Sara Bachiller

@us.es

Department of Medical Biochemistry, Molecular Biology, and Immunology. School of Medicine
University of Seville

Sara Bachiller


         Download Compact PDF  
https://researchid.co/sbachiller
28

Scopus Publications

Scopus Publications

  • Plasmacytoid and CD141+ Myeloid Dendritic Cells Cooperation with CD8+ T Cells in Lymph Nodes is Associated with HIV Control
    Joana Vitallé, Sara Bachiller, Beatriz Dominguez‐Molina, Eirini Moysi, Sara Ferrando‐Martínez, María Inés Camacho‐Sojo, Isabel Gallego, Alberto Pérez‐Gómez, María Reyes Jiménez‐Leon, Carmen Gasca‐Capote, Francisco José Ostos, Mohammed Rafii‐El‐Idrissi Benhnia, Laura E. Via, Antonio Mochón, Luis Fernando López‐Cortes, Constantinos Petrovas, Richard A. Koup, Ezequiel Ruiz‐Mateos
    Medcomm, 2025
    Dendritic cells (DC) are known to modulate antiviral immune responses; however, the knowledge about the role of different DC subsets in antiviral T cell priming in human tissues remains uncompleted. In the context of HIV infection, we determined the phenotype and location of plasmacytoid and CD141+ myeloid DCs (pDCs and mDCs) in lymph nodes of people living with HIV (PLWH). We found an interaction between pDCs and CD141+ mDCs with CD8+ T cells, being associated with participants’ viral levels in blood and tissue. Moreover, we demonstrated a higher and more polyfunctional superantigen‐ and HIV‐specific CD8+ T cell response after the coculture with Toll‐like receptor (TLR)‐primed pDCs and CD141+ mDCs. Last, we showed the potential of programmed cell death‐1 (PD‐1) blocking using pembrolizumab to further increase antigen‐specific CD8+ T cell response along with TLR agonists. Therefore, these results showed a cooperation between pDCs, CD141+ mDCs and CD8+ T cells in lymph nodes of PLWH, which is associated with higher HIV control, highlighting the importance of DC subsets crosstalk to achieve a more potent anti‐HIV response and support the use of DC‐based immunotherapies for HIV control.
  • HERC1 E3 Ubiquitin Ligase Is Necessary for Autophagy Processes and for the Maintenance and Homeostasis of Vesicles in Motor Nerve Terminals, but Not for Proteasomal Activity
    Miguel Ángel Pérez-Castro, Francisco Hernández-Rasco, Isabel María Alonso-Bellido, María S. Letrán-Sánchez, Eva María Pérez-Villegas, Joana Vitallé, Luis Miguel Real, Ezequiel Ruiz-Mateos, José Luis Venero, Lucía Tabares, Ángel Manuel Carrión, José Ángel Armengol, Sara Bachiller, Rocío Ruiz
    International Journal of Molecular Sciences, 2025
    The ubiquitin proteasome system (UPS) is implicated in protein homeostasis. One of the proteins involved in this system is HERC1 E3 ubiquitin ligase, which was associated with several processes including the normal development and neurotransmission at the neuromuscular junction (NMJ), autophagy in projection neurons, myelination of the peripheral nervous system, among others. The tambaleante (tbl) mouse model carries the spontaneous mutation Gly483Glu substitution in the HERC1 E3 protein. Using this model, we analyzed the implication of HERC1 E3 ubiquitin ligase in the activity of UPS, autophagy, and synaptic homeostasis in brain and muscle tissues. Regarding UPS, no differences were found in its activity nor in the specific gene expression in both brain and muscle tissues from tbl compared with the control littermates. Furthermore, the use of the specific UPS inhibitor (MG-132), did not alter the evoked neurotransmitter release in the levator auris longus (LAL) muscle. Interestingly, the expression of the autophagy-related gene p62 was significantly increased in the muscle of tbl compared to the control littermates. Indeed, impaired evoked neurotransmitter release was observed with the autophagy inhibitor Wortmannin. Finally, altered levels of Clathrin and Synaptophysin were detected in muscle tissues. Altogether, our findings show that HERC1 E3 ubiquitin ligase mutation found in tbl mice alters autophagy and vesicular recycling without affecting proteasomal function.
