Person: Cuartero Desviat, María Isabel
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First Name
María Isabel
Last Name
Cuartero Desviat
Affiliation
Universidad Complutense de Madrid
Faculty / Institute
Medicina
Department
Farmacología y Toxicología
Area
Farmacología
Identifiers
6 results
Search Results
Now showing 1 - 6 of 6
- Project number: PIMCD271/23-24
Item Charlas de investigación como vehículo para la integración de conceptos y la mejora del aprendizaje en ciencias de la salud(2024) Del Campo Milán, Lara; Castañer de Diego, Margarita; Cuartero Desviat, María Isabel; García Culebras, Alicia; García del Villar, Silvia; Gómez Del Moral Martín-Consuegra, Manuel María; López Gómez, Ana; Lozano Pérez, María Encarnación; Moraga Yébenes, Ana; Peña Martínez, Carolina Belén; Rodrigues Díez, Raúl; Vázquez Reyes, Sandra; Sánchez Álvarez, Miguel; Del Campo Milán, Lara Item Myeloid cells in vascular dementia and Alzheimer's disease: Possible therapeutic targets?(British Journal of Pharmacology, 2023) García Culebras, Alicia; Cuartero Desviat, María Isabel; Peña Martínez, Carolina Belén; Moraga Yébenes, Ana; Vázquez Reyes, Sandra; De Castro Millán, Francisco Javier; Cortes Canteli, Marta; Lizasoaín Hernández, Ignacio; Moro Sánchez, María ÁngelesGrowing evidence supports the suggestion that the peripheral immune system plays a role in different pathologies associated with cognitive impairment, such as vascular dementia (VD) or Alzheimer's disease (AD). The aim of this review is to summarize, within the peripheral immune system, the implications of different types of myeloid cells in AD and VD, with a special focus on post-stroke cognitive impairment and dementia (PSCID). We will review the contributions of the myeloid lineage, from peripheral cells (neutrophils, platelets, monocytes and monocyte-derived macrophages) to central nervous system (CNS)-associated cells (perivascular macrophages and microglia). Finally, we will evaluate different potential strategies for pharmacological modulation of pathological processes mediated by myeloid cell subsets, with an emphasis on neutrophils, their interaction with platelets and the process of immunothrombosis that triggers neutrophil-dependent capillary stall and hypoperfusion, as possible effector mechanisms that may pave the way to novel therapeutic avenues to stop dementia, the epidemic of our time.Item Ipsilesional Hippocampal Gaba is elevated and correlates with cognitive impairment and maladaptive neurogenesis after cortical stroke in mice(stroke, 2023) Cuartero Desviat, María Isabel; García Culebras, Alicia; Parra Gonzalo, Juan De La; Fernández Valle, María Encarnación; Benito, Marina; Vázquez Reyes, Sandra; Jareño Flores, Tania; Castro Millán, Francisco Javier de; Hurtado Moreno, Olivia; Buckwalter, Marion S.; García Segura, Juan Manuel; Lizasoaín Hernández, Ignacio; Moro Sánchez, María ÁngelesCognitive dysfunction is a frequent stroke sequela but its pathogenesis and treatment remain unresolved. Involvement of aberrant hippocampal neurogenesis and maladaptive circuitry remodelling has been proposed but their mechanisms are unknown. Our aim was to evaluate potential underlying molecular/cellular events implicated. Stroke was induced by permanent occlusion of the middle cerebral artery (MCAO) in 2-month-old C57BL/6 male mice. Hippocampal metabolites/neurotransmitters were analysed longitudinally by magnetic resonance spectroscopy (MRS). Cognitive function was evaluated with the contextual fear conditioning test. Microglia, astrocytes, neuroblasts and interneurons were analysed by immunofluorescence. Approximately 50% of mice exhibited progressive post-MCAO cognitive impairment. Notably, immature hippocampal neurons in the impaired group displayed more severe aberrant phenotypes than those from the non-impaired group. Using MRS, significant bilateral changes in hippocampal metabolites such as or N-acetylaspartic acid (NAA) were found that correlated, respectively, with numbers of glia and immature neuroblasts in the ischemic group. Importantly, some metabolites were specifically altered in the ipsilateral hippocampus suggesting its involvement in aberrant neurogenesis and remodelling processes. Specifically, MCAO animals with higher hippocampal GABA levels displayed worse cognitive outcome. Implication of GABA in this setting was supported by the amelioration of ischemia-induced memory deficits and aberrant hippocampal neurogenesis after blocking pharmacologically GABAergic neurotransmission. These data suggest that GABA exerts its detrimental effect, at least partly, by affecting morphology and integration of newborn neurons into the hippocampal circuits. Hippocampal GABAergic neurotransmission could be considered a novel diagnostic and therapeutic target for post-stroke cognitive impairment.Item Post-stroke Neurogenesis: Friend or Foe?