A5069557998- Parkinson's Disease Mechanisms and Treatments
- Neurological disorders and treatments
- Nerve injury and regeneration
- Neuroscience and Neuropharmacology Research
- Neurogenesis and neuroplasticity mechanisms
- Neural dynamics and brain function
- Olfactory and Sensory Function Studies
- Receptor Mechanisms and Signaling
- Nuclear Receptors and Signaling
- Conducting polymers and applications
- Fungal Plant Pathogen Control
- Phosphodiesterase function and regulation
- Oxidative Organic Chemistry Reactions
- Vagus Nerve Stimulation Research
- Functional Brain Connectivity Studies
- Catalytic C–H Functionalization Methods
- Cholinesterase and Neurodegenerative Diseases
- Medicinal Plants and Neuroprotection
- Neuroscience and Neural Engineering
- Photoreceptor and optogenetics research
- Neurological diseases and metabolism
- Neuroscience of respiration and sleep
- Transcranial Magnetic Stimulation Studies
- Radical Photochemical Reactions
- Nicotinic Acetylcholine Receptors Study
Philipps University of Marburg
2009-2024
New York University
2022-2024
Hebrew University of Jerusalem
2017-2021
Chung Yuan Christian University
2021
Institute of Neurobiology
2016-2017
Universitätsklinikum Gießen und Marburg
2017
Klinik und Poliklinik für Neurologie
2011
α-synuclein-induced neurotoxicity is a core pathogenic event in neurodegenerative synucleinopathies such as Parkinson's disease, dementia with Lewy bodies, or multiple system atrophy. There currently no disease-modifying therapy available for these diseases. We screened 1,600 FDA-approved drugs their efficacy to protect LUHMES cells from degeneration induced by wild-type α-synuclein and identified dipyridamole, non-selective phosphodiesterase inhibitor, top hit. Systematic analysis of other...
Degeneration of noradrenergic locus coeruleus neurons occurs during the prodromal phase Parkinson's disease and contributes to a variety non-motor symptoms, e.g. depression, anxiety REM sleep behavior disorder. This study was designed establish first α-synucleinopathy mouse model, which should provide sufficient information about time-course neurodegeneration, replicate cardinal histopathological features human neuropathology finally lead robust histological markers, are assess pathological...
Cholinergic interneurons (CINs) are believed to form synchronous cell assemblies that modulate the striatal microcircuitry and possibly orchestrate local dopamine release. We expressed GCaMP6s, a genetically encoded calcium indicator (GECIs), selectively in CINs, used microendoscopes visualize putative CIN dorsal striatum of freely moving mice. The GECI fluorescence signal from was composed signals individual somata were engulfed by widespread fluorescent neuropil. Bouts activation...
Abstract Parkinson’s disease (PD) is clinically defined by the presence of cardinal motor symptoms, which are associated with a loss dopaminergic nigrostriatal neurons in substantia nigra pars compacta (SNpc). While SNpc serve as prototypical cell-type to study cellular vulnerability PD, there an unmet need extent our efforts other at risk. The noradrenergic locus coeruleus (LC) represents one first brain structures affected and plays not only crucial role for evolving non-motor...
α-Synuclein overexpression (ASOX) drives the formation of toxic aggregates in neurons vulnerable Parkinson's disease (PD), including dopaminergic substantia nigra (SN) and cholinergic dorsal motor nucleus vagus (DMV). Just as these populations differ when they exhibit α-synucleinopathies during PD pathogenesis, could also their physiological responses to ASOX. An ASOX-mediated hyperactivity SN dopamine neurons, which was caused by oxidative dysfunction Kv4.3 potassium channels, recently...
The widely held view that the pathophysiology of Parkinson's disease arises from an under-activation direct pathway striatal spiny neurons (dSPNs) has gained support a recently described weakening glutamatergic projection parafascicular nucleus (PfN) to dSPNs in experimental parkinsonism. However, impact remodeling thalamostriatal cannot be fully appreciated without considering its on cholinergic interneurons (ChIs) themselves preferentially activate indirect (iSPNs). To study this...
Patients with schizophrenia frequently suffer from motor abnormalities, but underlying alterations in neuroarchitecture remain unclear. Here, we aimed to disentangle dyskinesia parkinsonism structures of patients and assess associated molecular architecture. We measured grey matter regions correlated volumetric estimates severity. Associations architecture were identified by cross-modal spatial correlations between ensuing maps abnormality-related volume neurotransmitter healthy populations....
Targeting α-synuclein to intact brainstem neurons drives gastrointestinal dysregulation seen in prodromal Parkinson’s disease.
Background and Purpose: Parkinson’s disease (PD) is clinically defined by the presence of cardinal motor symptoms, which are associated with a loss dopaminergic nigrostriatal neurons in substantia nigra pars compacta (SNpc). While SNpc serve as prototypical cell-type to study cellular vulnerability PD, there an unmet need extent our efforts other at risk. The noradrenergic locus coeruleus (LC) represents one first brain structures affected plays not only crucial role for evolving non-motor...
Abstract Cholinergic interneurons (CINs) are believed to form synchronous cell assemblies that modulate the striatal microcircuitry and possibly orchestrate local dopamine release. We expressed GCaMP6s, a genetically encoded calcium indicator (GECIs), selectively in CINs, used microendoscopes visualize putative CIN dorsal striatum of freely moving mice. The GECI fluorescence signal from was composed signals individual somata were engulfed by widespread fluorescent neuropil. Bouts activation...
α-Synuclein overexpression (ASOX) drives the formation of toxic aggregates in neurons vulnerable Parkinson9s disease (PD), including dopaminergic substantia nigra (SN) and cholinergic dorsal motor nucleus vagus (DMV). Just as these populations differ when they exhibit α-synucleinopathies during PD pathogenesis, could also their physiological responses to ASOX. An ASOX-mediated hyperactivity SN dopamine neurons, which was caused by oxidative dysfunction Kv4.3 potassium channels, recently...
Abstract No disease modifying therapy is currently available for Parkinson’s (PD), the second most common neurodegenerative disease. The long non-motor prodromal phase of PD a window opportunity early detection and intervention. However, we lack pathophysiological understanding to develop selective biomarkers interventions. By developing mutant α-synuclein selective-overexpression mouse model PD, identified cell-autonomous Kv4 channelopathy in dorsal motor nucleus vagus (DMV) neurons. This...
Abstract Alpha-7-nicotine-acetylcholine-receptor (α7-nAChRs) agonists modulate the cholinergic antiinflammatory pathway to attenuate proinflammatory signals and reduce dopaminergic neuronal cell loss in toxin-induced experimental murine models of Parkinson’s disease (PD). The protein α-synuclein (αSyn) is considered represent major pathogenic component etiology progression sporadic PD. However, no research has been performed evaluate effect α7-nAChR human αSyn mediated We, therefore,...
A 2,2-azobis(isobutyronitrile)-catalyzed oxidative cleavage of alkenes with molecular oxygen as the oxidant was described.