A5011542402- Trace Elements in Health
- Neuroinflammation and Neurodegeneration Mechanisms
- Alzheimer's disease research and treatments
- Heavy Metal Exposure and Toxicity
- Neurological Disease Mechanisms and Treatments
- Neurogenesis and neuroplasticity mechanisms
- Cholinesterase and Neurodegenerative Diseases
- Axon Guidance and Neuronal Signaling
- Mitochondrial Function and Pathology
- Neurological Disorders and Treatments
- Prion Diseases and Protein Misfolding
- Neuroscience and Neuropharmacology Research
- Immune Response and Inflammation
- Cellular Mechanics and Interactions
- Selenium in Biological Systems
- Exercise and Physiological Responses
- Traumatic Brain Injury and Neurovascular Disturbances
- Iron Metabolism and Disorders
- RNA Research and Splicing
- Liver Disease Diagnosis and Treatment
- Nerve injury and regeneration
- Adipokines, Inflammation, and Metabolic Diseases
- Receptor Mechanisms and Signaling
- Ion channel regulation and function
- Protein Kinase Regulation and GTPase Signaling
Universitat de Barcelona
2018-2024
Biomedical Research Networking Center on Neurodegenerative Diseases
2021-2024
Instituto de Salud Carlos III
2021-2024
Centro de Investigación Biomédica en Red
2021-2023
Columbia University
2022
Universitat Autònoma de Barcelona
2006-2020
Center of Regenerative Medicine in Barcelona
2020
University of Edinburgh
2014-2017
Centre de Recerca Matemàtica
2014
The brain’s white matter is highly vulnerable to reductions in cerebral blood flow via mechanisms that may involve elevated microgliosis and pro-inflammatory pathways. In the present study, effects of severe hypoperfusion were investigated on function inflammation. Male C57Bl/6J mice underwent bilateral common carotid artery stenosis was assessed at seven days with electrophysiology response evoked compound action potentials (CAPs) corpus callosum. peak latency CAPs axonal refractoriness...
Chronic cerebral hypoperfusion is a key mechanism associated with white matter disruption in vascular disease and dementia. In mouse model relevant to studying disease, we have previously shown that disrupts axon-glial integrity the distribution of paranodal internodal proteins subcortical myelinated axons. This axons accompanied by increased microglia cognitive decline. The aim present study was investigate whether impairs functional matter, its relation microglial number, targeting these...
Abstract Chronic cerebral hypoperfusion is a major cause of age-related vascular cognitive impairment. A well-characterised mouse model has shown that results in gliovascular and white matter damage impaired spatial working memory. In this study, we assessed whether cilostazol, phosphodiesterase III inhibitor, could protect against these changes. Adult, male C57Bl/6J mice were subjected to bilateral common carotid artery stenosis or sham operation fed normal cilostazol diet for three months....
The extracellular protein Reelin, expressed by Cajal-Retzius (CR) cells at early stages of cortical development and late GABAergic interneurons, regulates radial migration the "inside-out" pattern positioning. Current models Reelin functions in corticogenesis focus on CR cell-derived layer I. However, developmental disorders linked to deficits, such as schizophrenia autism, are related interneuron-derived although its role has not been established. Here we selectively inactivated Reln gene...
Chronic cerebral hypoperfusion, a sustained modest reduction in blood flow, is associated with damage to myelinated axons and cognitive decline ageing. Oligodendrocytes (the myelin producing cells) their precursor cells (OPCs) may be vulnerable the effects of hypoperfusion some forms injury OPCs have potential respond repair by increased proliferation differentiation. Using mouse model we characterised acute long term responses oligodendrocytes corpus callosum. Following 3 days numbers...
Organization of microtubules into ordered arrays is best understood in mitotic systems, but remains poorly characterized postmitotic cells such as neurons. By analyzing the cycling cell microtubule cytoskeleton proteome through expression profiling and targeted RNAi screening for candidates with roles neurons, we have identified kinase NEK7. We show that NEK7 regulates dendrite morphogenesis vitro vivo. activity required growth branching, well spine formation morphology. these processes part...
Mitochondrial dynamics and trafficking are essential to provide the energy required for neurotransmission neural activity. We investigated how G protein-coupled receptors (GPCRs) proteins control mitochondrial trafficking. The activation of Gα
Alzheimer's disease (AD) is a neurological of confusing causation with no cure or prevention available. The definitive diagnosis made postmortem, in part through the presence amyloid-beta plaques brain tissue, which can be done small molecule thioflavin-T (ThT). Plaques are also found to contain elevated amounts metal ions Cu(ii) and Zn(ii) that contribute neurotoxicity (Aβ). In this paper, we report silico, vitro, ex vivo studies ThT-derived binders 2-(2-hydroxyphenyl)benzoxazole (HBX),...