  • SARS-CoV-2 post-acute sequelae linked to inflammation via extracellular vesicles
    Sara Bachiller, Joana Vitallé, Lluís Camprubí-Ferrer, Manuel García, Isabel Gallego, Marina López-García, María Isabel Galvá, Julio Cañizares, Inmaculada Rivas-Jeremías, María Díaz-Mateos, Carmen Gasca-Capote, Cristina Moral-Turón, Lourdes Galán-Villamor, María Fontillón, Salvador Sobrino, José Miguel Cisneros, Luis Fernando López-Cortés, Tomas Deierborg, Ezequiel Ruiz-Mateos
    Frontiers in Immunology, 2025
    BackgroundDespite the efficacy of SARS-CoV-2 vaccines in reducing mortality and severe cases of COVID-19, a proportion of survivors experience long-term symptoms, known as post-acute sequelae of SARS-CoV-2 infection (PASC). This study investigates the long-term immunological and neurodegenerative effects associated with extracellular vesicles (EVs) in COVID-19 survivors, 15 months after SARS-CoV-2 infection.Methods13 Controls and 20 COVID-19 survivors, 15 months after SARS-CoV-2 infection, were recruited. Pro-inflammatory cytokines were analyzed in both plasma and EVs. A deep-immunophenotyping of monocytes, T-cells and dendritic cells (DCs) was performed, along with immunostainings of SARS-CoV-2 in the colon.ResultsHigher concentrations of pro-inflammatory cytokines and neurofilaments were found in EVs but not in plasma from COVID-19 survivors. Additionally, COVID-19 participants exhibited altered monocyte activation markers and elevated cytokine production upon lipopolysaccharide stimulation. Increased activation markers in CD4+ T-cells and decreased indoleamine 2,3-dioxygenase expression in DCs were observed in COVID-19 participants. Furthermore, the amount of plasmacytoid DCs expressing β7-integrin were higher in COVID-19, potentially associated with the viral persistence observed in the colon.ConclusionsCOVID-19 survivors exhibit long-term immune dysregulation and neurodegeneration, emphasizing the need for ongoing monitoring of PASC. The cargo of EVs can be a promising tool for early detection of virus-induced neurological disorders.
  • Vedolizumab and ART in recent HIV-1 infection unveil the role of α4β7 in reservoir size
    Maria Reyes Jimenez-Leon, Carmen Gasca-Capote, Cristina Roca-Oporto, Nuria Espinosa, Salvador Sobrino, Maria Fontillon-Alberdi, Ce Gao, Isabelle Roseto, Gregory Gladkov, Inmaculada Rivas-Jeremias, Karin Neukam, Jose German Sanchez-Hernandez, Raul Rigo-Bonnin, Antonio J. Cervera-Barajas, Rosario Mesones, Federico García, Ana Isabel Alvarez-Rios, Sara Bachiller, Joana Vitalle, Alberto Perez-Gomez, María Inés Camacho-Sojo, Isabel Gallego, Christian Brander, Ian McGowan, Beatriz Mothe, Pompeyo Viciana, Xu Yu, Mathias Lichterfeld, Luis F. Lopez-Cortes, Ezequiel Ruiz-Mateos
    Jci Insight, 2024
    BACKGROUND We evaluated the safety and viral rebound, after analytical treatment interruption (ATI), of vedolizumab and ART in recent HIV-1 infection. We used this model to analyze the effect of α4β7 on the HIV-1 reservoir size. METHODS Participants started ART with monthly vedolizumab infusions, and ATI was performed at week 24. Biopsies were obtained from ileum and cecum at baseline and week 24. Vedolizumab levels, HIV-1 reservoir, flow cytometry, and cell-sorting and antibody competition experiments were assayed. RESULTS Vedolizumab was safe and well tolerated. No participant achieved undetectable viremia off ART 24 weeks after ATI. Only a modest effect on the time to achieve more than 1,000 HIV-1 RNA copies/mL and the proportion of participants off ART was observed, being higher in the vedolizumab group compared with historical controls. Just before ATI, α4β7 expression was associated with HIV-1 DNA and RNA in peripheral blood and with PD1 and TIGIT levels. Importantly, a complete blocking of α4β7 was observed on peripheral CD4+ T cells