A5021418181- Neuroscience and Neuropharmacology Research
- Alzheimer's disease research and treatments
- Receptor Mechanisms and Signaling
- Cell death mechanisms and regulation
- Polyamine Metabolism and Applications
- Neuroinflammation and Neurodegeneration Mechanisms
- Neurogenesis and neuroplasticity mechanisms
- Memory and Neural Mechanisms
- Nuclear Receptors and Signaling
- Ion channel regulation and function
- Amino Acid Enzymes and Metabolism
- Mast cells and histamine
- Autophagy in Disease and Therapy
- Parkinson's Disease Mechanisms and Treatments
- Cellular transport and secretion
- Biochemical effects in animals
- Mitochondrial Function and Pathology
- Retinoids in leukemia and cellular processes
- Chemical Synthesis and Analysis
- Lipid Membrane Structure and Behavior
- Genetics and Neurodevelopmental Disorders
- Neurotransmitter Receptor Influence on Behavior
- Adipose Tissue and Metabolism
- Retinal Development and Disorders
- Metabolism and Genetic Disorders
Universitat Autònoma de Barcelona
2014-2025
Biomedical Research Networking Center on Neurodegenerative Diseases
2014-2025
Albert Einstein College of Medicine
2019-2024
Instituto de Salud Carlos III
2023
Achucarro Basque Center for Neuroscience
2015
University of the Basque Country
2015
Czech Academy of Sciences, Institute of Experimental Medicine
2008-2011
Centro de Investigación Biomédica en Red
2007-2011
The Open University
2003-2010
University of Manchester
2006-2008
Disturbance of calcium homeostasis and accumulation misfolded proteins in the endoplasmic reticulum (ER) are considered contributory components cell death after ischemia. However, signal-transducing events that activated by ER stress cerebral ischemia incompletely understood. In this study, we show caspase-12 PERK IRE pathways following oxygen-glucose deprivation (OGD) mixed cortical cultures or neonatal hypoxia–ischemia (HI). Activation led to a transient phosphorylation eIF2α, an increase...
Several evidences suggest that failure of synaptic function occurs at preclinical stages Alzheimer's disease (AD) preceding neuronal loss and the classical AD pathological hallmarks. Nowadays, there is an urgent need to identify reliable biomarkers could be obtained with non-invasive methods improve diagnosis early stages. Here, we have examined plasma levels a group miRNAs related proteins in cohort composed cognitive healthy controls (HC), mild impairment (MCI) subjects.Plasma brain were...
Activity-dependent gene expression mediating changes of synaptic efficacy is important for memory storage, but the mechanisms underlying transcriptional in age-related disorders are poorly understood. In this study, we report that transcription mediated by cAMP-response element binding protein (CREB)-regulated coactivator CRTC1 impaired neurons and brain from an Alzheimer9s disease (AD) transgenic mouse expressing human β-amyloid precursor (APP<sub>Sw,Ind</sub>). Suppression CRTC1-dependent...
Abstract Electron microscopic immunocytochemical methods were used to determine the localization, subcellular distribution and expression of activity‐regulated cytoskeletal protein (Arc/Arg3.1) in dentate gyrus after unilateral induction long‐term potentiation (LTP) perforant pathway anaesthetized rats. At 2 h post‐induction, immunoreaction product was visible both granule cell molecular layers. Arc higher potentiated than unstimulated contralateral hemisphere. Single‐section electron...
Epidemiological studies indicate that intellectual activity prevents or delays the onset of Alzheimer's disease (AD). Similarly, cognitive stimulation using environmental enrichment (EE), which increases adult neurogenesis and functional integration newborn neurons into neural circuits hippocampus, protects against memory decline in transgenic mouse models AD, but mechanisms involved are poorly understood. To study therapeutic benefits AD we examined effects EE hippocampal a model expressing...
β-Amyloid (Aβ), a peptide generated from the amyloid precursor protein, is widely believed to underlie pathophysiology of Alzheimer disease (AD). Emerging evidences suggest that soluble Aβ oligomers adversely affect synaptic function, leading cognitive failure associated with AD. The Aβ-induced dysfunction has been attributed removal α-amino-3-hydroxy-5-methylisoxazole-4-propionic acid (AMPA) receptors (AMPARs). However, molecular mechanisms underlying loss AMPAR induced by at synapses are...
Cognitive decline is associated with gene expression changes in the brain, but transcriptional mechanisms underlying memory impairments cognitive disorders, such as Alzheimer's disease (AD), are largely unknown. Here, we aimed to elucidate relevant responsible for early loss AD by examining pathological, behavioral, and transcriptomic control mutant β-amyloid precursor protein (APP Sw,Ind ) transgenic mice during aging. Genome-wide transcriptome analysis using mouse microarrays revealed...
Abstract Examination of the morphological correlates long‐term potentiation (LTP) in hippocampus requires analysis both presynaptic and postsynaptic elements. However, ultrastructural measurements synapses dendritic spines following LTP induced via tetanic stimulation presents difficulty that not all examined are necessarily activated. To overcome this limitation, to ensure a very large proportion have been potentiated, we acute hippocampal slices adult mice by addition tetraethylammonium...
Death receptors (DRs) and their ligands are expressed in developing nervous system. However, neurons generally resistant to death induction through DRs rather activation promotes neuronal outgrowth branching. These results suppose the existence of antagonists Fas apoptosis inhibitory molecule (FAIM S ) was first identified as a antagonist B-cells. Soon after, longer alternative spliced isoform with unknown function named FAIM L . is widely expressed, including system, we have shown...
Synapse-to-nucleus signaling regulates activity-dependent synaptic plasticity underlying memory by linking N-methyl-D-aspartate (NMDA) glutamate receptors (GluN) to gene transcription mediated the factor cAMP-response element binding protein (CREB), but programs mediating potentiation at excitatory synapses are unknown. Here, we analyzed genome-wide chromatin immunoprecipitation sequencing (ChIP-seq) datasets of mouse and human CREB synaptonuclear CREB-regulated coactivator1 (CRTC1) identify...
Alzheimer's disease (AD) is characterized by memory loss and neuropsychiatric symptoms associated with cerebral amyloid-β (Aβ) tau pathologies, but whether how these factors differentially disrupt neural circuits remains unclear. Here, we investigated the vulnerability of emotional to Aβ pathologies in mice expressing mutant human amyloid precursor protein (APP), Tau or both APP/Tau excitatory neurons. develop age- sex-dependent phosphorylated latter exacerbated at early stages, vulnerable...
Dysfunction of the vascular system contributes to brain damage and neurodegeneration, cerebral amyloid angiopathy (CAA) can be identified in a high percentage Alzheimer disease (AD) brains. Blood-brain barrier (BBB) alterations affect communication signalling between neurovascular unit (NVU) components through changes release angioneurins, among others. The two-hit hypothesis AD suggests that chronic risk factors cause an early microvasculature (hit 1) triggering cascade events leads...
Abstract The gyrus dentatus is one of the few areas brain that continues to produce neurons after birth. newborn cells differentiate into granule which project axons their postsynaptic targets. This step accompanied by transient expression polysialylated isoforms neuronal cell adhesion molecules (PSA‐NCAM) developing neurons. Glucocorticoid hormones have been shown inhibit neurogenesis. We noted a functional correlation between PSA‐NCAM and glucocorticoid action manipulation corticosterone...