A5076197620- Alzheimer's disease research and treatments
- Neurological diseases and metabolism
- Parkinson's Disease Mechanisms and Treatments
- Prion Diseases and Protein Misfolding
- Cancer Genomics and Diagnostics
- Cerebrovascular and genetic disorders
- Neuroscience and Neuropharmacology Research
- Nuclear Receptors and Signaling
- Dementia and Cognitive Impairment Research
- Neuroinflammation and Neurodegeneration Mechanisms
- Glioma Diagnosis and Treatment
- Amyotrophic Lateral Sclerosis Research
- Genetic Neurodegenerative Diseases
- Cholinesterase and Neurodegenerative Diseases
- Mitochondrial Function and Pathology
- Meningioma and schwannoma management
- Long-Term Effects of COVID-19
- Single-cell and spatial transcriptomics
- COVID-19 Clinical Research Studies
- Epigenetics and DNA Methylation
- Nerve injury and regeneration
- SARS-CoV-2 and COVID-19 Research
- Neurological disorders and treatments
- Intracerebral and Subarachnoid Hemorrhage Research
- Botulinum Toxin and Related Neurological Disorders
University Hospital of Basel
2015-2024
University of Basel
2007-2022
Case Western Reserve University
2020
University of Lausanne
2020
University of Regensburg
2020
Hospital Base
2020
Derriford Hospital
2018
Taipei Institute of Pathology
2004-2014
Institute of Molecular and Clinical Ophthalmology Basel
2000-2013
University Hospital of Zurich
2009-2010
Coronavirus disease 2019 (COVID-19), caused by severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2), has rapidly evolved into a sweeping pandemic. Its major manifestation is in the tract, and general extent of organ involvement microscopic changes lungs remain insufficiently characterised. Autopsies are essential to elucidate COVID-19-associated alterations.This article reports autopsy findings 21 COVID-19 patients hospitalised at University Hospital Basel Cantonal Baselland,...
Filamentous inclusions made of hyperphosphorylated tau are characteristic numerous human neurodegenerative diseases, including Alzheimer’s disease, tangle-only dementia, Pick argyrophilic grain disease (AGD), progressive supranuclear palsy, and corticobasal degeneration. In AGD, it has been shown that filamentous appears to spread in a stereotypic manner as the progresses. We previously demonstrated injection brain extracts from mutant P301S tau-expressing transgenic mice into brains for...
The presynaptic protein α-synuclein is a prime suspect for contributing to Lewy pathology and clinical aspects of diseases, including Parkinson9s disease, dementia with bodies, body variant Alzheimer9s disease. α-Synuclein accumulates in bodies neurites, two missense mutations (A53T A30P) the gene are genetically linked rare familial forms Under control mouse Thy1 regulatory sequences, expression A53T mutant human nervous system transgenic mice generated animals neuronal α-synucleinopathy,...
Abstract Intracellular inclusions composed of hyperphosphorylated filamentous tau are a hallmark Alzheimer’s disease, progressive supranuclear palsy, Pick’s disease and other sporadic neurodegenerative tauopathies. Recent in vitro vivo studies have shown that aggregates do not only seed further aggregation within neurons, but can also spread to neighbouring cells functionally connected brain regions. This process is referred as ‘tau propagation’ may explain the stereotypic progression...
Transgenic mice that overexpress mutant human amyloid precursor protein (APP) exhibit one hallmark of Alzheimer's disease pathology, namely the extracellular deposition plaques. Here, we describe significant beta (Abeta) in cerebral vasculature [cerebral angiopathy (CAA)] aging APP23 had striking similarities to observed and disease. Amyloid occurred preferentially arterioles capillaries within individual vessels showed a wide heterogeneity (ranging from thin ring vessel wall large...
The accumulation of insoluble proteins is a pathological hallmark several neurodegenerative disorders. Tauopathies are caused by the dysfunction and aggregation tau protein an impairment cellular degradation pathways may contribute to their pathogenesis. Thus, deficiency in autophagy can cause neurodegeneration, while activation protective against some proteinopathies. Little known about role animal models human tauopathy. In present report, we assessed effects stimulation trehalose...
It has been proposed that tau aggregation confined to entorhinal cortex and hippocampus, with no or only minimal Aβ deposition, should be considered as a 'primary age-related tauopathy' (PART) is not integral the continuum of sporadic Alzheimer disease (AD). Here, we examine evidence PART pathogenic mechanism prognosis which differ from those AD. We contend specific property entorhinal-hippocampal pathology makes it possible predict either limited progression development AD, biochemical...
Abstract Coronavirus Disease 19 (COVID-19) is a respiratory disease caused by severe acute syndrome coronavirus 2 (SARS-CoV-2), which has grown to worldwide pandemic with substantial mortality. Immune mediated damage been proposed as pathogenic factor, but immune responses in lungs of COVID-19 patients remain poorly characterized. Here we show transcriptomic, histologic and cellular profiles post mortem ( n = 34 tissues from 16 patients) normal lung 9 6 patients). Two distinct...
Altered autophagy contributes to the pathogenesis of Alzheimer's disease and other tauopathies, for which curative treatment options are still lacking. We have recently shown that trehalose reduces tau pathology in a tauopathy mouse model by stimulation autophagy. Here, we studied effect inducing drug rapamycin on progression P301S mutant transgenic mice. Rapamycin resulted significant reduction cortical tangles, less hyperphosphorylation, lowered levels insoluble forebrain. The favourable...
Studies on cases with incidental Lewy body disease (ILBD) suggest that α‐synuclein (αSN) pathology of Parkinson's (PD) starts in lower brainstem nuclei and the olfactory bulb. However, medullary structures as induction site αSN have been questioned large parts nervous system, including spinal cord peripheral autonomic system (PANS), not examined ILBD. Thus, time course PD lesions or PANS relation to remains unknown. We collected 98 post mortem no reference PD‐associated symptoms clinical...
A high risk factor for spontaneous and often fatal lobar hemorrhage is cerebral amyloid angiopathy (CAA). We now report that CAA in an precursor protein transgenic mouse model (APP23 mice) leads to a loss of vascular smooth muscle cells, aneurysmal vasodilatation, rare cases, vessel obliteration severe vasculitis. This weakening the wall followed by rupture bleedings range from multiple, recurrent microhemorrhages large hematomas. Our results demonstrate that, APP mice, extracellular...
Alzheimer's disease presents morphologically with senile plaques, primarily made of extracellular amyloid-β (Aβ) deposits, and neurofibrillary lesions, which consist intracellular aggregates hyperphosphorylated tau protein. To study the in vivo induction pathology, dilute brain extracts from aged Aβ-depositing APP23 transgenic mice were intracerebrally infused young B6/P301L mice. Six months after infusion, pathology was induced injected hippocampus but also regions well beyond injection...
Chronic, daytime sleepiness is a major, disabling symptom for many patients with traumatic brain injury (TBI), but thus far, its etiology not well understood. Extensive loss of the hypothalamic neurons that produce wake-promoting neuropeptide hypocretin (orexin) causes severe narcolepsy, and partial these cells may contribute to Parkinson disease other disorders. We have found number significantly reduced in TBI. This observation highlights often overlooked TBI provides new insights into chronic