but not in gut (ileum and cecum), where α4β7 blockade and vedolizumab levels were inversely associated with HIV-1 DNA. CONCLUSION Our findings support α4β7 as an important determinant in HIV-1 reservoir size, suggesting the complete α4β7 blockade in tissue as a promising tool for HIV-cure combination strategies. TRIAL REGISTRATION ClinicalTrials.gov NCT03577782. FUNDING This work was supported by the Instituto de Salud Carlos III (Fondo Europeo de Desarrollo Regional, “a way to make Europe,” research contracts FI17/00186 and FI19/00083 and research projects PI18/01532, PI19/01127, PI22/01796), Conserjería de Economía, Conocimiento, Empresas y Universidad, Junta de Andalucía (research projects P20/00906), the Red Temática de Investigación Cooperativa en SIDA (RD16/0025/0020), and the Spanish National Research Council.
  • Dopaminergic neurons lacking Caspase-3 avoid apoptosis but undergo necrosis after MPTP treatment inducing a Galectin-3-dependent selective microglial phagocytic response
    Juan García-Revilla, Rocío Ruiz, Ana M. Espinosa-Oliva, Marti Santiago, Irene García-Domínguez, Lluís Camprubí-Ferrer, Sara Bachiller, Tomas Deierborg, Bertrand Joseph, Rocío M. de Pablos, José A. Rodríguez-Gómez, José Luis Venero
    Cell Death and Disease, 2024
    Parkinson’s Disease (PD) is a progressive neurodegenerative disorder characterized by the loss of dopaminergic neurons in the Substantia nigra pars compacta (SNpc). Apoptosis is thought to play a critical role in the progression of PD, and thus understanding the effects of antiapoptotic strategies is crucial for developing potential therapies. In this study, we developed a unique genetic model to selectively delete Casp3, the gene encoding the apoptotic protein caspase-3, in dopaminergic neurons (TH-C3KO) and investigated its effects in response to a subacute regime of 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP) administration, which is known to trigger apoptotic loss of SNpc dopaminergic neurons. We found that Casp3 deletion did not protect the dopaminergic system in the long term. Instead, we observed a switch in the cell death pathway from apoptosis in wild-type mice to necrosis in TH-C3KO mice. Notably, we did not find any evidence of necroptosis in our model or in in vitro experiments using primary dopaminergic cultures exposed to 1-methyl-4-phenylpyridinium in the presence of pan-caspase/caspase-8 inhibitors. Furthermore, we detected an exacerbated microglial response in the ventral mesencephalon of TH-C3KO mice in response to MPTP, which mimicked the microglia neurodegenerative phenotype (MGnD). Under these conditions, it was evident the presence of numerous microglial phagocytic cups wrapping around apparently viable dopaminergic cell bodies that were inherently associated with galectin-3 expression. We provide evidence that microglia exhibit phagocytic activity towards both dead and stressed viable dopaminergic neurons through a galectin-3-dependent mechanism. Overall, our findings suggest that inhibiting apoptosis is not a beneficial strategy for treating PD. Instead, targeting galectin-3 and modulating microglial response may be more promising approaches for slowing PD progression.
  • Biocompatible metal-organic frameworks as promising platforms to eradicate HIV reservoirs ex vivo in people living with HIV
    José A. Lebrón, Francisco J. Ostos, Marta Martínez-Santa, Francisco García-Moscoso, Manuel López-López, María L. Moyá, Eva Bernal, Sara Bachiller, Gabriel González-Ulloa, David Rodríguez-Lucena, Tania Lopes-Costa, Rut Fernández-Torres, Ezequiel Ruiz-Mateos, José M. Pedrosa, Mohammed Rafii-El-Idrissi Benhnia, Pilar López-Cornejo
    Journal of Materials Chemistry B, 2024
    The HIV attacks the immune system provoking an infection that is considered a global health challenge.
