María‐Ángeles Arévalo

ORCID: 0000-0002-4303-9576
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About
Contact & Profiles
Research Areas
  • Estrogen and related hormone effects
  • Neuroinflammation and Neurodegeneration Mechanisms
  • Stress Responses and Cortisol
  • Menopause: Health Impacts and Treatments
  • Neurogenesis and neuroplasticity mechanisms
  • Genetic and Clinical Aspects of Sex Determination and Chromosomal Abnormalities
  • Neuroscience and Neuropharmacology Research
  • Hypothalamic control of reproductive hormones
  • Nerve injury and regeneration
  • Epigenetics and DNA Methylation
  • Alzheimer's disease research and treatments
  • Autophagy in Disease and Therapy
  • Nuclear Receptors and Signaling
  • Tryptophan and brain disorders
  • Mitochondrial Function and Pathology
  • Neuroendocrine regulation and behavior
  • MicroRNA in disease regulation
  • Neuropeptides and Animal Physiology
  • Sleep and Wakefulness Research
  • Sexual Differentiation and Disorders
  • Genetics and Neurodevelopmental Disorders
  • Adipose Tissue and Metabolism
  • Circadian rhythm and melatonin
  • S100 Proteins and Annexins
  • Growth Hormone and Insulin-like Growth Factors

Instituto Cajal
2016-2025

Instituto de Salud Carlos III
2017-2025

Centro de Investigación Biomédica en Red de Fragilidad y Envejecimiento Saludable
2017-2025

Consejo Superior de Investigaciones Científicas
2013-2023

Health Research Institute of the Balearic Islands
2023

Biomedical Research Networking Center on Neurodegenerative Diseases
2009

Unidades Centrales Científico-Técnicas
2009

Universidad de Salamanca
1993-2008

Charité - Universitätsmedizin Berlin
2006

Centro de Biología Molecular Severo Ochoa
1988-1989

Daniel J. Klionsky Amal Kamal Abdel‐Aziz Sara Abdelfatah Mahmoud Abdellatif Asghar Abdoli and 95 more Steffen Abel Hagai Abeliovich Marie H. Abildgaard Yakubu Princely Abudu Abraham Acevedo‐Arozena Iannis E. Adamopoulos Khosrow Adeli Timon E. Adolph Annagrazia Adornetto Elma Aflaki Galila Agam Anupam Agarwal Bharat B. Aggarwal Maria Agnello Patrizia Agostinis Javed N. Agrewala Alexander Agrotis Patricia V. Aguilar S. Tariq Ahmad Zubair M. Ahmed Ulises Ahumada-Castro Sonja Aits Shu Aizawa Yunus Akkoç Tonia Akoumianaki Hafize Aysin Akpinar Ahmed M. Al‐Abd Lina Al-Akra Abeer Gharaibeh Moulay A. Alaoui‐Jamali Simon Alberti Elísabet Alcocer‐Gómez Cristiano Alessandri Muhammad Ali Md. Abdul Alim Al‐Bari Saeb Aliwaini Javad Alizadeh Eugènia Almacellas Alexandru Almasan Alicia Alonso G. Alonso Nihal Altan‐Bonnet Dario C. Altieri Élida Álvarez Sara Alves Cristine Alvès da Costa Mazen M. Alzaharna Marialaura Amadio Consuelo Amantini Cristina Amaral Susanna Ambrosio Amal O. Amer Veena Ammanathan Zhenyi An Stig Uggerhøj Andersen Shaida A. Andrabi Magaiver Andrade-Silva Allen M. Andres Sabrina Angelini David K. Ann Uche C. Anozie Mohammad Y. Ansari Pedro Antas Adam Antebi Zuriñe Antón Tahira Anwar Lionel Apétoh Nadezda Apostolova Toshiyuki Araki Yasuhiro Araki Kohei Arasaki Wagner L. Araújo Jun Araya Catherine Arden María‐Ángeles Arévalo Sandro Argüelles Esperanza Arias Jyothi Arikkath Hirokazu Arimoto Aileen Ariosa Darius Armstrong‐James Laetitia Pelloquin Ángeles Aroca Daniela S. Arroyo Ivica Arsov Rubén Artero Dalia Maria Lucia Asaro Michael Aschner Milad Ashrafizadeh Osnat Ashur‐Fabian Atanas G. Atanasov Alicia K. Au Patrick Auberger Holger W. Auner Laure Aurelian

In 2008, we published the first set of guidelines for standardizing research in autophagy. Since then, this topic has received increasing attention, and many scientists have entered field. Our knowledge base relevant new technologies also been expanding. Thus, it is important to formulate on a regular basis updated monitoring autophagy different organisms. Despite numerous reviews, there continues be confusion regarding acceptable methods evaluate autophagy, especially multicellular...

10.1080/15548627.2020.1797280 article EN cc-by-nc-sa Autophagy 2021-01-02

Abstract Expression of proinflammatory molecules by glial cells is involved in the pathophysiological changes associated with chronic neurological diseases. Under pathological conditions, astrocytes release a number molecules, such as interleukin‐6 (IL‐6) and interferon‐γ‐inducible protein‐10 (IP‐10). The ovarian hormone estradiol exerts protective effects central nervous system that, at least part, may be mediated reduction local inflammation. This study was designed to assess whether...

