A5087140749- Alzheimer's disease research and treatments
- Neuroinflammation and Neurodegeneration Mechanisms
- Cholinesterase and Neurodegenerative Diseases
- S100 Proteins and Annexins
- Traumatic Brain Injury and Neurovascular Disturbances
- Neurological Disease Mechanisms and Treatments
- Computational Drug Discovery Methods
- Dementia and Cognitive Impairment Research
- Drug Transport and Resistance Mechanisms
- Nuclear Receptors and Signaling
- Advanced Glycation End Products research
- Immune cells in cancer
- Mitochondrial Function and Pathology
- Immune Response and Inflammation
- Protein Hydrolysis and Bioactive Peptides
- Neurological Disorders and Treatments
- Tryptophan and brain disorders
- Fibromyalgia and Chronic Fatigue Syndrome Research
- Neuroscience and Neuropharmacology Research
- Traumatic Brain Injury Research
- NF-κB Signaling Pathways
- Protein Structure and Dynamics
- Axon Guidance and Neuronal Signaling
- Cardiovascular Syncope and Autonomic Disorders
- Medicinal Plants and Neuroprotection
University of Basel
2023-2025
Swiss Tropical and Public Health Institute
2023-2025
Roskamp Institute
2016-2025
Radboud University Nijmegen
2024
Radboud University Medical Center
2024
University of Leicester
2024
St. Vincent's University Hospital
2024
Trinity College Dublin
2024
University of Copenhagen
2024
The Open University
2014-2021
Alzheimer's disease (AD) has a substantial inflammatory component, and activated microglia may play central role in neuronal degeneration. CD40 expression was increased on cultured treated with freshly solublized amyloid-β (Aβ, 500 nanomolar) from transgenic murine model of AD (Tg APP sw ). Increased tumor necrosis factor α production induction injury occurred when Aβ-stimulated were ligand (CD40L). Microglia Tg mice deficient for CD40L demonstrated reduction activation, suggesting that the...
BACKGROUND: Inflammation is believed to play an important role in the pathology of Alzheimer's disease (AD) and cytokine production a key pathologic event progression inflammatory cascades. The current study characterizes expression profile brain two transgenic mouse models AD (TgAPPsw PS1/APPsw) explores correlations between level soluble insoluble forms Abeta. METHODS: Organotypic slice cultures from 15-month-old mice (TgAPPsw, PS1/APPsw control littermates) were established multiple...
Aβ deposits represent a neuropathological hallmark of Alzheimer's disease (AD). Both soluble and insoluble species are considered to be responsible for initiating the pathological cascade that eventually leads AD. Therefore, identification therapeutic approaches can lower production or accumulation remains priority. NFκB has been shown regulate BACE-1 expression level, rate limiting enzyme Aβ. We therefore explored whether known inhibitor celastrol could suitable compound decreasing in vivo....
Alzheimer’s disease (AD) is characterized by the deposition of β-sheet–rich, insoluble amyloid β-peptide (Aβ) plaques; however, plaque burden not correlated with cognitive impairment in AD patients; instead, it presence toxic soluble oligomers. Here, we show, a variety different techniques, that these Aβ oligomers adopt nonstandard secondary structure, termed “α-sheet.” These form lag phase aggregation, when Aβ-associated cytotoxicity peaks, en route to forming nontoxic β-sheet fibrils. De...
Exposure to repetitive concussion, or mild traumatic brain injury (mTBI), has been linked with increased risk of long-term neurodegenerative changes, specifically chronic encephalopathy (CTE). To date, preclinical studies largely have focused on the immediate aftermath mTBI, no literature lifelong consequences mTBI in these models. This study provides first account neurobehavioral and histological providing unique insight into constellation evolving ongoing pathologies late survival.Male...
Several genetic variants of the Triggering Receptor Expressed on Myeloid Cells-2 (TREM2) have been shown to increase risk developing Alzheimer's disease (AD) supporting a role microglia and immune cells in pathobiology AD. We developed an ectopic model TREM2 DAP12 expression HEK293 study selectively dependent signaling phagocytic functions evaluated effects some mutations associated with show that shedding N-terminal domain does not affect its anti-inflammatory activity while it completely...
Mounting evidence suggests that cholesterol may contribute to the pathogenesis of Alzheimer disease (AD). We examined whether might be present in senile plaques, a hallmark neuropathological feature AD. employed 2 different fluorometric-staining techniques (filipin staining and an enzymatic technique) for determination brains postmortem confirmed AD patients nondemented, age-matched histopathologically normal controls. patient showed abnormal accumulation congophilic/birefringent dense cores...
Several large population-based or clinical trial studies have suggested that certain dihydropyridine (DHP) L-type calcium channel blockers (CCBs) used for the treatment of hypertension may confer protection against development Alzheimer disease (AD). However, other with drugs same class shown no beneficial effects. To determine whether DHPs are able to impact underlying processes in AD (specifically accumulation Aβ peptide), we investigated effect several antihypertensive and non-DHP CCBs on...
Beta-amyloid peptides (Abeta) are the major constituents of senile plaques and cerebrovascular deposits in brains Alzheimer's disease patients. We have shown previously that soluble forms Abeta anti-angiogenic both vitro vivo. However, mechanism activity is unclear. In this study, we examined effects Abeta1-42 on vascular endothelial growth factor receptor 2 (VEGFR-2) signaling, which plays a key role angiogenesis. inhibited VEGF-induced migration cells, as well permeability an model blood...
Abstract Background Matrix metallopeptidase 9 (MMP9) has been implicated in a variety of neurological disorders, including Alzheimer’s disease (AD), where MMP9 levels are elevated the brain and cerebrovasculature. Previously our group demonstrated apolipoprotein E4 (apoE4) was less efficient regulating activity than other apoE isoforms, that inhibition facilitated beta-amyloid (Aβ) elimination across blood–brain barrier (BBB) Methods In current studies, we evaluated impact modulation on Aβ...
Myalgic Encephalomyelitis/Chronic Fatigue Syndrome (ME/CFS) is a multi-factorial systemic chronic debilitating disease of poorly understood etiology and limited systematic evidence. The questionnaire interview-based survey included 169 ME/CFS patients from the Swiss association. majority were females (72.2%), single (55.7%) without children (62.5%). Only one third working (full/part-time). mean onset was 31.6 years age with 15% being symptomatic before their 18th birthday. In this cohort,...
Myalgic Encephalomyelitis/Chronic Fatigue Syndrome (ME/CFS) is a debilitating chronic disease of significant public health and clinical importance. It affects multiple systems in the body has neuro-immunological characteristics. The characterized by prominent symptom called post-exertional malaise (PEM), as well abnormalities immune-inflammatory pathways, mitochondrial dysfunctions disturbances neuroendocrine pathways. purpose this study was to evaluate impact ME/CFS on mental secondary...
Aβ peptides are the major protein constituents of Alzheimer's disease (AD) senile plaques and also form some deposits in cerebrovasculature leading to cerebral amyloid angiopathy hemorrhagic stroke. Functional vascular abnormalities one earlier clinical manifestations both sporadic familial forms AD. Most cardiovascular risk factors (for instance, diabetes, hypertension, high cholesterol levels, atherosclerosis smoking) constitute for AD as well, suggesting that functional may contribute...