  • The HIV-1 reservoir landscape in persistent elite controllers and transient elite controllers
    Carmen Gasca-Capote, Xiaodong Lian, Ce Gao, Isabelle C. Roseto, María Reyes Jiménez-León, Gregory Gladkov, María Inés Camacho-Sojo, Alberto Pérez-Gómez, Isabel Gallego, Luis E. Lopez-Cortes, Sara Bachiller, Joana Vitalle, Mohamed Rafii-El-Idrissi Benhnia, Francisco J. Ostos, Antonio R. Collado-Romacho, Jesús Santos, Rosario Palacios, Cristina Gomez-Ayerbe, Leopoldo Muñoz-Medina, Andrés Ruiz-Sancho, Mario Frias, Antonio Rivero-Juarez, Cristina Roca-Oporto, Carmen Hidalgo-Tenorio, Anna Rull, Julian Olalla, Miguel A. Lopez-Ruz, Francesc Vidal, Consuelo Viladés, Andrea Mastrangelo, Matthias Cavassini, Nuria Espinosa, Matthieu Perreau, Joaquin Peraire, Antonio Rivero, Luis F. López-Cortes, Mathias Lichterfeld, Xu G. Yu, Ezequiel Ruiz-Mateos
    Journal of Clinical Investigation, 2024
    BACKGROUND Persistent controllers (PC) maintain antiretroviral-free HIV-1 control indefinitely over time while transient controllers (TC) eventually lose virological control. It is essential to characterize the quality of the HIV reservoir of these phenotypes to identify the factors that lead to HIV progression and to open new avenues in HIV cure strategies. METHODS The characterization of HIV-1 reservoir, from peripheral blood mononuclear cells, was performed using next-generation sequencing techniques, such as full-length individual and matched integration site proviral sequencing (FLIP-seq; MIP-seq). RESULTS PC and TC before losing virological control, presented significantly lower total, intact and defective proviruses compared to participants on antiretroviral therapy (ART). No differences were found in total and defective proviruses between PC and TC. However, intact provirus levels were lower in PC compared to TC, being the intact/defective HIV-DNA ratio significantly higher in TC. Clonally expanded intact proviruses were found only in PC and located in centromeric satellite DNA or zinc-finger genes, both associated with heterochromatin features. In contrast, sampled intact proviruses were located in permissive genic euchromatic positions in TC. CONCLUSIONS These results suggest the need for, and can give guidance to the design of, future research to identify a distinct proviral landscape that may be associated with the persistent control of HIV-1 without ART. FUNDING Instituto de Salud Carlos III (FI17/00186, FI19/00083, MV20/00057 PI18/01532, PI19/01127 and PI22/01796), Consejería de Economía, Conocimiento, Empresas y Universidad, Junta de Andalucía (PI20/1276), Gilead Fellowships (GLD22/00147) and I+D+iFEDER Andalucía 2014-2020 (US-1380938).
