorylation tau protein, biochemical substrate for neurofibrillary tangles Alzheimer's brain. Exposure peptide (betaAP) induced expression secreted glycoprotein Dickkopf-1 (DKK1). DKK1 negatively modulates canonical Wnt signaling pathway, thus activating tau-phosphorylating enzyme glycogen synthase kinase-3beta. was at late times after betaAP exposure, its dependent on tumor...
To determine how amyloid β 42 (Aβ42), total tau (t-tau), and phosphorylated (p-tau) levels in CSF behave a large cohort of patients with different types dementia.Baseline was collected from 512 Alzheimer disease (AD) 272 other dementia (OD), 135 psychiatric disorder (PSY), 275 subjective memory complaints (SMC). Aβ42, t-tau, p-tau (at amino acid 181) were measured by ELISA. Autopsy obtained subgroup 17 patients.A correct classification AD (92%) OD (66%) accomplished when Aβ42 combined....
When 22 members of the BrainNet Europe (BNE) consortium assessed 31 cases with α-synuclein (αS) immunoreactive (IR) pathology applying consensus protocol described by McKeith and colleagues in 2005, inter-observer agreement was 80%, being lowest limbic category (73%). staging Braak 2003, only 65%, some as low 36%. modifications these strategies, i.e., McKeith's Leverenz from 2009, Braak's Müller 2005 were applied then increased to 78 82%, respectively. In both modifications, a reduced number...
Cerebral amyloid angiopathy (CAA) is frequently observed in Alzheimer's disease (AD) and characterized by deposition of beta (Aβ) leptomeningeal cortical brain vasculature. In 40% AD cases, Aβ mainly accumulates capillaries, a phenomenon referred to as capillary CAA (capCAA). The aim this study was investigate blood–brain barrier (BBB) alterations CAA-affected capillaries with the emphasis on tight junction (TJ) changes. First, capCAA tissue analyzed for distribution TJs. Here, we show first...
There is increasing evidence that frontotemporal dementia and amyotrophic lateral sclerosis are part of a disease continuum. Recently, hexanucleotide repeat expansion in C9orf72 was identified as major cause both sporadic familial sclerosis. The aim this study to investigate clinical neuropathological characteristics expansions large cohort Dutch patients with dementia. Repeat were successfully determined 353 or without sclerosis, 522 neurologically normal controls. Immunohistochemistry...
Abstract We examined the regulation of glutamate transporter protein expression after stimulation with selective metabotropic receptor (mGluR) agonists in cultured human glial cells. mGluR3 and mGluR5 are expressed astrocytes glioma cells vivo as well vitro , shown by either RT‐PCR or western blot analysis. The group I agonist (S)‐3,5‐dihydroxyphenylglycine produced a significant down‐regulation both GLAST GLT‐1 presence growth factors. This condition mimics morphology reactive including an...
Amyloid plaques in Alzheimer's dementia contain complement factors C1q, C4 and C3. In the present study we demonstrate activation amyloid using immunoenzymatical techniques specific antibodies against subunits of individual components activated products. C1q C3 fragments (C3c C3d, g) but no C1s C3a. These findings that are not passively bound to plaque structures result an process. The role genesis senile is discussed.
White matter hyperintensities (WMH) are frequently seen on T2-weighted MRI scans of elderly subjects with and without Alzheimer's disease. WMH only weakly inconsistently associated cognitive decline, which may be explained by heterogeneity the underlying neuropathological substrates. The use quantitative could increase specificity for these changes. We assessed whether post-mortem is able to reflect differences in correlates tissue samples obtained from disease patients non-demented elderly....
This study was designed to investigate the role of serum proteins, microglia, glial fibrillary acidic protein (GFAP) positive cells and dystrophic neurites in genesis cerebral amyloid. Using A4 antisera, we found an amorphous non-congophilic, form plaque, which not seen Bielschowsky silver staining or Bodian impregnations. GFAP-positive cells, immunolabelled for some macrophage markers were detected congophilic plaques with crystalline amyloid, but amorphous, non-congophilic plaques. The...