Cristina Lao‐Peregrín

ORCID: 0000-0002-3733-195X
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About
Contact & Profiles
Research Areas
  • Neuroscience and Neuropharmacology Research
  • Nerve injury and regeneration
  • Receptor Mechanisms and Signaling
  • Cell Image Analysis Techniques
  • Retinal Development and Disorders
  • Nicotinic Acetylcholine Receptors Study
  • Neurological disorders and treatments
  • Virus-based gene therapy research
  • Down syndrome and intellectual disability research
  • Genetic Neurodegenerative Diseases
  • Neuroinflammation and Neurodegeneration Mechanisms
  • Lipid Membrane Structure and Behavior
  • Autism Spectrum Disorder Research
  • Neurogenesis and neuroplasticity mechanisms
  • Advanced Fluorescence Microscopy Techniques
  • Sirtuins and Resveratrol in Medicine
  • Epilepsy research and treatment
  • Genetics and Neurodevelopmental Disorders

Cornell University
2015-2023

Weill Cornell Medicine
2023

New York Proton Center
2023

University of Castilla-La Mancha
2009-2016

Wellcome/MRC Cambridge Stem Cell Institute
2015

Medical Research Council
2015

University of Cambridge
2015

Myelin regeneration can occur spontaneously in demyelinating diseases such as multiple sclerosis (MS). However, the underlying mechanisms and causes of its frequent failure remain incompletely understood. Here we show, using an in-vivo remyelination model, that demyelinated axons are electrically active generate de novo synapses with recruited oligodendrocyte progenitor cells (OPCs), which, early after lesion induction, sense neuronal activity by expressing AMPA...

10.1038/ncomms9518 article EN cc-by Nature Communications 2015-10-06

Although ubiquitous in biological studies, the enhanced green and yellow fluorescent proteins (EGFP EYFP) were not specifically optimized for neuroscience, their underwhelming brightness slow expression brain tissue limits fidelity of dendritic spine analysis other indispensable techniques studying neurodevelopment plasticity. We hypothesized that EGFP's low solubility mammalian systems must limit total fluorescence output whole cells, improving folding efficiency could therefore translate...

10.1073/pnas.2000942117 article EN cc-by-nc-nd Proceedings of the National Academy of Sciences 2020-11-18

Brain-Derived Neurotrophic Factor (BDNF) is the main candidate for neuroprotective therapy Huntington's disease (HD), but its conditional administration one of most challenging problems.Here we used transgenic mice that over-express BDNF under control Glial Fibrillary Acidic Protein (GFAP) promoter (pGFAP-BDNF mice) to test whether up-regulation and release BDNF, dependent on astrogliosis, could be protective in HD. Thus, cross-mated pGFAP-BDNF with R6/2 generate a double-mutant mouse mutant...

10.1186/1750-1326-6-71 article EN cc-by Molecular Neurodegeneration 2011-10-10

Abstract Caffeine has cognitive‐enhancing properties with effects on learning and memory, concentration, arousal mood. These imply changes at circuital synaptic level, but the mechanism by which caffeine modifies plasticity remains elusive. Here we report that caffeine, concentrations representing moderate to high levels of consumption in humans, induces an NMDA receptor‐independent form LTP ( CAF LTP) CA1 region hippocampus promoting calcium‐dependent secretion BDNF, subsequently activates...

10.1111/adb.12433 article EN cc-by Addiction Biology 2016-07-25

In this study, we explore the antiepileptic effects of flufenamic acid (FFA) in order to identify cellular mechanisms that underlie potential anticonvulsant properties nonsteroidal antiinflammatory compound.The FFA action were analyzed using an vitro model which epileptiform activity was induced hippocampal slices by perfusion with 100 microm 4-aminopyridine (4-AP) added a modified Mg(2+)-free solution. The CA1 pyramidal neurons as well synaptic connection between CA3 and monitored...

10.1111/j.1528-1167.2009.02279.x article EN Epilepsia 2009-09-03

Cellular signaling involves a large repertoire of membrane receptors operating in overlapping spatiotemporal regimes and targeting many common intracellular effectors. However, both the molecular mechanisms physiological roles crosstalk between receptors, especially those from different superfamilies, are poorly understood. We find that receptor tyrosine kinase (RTK), TrkB, G protein-coupled (GPCR), metabotropic glutamate 5 (mGluR5), together mediate novel form hippocampal synaptic...

10.1101/2023.08.28.555210 preprint EN bioRxiv (Cold Spring Harbor Laboratory) 2023-08-28
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