A5013012959- Neuroinflammation and Neurodegeneration Mechanisms
- Stress Responses and Cortisol
- Prion Diseases and Protein Misfolding
- Multiple Sclerosis Research Studies
- Tryptophan and brain disorders
- Muscle Physiology and Disorders
- Phagocytosis and Immune Regulation
- Immunotherapy and Immune Responses
- Neurological diseases and metabolism
- Genetic Neurodegenerative Diseases
- Fibromyalgia and Chronic Fatigue Syndrome Research
- Autoimmune Neurological Disorders and Treatments
- Nuclear Structure and Function
- Immune Response and Inflammation
- Neurogenetic and Muscular Disorders Research
- Trace Elements in Health
- Glaucoma and retinal disorders
- Advanced MIMO Systems Optimization
- Glioma Diagnosis and Treatment
- Systemic Sclerosis and Related Diseases
- T-cell and B-cell Immunology
- Retinal and Optic Conditions
- Inflammatory Myopathies and Dermatomyositis
- Neurofibromatosis and Schwannoma Cases
- Wireless Body Area Networks
University Hospital of Zurich
2012-2025
University of Zurich
2007-2025
National Hospital for Neurology and Neurosurgery
2023
University College London
2023
Klinikum rechts der Isar
2023
Neurosciences Institute
2023
Munich Cluster for Systems Neurology
2023
Technical University of Munich
2023
Icahn School of Medicine at Mount Sinai
2015-2021
Tisch Hospital
2015-2021
Abstract Major depressive disorder is associated with abnormalities in the brain and immune system. Chronic stress animals showed that epigenetic inflammatory mechanisms play important roles mediating resilience susceptibility to depression. Here, through a high-throughput screening, we identify two phytochemicals, dihydrocaffeic acid (DHCA) malvidin-3′- O -glucoside (Mal-gluc) are effective promoting against by modulating synaptic plasticity peripheral inflammation. DHCA/Mal-gluc also...
Microglia, the brain resident macrophages, critically shape forebrain neuronal circuits. However, their precise function in cerebellum is unknown. Here we show that human and mouse cerebellar microglia express a unique molecular program distinct from microglia. Cerebellar microglial identity was driven by CSF-1R ligand CSF-1, independently of alternate ligand, IL-34. Accordingly, CSF-1 depletion Nestin+ cells led to severe transcriptional alterations microglia, while remained intact....
To analyze antisynthetase syndrome-associated myositis by modern myopathologic methods and to define its place in the spectrum of idiopathic inflammatory myopathies (IIMs).Skeletal muscle biopsies from other IIMs different institutions worldwide were analyzed histopathology, quantitative PCR, electron microscopy.Myonuclear actin filament inclusions identified as a unique morphologic hallmark myositis. Nuclear never found dermatomyositis, polymyositis, sporadic inclusion body myositis,...
Abstract Multiple sclerosis (MS) is a neurological disease of the central nervous system that leading cause non-traumatic disability in young adults. Clinical laboratory tests and neuroimaging studies are standard methods to diagnose monitor MS. However, due infrequent clinic visits, it fundamental identify remote frequent approaches for monitoring MS, which enable timely diagnosis, early access treatment, slowing down progression. In this work, we investigate most reliable , clinically...
Langerhans cell histiocytosis (LCH) is an inflammatory myeloid neoplasia characterized by granulomatous lesions containing pathological CD207+ dendritic cells (DCs) with constitutively activated mitogen-activated protein kinase (MAPK) pathway signaling. Approximately 60% of LCH patients harbor somatic BRAFV600E mutations localizing to DCs within lesions. However, the mechanisms driving BRAFV600E+ accumulation in remain unknown. Here we show that sustained extracellular signal–related...
Prnp−/− mice lack the prion protein PrPC and are resistant to infections, but variable phenotypes have been reported in physiological function of remains poorly understood. Here we examined a cell-autonomous phenotype, inhibition macrophage phagocytosis apoptotic cells, previously mice. Using formal genetic, genomic, immunological analyses, found that regulation ascribed is instead controlled by linked locus encoding signal regulatory α (Sirpa). These findings indicate control was...
The structural complexity of chromosome 1p centromeric region has been an obstacle for fine mapping tumor suppressor genes in this area. Loss heterozygosity (LOH) on is associated with the longer survival oligodendroglioma (OD) patients. To test clinical relevance loss glioblastomas (GBM) patients and identifiy underlying locus, we constructed a somatic deletion map 26 OG 118 GBM. Deletion hotspots at 4 microsatellite markers located 1p36.3, 1p36.1, 1p22 1p11 defined 10 distinct haplotypes...
Nusinersen, an intrathecally-administered antisense oligonucleotide for the treatment of spinal muscular atrophy (SMA), may rarely cause mild aseptic meningitis early in treatment. We report a severe late-onset brain stem meningoencephalitis 42-year-old man with type III SMA, occurring 38 months after starting nusinersen. The patient showed clinical and radiological signs significant CSF neutrophilic pleocytosis, despite negative infectious disease tests. After high-dose steroids tapering,...
Misfolding of the cellular prion protein (PrPC) into scrapie (PrPSc) results in progressive, fatal, transmissible neurodegenerative conditions termed diseases. Experimental and epidemiological evidence point toward a protracted, clinically silent phase diseases, yet there is no diagnostic test capable identifying asymptomatic individuals incubating prions. In an effort to identify early biomarkers we have compared global transcriptional profiles brains from pre-symptomatic prion-infected...
Dysferlin is reduced in patients with limb girdle muscular dystrophy type 2B, Miyoshi myopathy, distal anterior compartment and certain Ethnic clusters. We evaluated clinical genetic patient data from three different Swiss Neuromuscular Centers. Thirteen 6 non-related families were included. Age of onset was 18.8 ± 4.3 years. In all patients, diallelic disease-causing mutations identified the DYSF gene. Nine 3 Central Switzerland carried identical homozygous mutation, c.3031 + 2T>C. A...