10.1002/glia.20904 article EN Glia 2009-06-16

Several brain disorders associated with neuroinflammation show sex differences in their incidence, onset, progression and/or outcome. The different regulation of the neuroinflammatory response males and females could underlie these differences. In this study, we have explored whether reactive gliosis after a penetrating cortical injury exhibits Males presented higher density Iba1 immunoreactive cells proximity wound (0-220 μm) than females. This difference was due to number nonreactive...

10.1002/glia.22867 article EN Glia 2015-06-02

Abstract Sex differences in the incidence, clinical manifestation, disease course, and prognosis of neurological diseases, such as autism spectrum disorders or Alzheimer's disease, have been reported. Obesity has postulated a risk factor for cognitive decline and, during pregnancy, increases offspring. is associated with increased serum brain levels free fatty acids, palmitic acid, which activate microglial cells triggering potent inflammatory cascade. In this study, we determined effect...

10.1002/glia.23263 article EN Glia 2017-11-15

Neuroglobin (Ngb), so named after its initial discovery in brain neurones, has received great attention as a result of neuroprotective effects both vitro and vivo . Recently, we demonstrated that, Ngb is 17β‐oestradiol (E 2 ) inducible protein that pivotal for hormone‐induced anti‐apoptotic against H O toxicity. The involvement other cell populations, well E , completely unknown at present. We demonstrate immunoreactivity reactive astrocytes located the proximity penetrating cortical injury...

10.1111/jne.12007 article EN Journal of Neuroendocrinology 2012-11-29

Abstract Microglia dysfunction and activation are important hallmarks of the aging brain concomitant with age‐related neurodegeneration cognitive decline. Age‐associated changes in microglia migration phagocytic capacity result maladaptive responses, chronic neuroinflammation, worsened outcomes neurodegenerative disorders. Given sex bias incidence, prevalence, therapy response most neurological disorders, we have here examined whether activity aged is different males females. With this aim,...

10.1111/acel.13182 article EN cc-by Aging Cell 2020-07-29

In the nervous system, Notch pathway has a prominent role in control of neuronal morphology and determination astrocyte fate. However, morphological plasticity is unknown. Here, we have explored activity on reactivity primary astrocytes response to LPS, an inflammatory stimulus. We found that LPS induces reactive by inhibition signaling via NFκB activation Jagged upregulation. contrast, IGF-1, anti-inflammatory molecule, inhibits LPS-induced phenotype enhancing through MAPK. Therefore,...

10.1038/s41420-019-0166-6 article EN cc-by Cell Death Discovery 2019-04-03

Insulin-like growth factor-I (IGF-I) signaling plays a key role in neuroinflammation. Here we show that IGF-1 also regulates phagocytosis of reactive astrocytes through p110α isoform phosphatidylinositol 3-kinase (PI3K), differentially both sexes. Systemic bacterial lipopolysaccharide (LPS)-treatment increased the expression GFAP, astrocyte marker, cortex mice sexes and was blocked by only males. In primary astrocytes, LPS enhanced mRNA Toll-like receptors (TLR2,4) proinflammatory factors:...

10.1002/glia.24163 article EN Glia 2022-02-17

The developmental regulation of insulin-like growth factor I (IGF-I), its receptor, and binding proteins (IGFBPs) was studied in the rat cerebellum. All components IGF-I system were detectable cerebellum at least by embryonic day 19. Levels receptor mRNA highest perinatal ages steadily decrease thereafter, although a partial recovery found adults. also peaked early ages, immunoreactive showed second peak during adulthood. Finally, levels IGFBPs postnatal abruptly decreased thereafter to...

10.1002/jnr.490390202 article EN Journal of Neuroscience Research 1994-10-01

Abstract We have previously shown that dendrite morphology of cultured hippocampal neurones is controlled by Notch receptor activation or binding nerve growth factor (NGF) to its low affinity p75 NTR , i.e. processes up‐regulate the expression Homologue enhancer split 1 and 5 . Thus, increased these genes decreases number dendrites, whereas abrogation 1/5 activity stimulates outgrowth new dendrites. Here, we show Neurogenin 3 a proneural gene negatively regulated It also influences...

10.1111/j.1471-4159.2006.03783.x article EN Journal of Neurochemistry 2006-03-15

Although discovered in 2000, neuroglobin (Ngb) functions are still uncertain. A contribution to the role played by Ngb neurons could certainly derive from identification of endogenous modulators. Here, we evaluate possibility that be regulated 17β-estradiol (E2) signaling both SK-N-BE human neuroblastoma cell line and mouse hippocampal neurons. 1 nM E2 rapidly induced a 300% increase levels models. The effect was specific, being not testosterone or dihydrotestosterone. E2-induced requires...

10.1159/000323906 article EN Neurosignals 2010-01-01
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