(Frontiers in Cell and Developmental Biology, 2021) Cuartero Desviat, María Isabel; García Culebras, Alicia; Torres López, Cristina; Medina, Violeta ; Fraga, Enrique ; Vázquez-Reyes, Sandra ; Jareño-Flores, Tania; García Segura, Juan Manuel; Lizasoaín Hernández, Ignacio; Moro Sánchez, María ÁngelesThe substantial clinical burden and disability after stroke injury urges the need to explore therapeutic solutions. Recent compelling evidence supports that neurogenesis persists in the adult mammalian brain and is amenable to regulation in both physiological and pathological situations. Its ability to generate new neurons implies a potential to contribute to recovery after brain injury. However, post-stroke neurogenic response may have different functional consequences. On the one hand, the capacity of newborn neurons to replenish the damaged tissue may be limited. In addition, aberrant forms of neurogenesis have been identified in several insult settings. All these data suggest that adult neurogenesis is at a crossroads between the physiological and the pathological regulation of the neurological function in the injured central nervous system (CNS). Given the complexity of the CNS together with its interaction with the periphery, we ultimately lack in-depth understanding of the key cell types, cell–cell interactions, and molecular pathways involved in the neurogenic response after brain damage and their positive or otherwise deleterious impact. Here we will review the evidence on the stroke-induced neurogenic response and on its potential repercussions on functional outcome. First, we will briefly describe subventricular zone (SVZ) neurogenesis after stroke beside the main evidence supporting its positive role on functional restoration after stroke. Then, we will focus on hippocampal subgranular zone (SGZ) neurogenesis due to the relevance of hippocampus in cognitive functions; we will outline compelling evidence that supports that, after stroke, SGZ neurogenesis may adopt a maladaptive plasticity response further contributing to the development of post-stroke cognitive impairment and dementia. Finally, we will discuss the therapeutic potential of specific steps in the neurogenic cascade that might ameliorate brain malfunctioning and the development of post-stroke cognitive impairment in the chronic phase.Item Defective hippocampal neurogenesis underlies cognitive impairment by carotid stenosis-induced cerebral hypoperfusion in mice(Front. Cell. Neurosci., 2023) Fraga, Enrique; Medina, Violeta; Cuartero Desviat, María Isabel; García Culebras, Alicia; Bravo Ferrer, Isabel; Hernández Jiménez, Macarena; García Segura, Juan Manuel; Hurtado Moreno, Olivia; Pradillo Justo, Jesús Miguel; Lizasoaín Hernández, Ignacio; Moro Sánchez, María ÁngelesChronic cerebral hypoperfusion due to carotid artery stenosis is a major cause of vascular cognitive impairment and dementia (VCID). Bilateral carotid artery stenosis (BCAS) in rodents is a well-established model of VCID where most studies have focused on white matter pathology and subsequent cognitive deficit. Therefore, our aim was to study the implication of adult hippocampal neurogenesis in hypoperfusion-induced VCID in mice, and its relationship with cognitive hippocampal deficits. Mice were subjected to BCAS; 1 and 3 months later, hippocampal memory and neurogenesis/cell death were assessed, respectively, by the novel object location (NOL) and spontaneous alternation performance (SAP) tests and by immunohistology. Hypoperfusion was assessed by arterial spin labeling-magnetic resonance imaging (ASL-MRI). Hypoperfused mice displayed spatial memory deficits with decreased NOL recognition index. Along with the cognitive deficit, a reduced number of newborn neurons and their aberrant morphology indicated a remarkable impairment of the hippocampal neurogenesis. Both increased cell death in the subgranular zone (SGZ) and reduced neuroblast proliferation rate may account for newborn neurons number reduction. Our data demonstrate quantitative and qualitative impairment of adult hippocampal neurogenesis disturbances associated with cerebral hypoperfusion-cognitive deficits in mice. These findings pave the way for novel diagnostic and therapeutic targets for VCID.Item The role of gut microbiota in cerebrovascular disease and related dementia(British Journal of Pharmacology, 2023) Cuartero Desviat, María Isabel; García Culebras, Alicia; Nieto Vaquero, Carmen; Fraga, Enrique; Torres López, Cristina; Pradillo Justo, Jesús Miguel; Lizasoaín Hernández, Ignacio; Moro Sánchez, María ÁngelesIn recent years, increasing evidence suggests that commensal microbiota may play an important role not only in health but also in disease including cerebrovascular disease. Gut microbes impact physiology, at least in part, by metabolizing dietary factors and host-derived substrates and then generating active compounds including toxins. The purpose of this current review is to highlight the complex interplay between microbiota, their metabolites. and essential functions for human health, ranging from regulation of the metabolism and the immune system to modulation of brain development and function. We discuss the role of gut dysbiosis in cerebrovascular disease, specifically in acute and chronic stroke phases, and the possible implication of intestinal microbiota in post-stroke cognitive impairment and dementia, and we identify potential therapeutic opportunities of targeting microbiota in this context.