A5063244086- Genetic Neurodegenerative Diseases
- Neuroscience and Neuropharmacology Research
- Neurological disorders and treatments
- Neuroinflammation and Neurodegeneration Mechanisms
- Mitochondrial Function and Pathology
- Cell Image Analysis Techniques
- Neuroscience and Neural Engineering
- Alzheimer's disease research and treatments
- RNA Interference and Gene Delivery
- Pluripotent Stem Cells Research
- Nicotinic Acetylcholine Receptors Study
- Immune cells in cancer
- Inflammation biomarkers and pathways
- Gut microbiota and health
- Nanoplatforms for cancer theranostics
- Lipid Membrane Structure and Behavior
- Neurogenesis and neuroplasticity mechanisms
- Cardiac electrophysiology and arrhythmias
- Ion channel regulation and function
- Epigenetics and DNA Methylation
- Sphingolipid Metabolism and Signaling
- Connective tissue disorders research
- Medicinal Plants and Bioactive Compounds
- Medicinal Plants and Neuroprotection
- S100 Proteins and Annexins
University of Antwerp
2019-2024
Universitat de Barcelona
2014-2022
Departament de Salut
2020
Biomedical Research Networking Center on Neurodegenerative Diseases
2014-2020
Consorci Institut D'Investigacions Biomediques August Pi I Sunyer
2014-2020
Huntington's disease (HD) is a hereditary neurodegenerative disorder characterized by motor and cognitive impairments, involving striatum, cortex hippocampus. Synaptic memory dysfunction in HD mouse models have been related to low levels of brain-derived neurotrophic factor (BDNF) imbalance between TrkB p75NTR receptors. In addition, astrocyte over-activation has also suggested contribute deficits. Fingolimod (FTY720), modulator sphingosine-1 phosphate (S1P) receptors, shown increase BDNF...
See Brouillet and Merienne (doi:10.1093/brain/awz274) for a scientific commentary on this article. Creus-Muncunill et al. report that protein translation is altered in the striatum of Huntington’s disease mouse models, with upregulated expression proteins from ribosomal oxidative phosphorylation pathways. Pharmacological normalization R6/1 mice ameliorates motor disturbances normalizes content striatum.
Epidemiologic associations and preclinical studies suggest that amyloid pathology observed in the brain may be preceded by gastrointestinal amyloidosis.We identify a pathogenic program becomes activated enteric nervous system after exposure to bacterial amyloids, show serum A3 is an important self-amplifying mediator of this proinflammatory response.responsible for SAA3 production, attenuated curli-and recombinant SAA3-induced Saa3 up-regulation, DNA damage, replication glia.CONCLUSIONS: Our...
Huntington's disease (HD) is a fatal neurodegenerative with motor, cognitive and psychiatric impairment. Dysfunctions in HD models have been related to reduced levels of striatal brain-derived neurotrophic factor (BDNF) imbalance between its receptors TrkB p75(NTR). Thus, molecules activity on the BDNF/TrkB/p75 system can therapeutic potential. 7,8-Dihydroxyflavone (7,8-DHF) was described as agonist several neuro-degenerative diseases, however, activation profile needs further investigation...
Huntington’s disease (HD) is a neurological disorder characterized by motor disturbances. HD pathology most prominent in the striatum, central hub of basal ganglia. The cerebral cortex main striatal afferent, and progressive cortico-striatal disconnection characterizes HD. We mapped network dysfunction mice to ultimately modulate activity specific circuit ameliorate symptoms recover synaptic plasticity. Multimodal MRI vivo indicates thalamo-striatal functional deficits reduced...
Microglia, the main resident immune cells in CNS, are thought to participate pathogenesis of various neurological disorders. LPS and + IFNγ stimuli that widely used activate microglia. However, transcriptomic profiles microglia treated with have not been properly compared. Here, we murine primary microglial cultures or for 6 hours then performed RNA-Sequencing. Gene expression patterns induced by treatments were obtained WGCNA 11 different found, showing differential responses many genes....
Most neurological disorders display impaired synaptic connectivity. Hence, modulation of synapse formation may have therapeutic relevance. However, the high density and small size synapses complicate their quantification. To improve synapse-oriented screens, we analyzed labeling performance synapse-targeting antibodies on neuronal cell cultures using segmentation-independent image analysis based sliding window correlation. When assessing pairwise colocalization, a common readout for mature...
CCAAT/enhancer binding protein β (C/EBPβ) is a transcription factor that regulates the expression of important pro-inflammatory genes in microglia. Mice deficient for C/EBPβ show protection against excitotoxic and ischemic CNS damage, but involvement this neuroprotective effect various C/EBPβ-expressing cell types not solved. Since C/EBPβ-deficient microglia attenuated neurotoxicity culture, we hypothesized specific deficiency could be vivo. In study, have tested hypothesis by generating...
Therapeutic developments for neurodegenerative disorders are redirecting their focus to the mechanisms that contribute neuronal connectivity and loss thereof. Using a high-throughput microscopy pipeline integrates morphological functional measurements, we found inhibition of dual leucine zipper kinase (DLK) increased in primary cortical cultures. This neuroprotective effect was not only observed basal conditions but also cultures depleted from antioxidants which microtubule stability...
Here, we unravel the mechanism of action Ikaros family zinc finger protein Helios (He) during development striatal medium spiny neurons (MSNs). He regulates second wave neurogenesis involved in generation striatopallidal neurons, which express dopamine 2 receptor and enkephalin. To exert this effect, is expressed neural progenitor cells (NPCs) keeping them G1/G0 phase cell cycle. Thus, a lack results an increase S-phase entry length NPCs, turn impairs produces accumulation number cycling...
A systematic characterization of the spatio-temporal gene expression during human neurodevelopment is essential to understand brain function in both physiological and pathological conditions. In recent years, stem cell technology has provided an vitro tool recapitulate development, permitting also generation models for many diseases. The correct differentiation pluripotent (hPSC) into specific types should be evaluated by comparison with cells/tissue profiles from equivalent adult vivo...
Abstract Background Network alterations underlying neurodegenerative diseases often precede symptoms and functional deficits. Thus, their early identification is central for improved prognosis. In Huntington’s disease (HD), the cortico-striatal networks, involved in motor function processing, are most compromised neural substrate. However, whether network intrinsic of striatum or cortex not fully understood. Results order to identify HD deficits, we characterized neuronal ensemble calcium...
Kv7 channels determine the resting membrane potential of neurons and regulate their excitability. Even though dysfunction has been linked to several debilitating childhood neuronal disorders, ontogeny constituent genes, which encode (KNCQ), expression subunits have largely unexplored. Here, we show that developmentally regulated specific KCNQ mRNA channel in mouse human striatum is crucial functional maturation striatal human-induced pluripotent stem cell-derived neurons. This demonstrates...
Abstract Vapor nanobubble (VNB) photoporation is a physical method for intracellular delivery that has gained significant interest in the past decade. It successfully been used to introduce molecular cargo of diverse nature into different cell types with high throughput and minimal cytotoxicity. For translational purposes, it important understand whether how affects homeostasis. To obtain comprehensive view on transcriptional rewiring takes place after VNB photoporation, we performed...
Abstract Huntington’s disease (HD) is a neurological disorder characterized by motor disturbances. HD pathology most prominent in the striatum, central hub of basal ganglia. The cortex main striatal afference and progressive cortico-striatal disconnection characterizes HD. We mapped dysfunction mice to ultimately modulate activity selected circuits ameliorate symptoms recover synaptic plasticity. Multimodal MRI vivo suggested functional network deficits fronto-striatal compared...