A5033619508- Neuroscience and Neuropharmacology Research
- Alzheimer's disease research and treatments
- Photoreceptor and optogenetics research
- Topological and Geometric Data Analysis
- Cell Image Analysis Techniques
- Prion Diseases and Protein Misfolding
- HIV Research and Treatment
- Functional Brain Connectivity Studies
- Calcium signaling and nucleotide metabolism
- Amino Acid Enzymes and Metabolism
- Neural dynamics and brain function
- Neural and Behavioral Psychology Studies
- Autophagy in Disease and Therapy
- Cholinesterase and Neurodegenerative Diseases
- Mitochondrial Function and Pathology
- Neuroscience and Neural Engineering
- Neurological disorders and treatments
- Retinal Development and Disorders
- Genetic Neurodegenerative Diseases
- EEG and Brain-Computer Interfaces
King's College London
2019-2024
ETH Zurich
2017
University of Zurich
2017
University Hospital of Zurich
2017
Royal Holloway University of London
2013
Charing Cross Hospital
2013
Imperial College London
2013
Hammersmith Hospital
2013
<h3>Objective:</h3> To determine whether behavioral dissociations and interactions occur between the attentional functions—alerting, orienting, conflict resolution—depending upon stroke location to approximate proportion of patients who can be classified into 1 these 3 anatomical networks. <h3>Methods:</h3> We recruited 110 anatomically unselected acute 62 age-matched controls. Subjects underwent attention network test (ANT), which provides a measure each type. Their performance was related...
Genetically encoded calcium indicators (GECIs) enable imaging of in vivo brain cell activity with high sensitivity and specificity. In contrast to viral infection or utero electroporation, indicator expression transgenic reporter lines is induced noninvasively, reliably, homogenously. Recently, Cre/tTA-dependent mice were introduced, which provide high-level green fluorescent GECIs a cell-type-specific inducible manner when crossed Cre tTA driver mice. Here, we generated characterized the...
Prion infections cause inexorable, progressive neurological dysfunction and neurodegeneration. Expression of the cellular prion protein PrPC is required for toxicity, suggesting existence deleterious PrPC-dependent signaling cascades. Because group-I metabotropic glutamate receptors (mGluR1 mGluR5) can form complexes with (PrPC), we investigated impact mGluR1 mGluR5 inhibition on toxicity ex vivo in vivo. We found that pharmacological antagonized dose-dependently neurotoxicity triggered by...
Abstract INTRODUCTION In tauopathies, altered tau processing correlates with impairments in synaptic density and function. Changes hyperpolarization‐activated cyclic nucleotide‐gated (HCN) channels contribute to disease‐associated abnormalities multiple neurodegenerative diseases. METHODS To investigate the link between HCN channels, we performed histological, biochemical, ultrastructural, functional analyses of hippocampal tissues from Alzheimer's disease (AD), age‐matched controls, Tau35...
Tauopathies are characterized by the progressive accumulation of abnormal tau species, which disrupt autophagy-lysosomal pathway (ALP), a critical system for degrading intracellular macromolecules and aggregated proteins, causing toxicity cell death. This study investigates impact N-terminally truncated Tau35 protein overexpression on proteolytic pathways, including effects autophagy endo-lysosomal processes. Using mouse model SH-SY5Y lines stably expressing either fragment or full-length...
Huntington's disease (HD) is a devastating neurodegenerative disorder caused by abnormal polyglutamine expansion in the huntingtin protein (Exp-Htt). Currently, there are no effective treatments for HD. We used bidirectional lentiviral transfer vectors to generate vitro and vivo models of HD test therapeutic potential vascular endothelial growth factor 165 (VEGF₁₆₅). Lentiviral-mediated expression Exp-Htt cell death aggregate formation human neuroblastoma SH-SY5Y rat primary striatal...
The TMD is a morphology descriptor for neurons which, when applied to path length, equivalent extended persistent homology and can be used characterize differences between healthy diseased mouse neurons.
Abstract Progressive neurodegeneration in tauopathies is mediated through an elusive mechanism. Here, we show that hyperpolarization-activated cyclic nucleotide-gated (HCN) channels are functionally linked to disease-associated abnormalities tau. Selective rises the proportion of HCN-positive neurons detected both post-mortem human brain from Alzheimer’s disease and Tau35 mouse model tauopathy. mice develop progressive including increased phosphorylated tau, enhanced HCN channel expression...
Deficits in synaptic function and neurite connectivity are early correlates of tauopathies. Altered tau processing mis-localization coincide with reductions synapse density function, suggesting a causal role for disease pathogenesis. In parallel, altered activity hyperpolarization-activated cyclic nucleotide-gated (HCN) channels, involved integration, is implicated progression animal models tauopathy. However, the mechanisms underlying these pathological events not fully understood.We...
The geometry of neurons is known to be important for their functions. Hence, are often classified by morphology. Two recent methods, persistent homology and the topological morphology descriptor, assign a descriptor called barcode neuron equipped with given function, such as Euclidean distance from root neuron. These barcodes can converted into matrices persistence images, which then averaged across groups. We show that when defining function path length root, both equivalent. further images...