In addition to neuronal migration, brain development, and adult plasticity, the extracellular matrix protein Reelin has been extensively implicated in human psychiatric disorders such as schizophrenia, bipolar disorder, autism spectrum disorder. Moreover, heterozygous reeler mice exhibit features reminiscent of these disorders, while overexpression protects against its manifestation. However, how influences structure circuits striatal complex, a key region for above-mentioned is far from...
Alzheimer's disease (AD) is the most commonly diagnosed dementia, where signs of neuroinflammation and oxidative stress are prominent. In this study we intend to further characterize roles antioxidant, anti-inflammatory, heavy metal binding protein, metallothionein-1 (MT-1), by cross ing Mt1 overexpressing mice with a well-known mouse model AD, Tg2576 mice, which express human amyloid-β protein precursor (hAβPP) Swedish K670N/M671L mutations. overexpression increased overall perinatal...
Abstract Cytokines, such as tumour necrosis factor (TNF)‐α and lymphotoxin‐α, have been described widely to play important roles in the brain physiologic conditions after traumatic injury. However, exact mechanisms involved their function not fully elucidated. We give some insight on role by using animals lacking either Type 1 receptor (TNFR1KO) or 2 (TNFR2KO) controls (C57Bl/6). Both TNFR1KO a greater extent TNFR2KO mice showed increased exploration/activity neurobehavioral traits hole...
ARMCX3 is encoded by a member of the Armcx gene family and known to be involved in nervous system development function. We found that markedly upregulated mouse liver response high lipid availability, hepatic patients with NAFLD hepatocellular carcinoma (HCC). Mice were subjected invalidation (inducible knockout) then exposed high-fat diet diethylnitrosamine-induced hepatocarcinogenesis. The effects experimental knockdown or overexpression HCC cell lines also analyzed. protected mice against...
The role of metals in the pathophysiology Alzheimer′s disease (AD) has gained considerable support recent years, with both vitro and vivo data demonstrating that a mis‐metabolism metal ions, such as copper zinc, may affect various cellular cascades ultimately leads to development and/or potentiation AD. In this paper, we will provide an overview preclinical clinical literature specifically relates attempts AD cascade by modulation brain levels. We also detail our own novel animal data, where...
The mouse model of Alzheimer’s disease (AD), Tg2576 mice (APP), has provided valuable information, such as the role metallothionein (MT) family in their behavioral and amyloidosis phenotypes. In this study, we further characterize MT-1 by crossing Mt1-overexpressing with (APPTgMT). 14-month-old mice, MT-1(/2) protein levels were dramatically increased Mt1 overexpression throughout cortex (Cx), which showed a prominent caudal-rostral gradient, hippocampus (HC). There was trend for...
Abstract Traumatic injury to the brain is one of leading causes injury‐related death or disability, but current therapies are limited. Previously it has been shown that antioxidant proteins metallothioneins (MTs) potent neuroprotective factors in animal models injury. The exogenous administration MTs effects consistent with roles proposed from studies knock‐out mice. We herewith report results comparing full mouse MT‐1 independent α and β domains, alone together, a cryoinjury model. lesion...
Abstract Cryolesion of the frontoparietal cortex in mice is a well‐described brain injury paradigm that results increased astrogliosis surrounding lesion site and accompanied by prominent increase MAO‐B levels astrocytes. Whether these contribute to cellular damage or modulate reactive astrocytosis remains unclear. activity may damage, since its metabolism products are highly toxic cells. Additionally, it has been suggested inhibition regulate astrocytic reaction. In this study, we have...
Abstract In addition to neuronal migration, brain development and adult plasticity, the extracellular matrix protein Reelin has been extensively implicated in human psychiatric disorders such as schizophrenia, bipolar disorder autistic spectrum disorder. Moreover, heterozygous reeler mice exhibit features reminiscent of these disorders, while overexpression protects against its manifestation. However, how influences structure circuits striatal complex, a key region for above-mentioned is far...
Chronic cerebral hypoperfusion contributes to age-related cognitive decline and dementia such as Alzheimer's disease. The causative link is not yet defined but proposed involve damage the brain's white matter mediated by oxidative stress inflammation. Dimethyl fumarate (DMF) an anti-inflammatory drug which acts in part activating Nrf2-signalling, a master regulator of anti-oxidant pathways. In present study, effects severe DMF administration were investigated on function Male C57Bl/6J mice...