Alfonsa Zamora‐Moratalla

ORCID: 0000-0002-1870-1003
Publications
Citations
Views
---
Saved
---
About
Contact & Profiles
Research Areas
  • Neuroscience and Neuropharmacology Research
  • Genetic Neurodegenerative Diseases
  • Memory and Neural Mechanisms
  • Neurogenesis and neuroplasticity mechanisms
  • Neurological disorders and treatments
  • Neuroendocrine regulation and behavior
  • Nerve injury and regeneration
  • RNA modifications and cancer
  • Down syndrome and intellectual disability research
  • Cancer-related molecular mechanisms research
  • Zebrafish Biomedical Research Applications
  • Autism Spectrum Disorder Research
  • Neural dynamics and brain function
  • Thyroid Disorders and Treatments
  • Spaceflight effects on biology
  • RNA Research and Splicing
  • Cellular Mechanics and Interactions
  • Sirtuins and Resveratrol in Medicine
  • Congenital heart defects research
  • Advanced Materials and Mechanics
  • Birth, Development, and Health
  • Stress Responses and Cortisol
  • Advanced Fluorescence Microscopy Techniques
  • Digestive system and related health
  • Ion channel regulation and function

Centre for Genomic Regulation
2021-2024

Barcelona Institute for Science and Technology
2023

Instituto Cajal
2019-2020

Consejo Superior de Investigaciones Científicas
2020

Université Laval
2018

University of Castilla-La Mancha
2013-2016

Synaptic Research (United States)
2014

Learning and memory deficits are early clinical manifestations of Huntington's disease (HD). These cognitive impairments have been mainly associated with frontostriatal HD pathology; however, compelling evidence provided by several murine models suggests that the hippocampus may contribute to synaptic dysfunction in HD. The neurotrophin receptor p75(NTR) negatively regulates spine density, which is learning memory; therefore, we explored whether disturbed function could Here, determined...

10.1172/jci74809 article EN Journal of Clinical Investigation 2014-09-01

Cognitive dysfunction is an early clinical hallmark of Huntington's disease (HD) preceding the appearance motor symptoms by several years. Neuronal and altered corticostriatal connectivity have been postulated to be fundamental explain these disturbances. However, no treatments attenuate cognitive changes successful: reason may rely on idea that temporal sequence pathological as critical per se when new therapies are in development. To this aim, it becomes use HD mouse models which...

10.1093/hmg/ddv426 article EN Human Molecular Genetics 2015-10-12

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

Abstract Actin cytoskeleton dynamics is critical for nervous system development and function, yet the role of alternative splicing in controlling these processes poorly understood. A highly conserved subset neuronal-specific microexons coordinates fundamental aspects biology. exons enriched genes involved actin cytoskeleton, their functions are unknown. Here, we focus on a microexon DAAM1, member formin-homology-2 (FH2) domain class proteins, which have diverse associated with reorganization...

10.1101/2023.01.12.523772 preprint EN cc-by-nc bioRxiv (Cold Spring Harbor Laboratory) 2023-01-12

Abstract Dynamic signaling between the endocrine system (ES) and nervous (NS) is essential for brain body homeostasis. In particular, reciprocal interaction occurs during pregnancy motherhood that may involve changes in some plasticity processes. Prolactin (PRL), a hormone with pleiotropic effects on NS, promotes maternal behavior has been linked to modifications circuits motherhood; however, it unclear whether PRL regulate synaptic plasticity. Therefore, main aim of present work was...

10.1002/hipo.23288 article EN cc-by-nc-nd Hippocampus 2020-12-07

Down syndrome (DS) stands as the prevalent genetic cause of intellectual disability, yet comprehensive understanding its cellular and molecular underpinnings remains limited. In this study, we explore landscape hippocampus in a DS mouse model through single-nuclei transcriptional profiling. Our findings demonstrate that trisomy manifests highly specific modification transcriptome within distinct cell types. Remarkably, observed significant shift transcriptomic profile granule cells dentate...

10.21203/rs.3.rs-3184329/v1 preprint EN cc-by Research Square (Research Square) 2023-09-25

Currently, molecular, electrophysiological and structural studies delineate several neural subtypes in the hippocampus. However, precise developmental mechanisms that lead to this diversity are still unknown. Here we show alterations a concrete hippocampal neuronal subpopulation during development specifically affect hippocampal-dependent spatial memory. We observed genetic deletion of transcription factor Helios mice, which is expressed developing calbindin-positive CA1 pyramidal neurons...

10.1016/j.expneurol.2019.113095 article EN cc-by-nc-nd Experimental Neurology 2019-11-08

One of the current challenges in field neurodevelopmental disorders (NDDs) is still to determine their underlying aetiology and risk factors. NDDs comprise a diverse group primarily related dysfunction including autism spectrum disorder (ASD), developmental delay, intellectual disability (ID), attention-deficit/hyperactivity (ADHD) that may present with certain degree cognitive high prevalence neuropsychiatric outcomes. Last year, advances human genomics have begun shed light on genetic...

10.17879/freeneuropathology-2021-3268 article EN DOAJ (DOAJ: Directory of Open Access Journals) 2021-01-01

Down syndrome (DS) is the most common genetic form of intellectual disability (ID). The cellular and molecular mechanisms contributing to ID in DS are not completely understood. Recent evidence indicates that a given memory encoded by sparsely distributed neurons, highly activated during learning, engram cells. Intriguingly, paramount importance for formation impaired DS. Here we explored mouse model, Ts65Dn found reduced number cells dentate gyrus (DG), suggesting neuronal allocation...

10.1101/2023.01.11.523460 preprint EN bioRxiv (Cold Spring Harbor Laboratory) 2023-01-11
Coming Soon ...