  • Targeting galectin-3 to counteract spike-phase uncoupling of fast-spiking interneurons to gamma oscillations in Alzheimer’s disease
    Luis Enrique Arroyo-García, Sara Bachiller, Rocío Ruiz, Antonio Boza-Serrano, Antonio Rodríguez-Moreno, Tomas Deierborg, Yuniesky Andrade-Talavera, André Fisahn
    Translational Neurodegeneration, 2023
    Background Alzheimer’s disease (AD) is a progressive multifaceted neurodegenerative disorder for which no disease-modifying treatment exists. Neuroinflammation is central to the pathology progression, with evidence suggesting that microglia-released galectin-3 (gal3) plays a pivotal role by amplifying neuroinflammation in AD. However, the possible involvement of gal3 in the disruption of neuronal network oscillations typical of AD remains unknown. Methods Here, we investigated the functional implications of gal3 signaling on experimentally induced gamma oscillations ex vivo (20–80 Hz) by performing electrophysiological recordings in the hippocampal CA3 area of wild-type (WT) mice and of the 5×FAD mouse model of AD. In addition, the recorded slices from WT mice under acute gal3 application were analyzed with RT-qPCR to detect expression of some neuroinflammation-related genes, and amyloid-β (Aβ) plaque load was quantified by immunostaining in the CA3 area of 6-month-old 5×FAD mice with or without Gal3 knockout (KO). Results Gal3 application decreased gamma oscillation power and rhythmicity in an activity-dependent manner, which was accompanied by impairment of cellular dynamics in fast-spiking interneurons (FSNs) and pyramidal cells. We found that the gal3-induced disruption was mediated by the gal3 carbohydrate-recognition domain and prevented by the gal3 inhibitor TD139, which also prevented Aβ42-induced degradation of gamma oscillations. Furthermore, the 5×FAD mice lacking gal3 (5×FAD-Gal3KO) exhibited WT-like gamma network dynamics and decreased Aβ plaque load. Conclusions We report for the first time that gal3 impairs neuronal network dynamics by spike-phase uncoupling of FSNs, inducing a network performance collapse. Moreover, our findings suggest gal3 inhibition as a potential therapeutic strategy to counteract the neuronal network instability typical of AD and other neurological disorders encompassing neuroinflammation and cognitive decline.
  • Maternal separation differentially modulates early pathology by sex in 5xFAD Alzheimer's disease-transgenic mice
    M.G. Garcia, A. Paulus, S. Vázquez-Reyes, O. Klementieva, G.K. Gouras, S. Bachiller, T. Deierborg
    Brain Behavior and Immunity Health, 2023
    Alzheimer’s disease (AD) is the most common neurodegenerative disease. Most cases of AD are considered idiopathic and likely due to a combination of genetic, environmental, and lifestyle-related risk factors. Despite occurring decades before the typical age of an AD diagnosis, early-life stress (ELS) has been suggested to have long-lasting effects that may contribute to AD risk and pathogenesis. Still, the mechanisms that underlie the role of ELS on AD risk remain largely unknown. Here, we used 5xFAD transgenic mice to study relatively short-term alterations related to ELS in an AD-like susceptible mouse model at 6 weeks of age. To model ELS, we separated pups from their dams for 3 h per day from postnatal day 2–14. Around 6 weeks of age, we found that maternally separated (MS) 5xFAD mice, particularly female mice, displayed increased amyloid-β-immunoreactivity in the anterior cingulate cortex (ACC) and basolateral amygdala (BLA). In anterior cingulate cortex, we also noted significantly increased intraneuronal amyloid-β-immunoreactivity associated with MS but only in female mice. Moreover, IBA1-positive DAPI density was significantly increased in relation to MS in ACC and BLA, and microglia in BLA of MS mice had significantly different morphology compared to microglia in non-MS 5xFAD mice. Cytokine analysis showed that male MS mice, specifically, had increased levels of neuroinflammatory markers CXCL1 and IL-10 in hippocampal extracts compared to non-MS counterparts. Additionally, hippocampal extracts from both male and female MS 5xFAD mice had decreased levels of synapse- and activity-related markers Bdnf, 5htr6, Cox2, and Syp in hippocampus. Lastly, we performed behavioral tests to evaluate anxiety- and depressive-like behavior and working memory but could not detect any significant differences between groups. Overall, we detected several sex-specific molecular and cellular alterations in 6-week-old adolescent 5xFAD mice associated with MS that may help explain the connection between ELS and AD risk.
  • LPS priming before plaque deposition impedes microglial activation and restrains Aβ pathology in the 5xFAD mouse model of Alzheimer's disease
    Yiyi Yang, Marta García-Cruzado, Hairuo Zeng, Lluís Camprubí-Ferrer, Bazhena Bahatyrevich-Kharitonik, Sara Bachiller, Tomas Deierborg
    Brain Behavior and Immunity, 2023
    Microglia have an innate immunity memory (IIM) with divergent functions in different animal models of neurodegenerative diseases, including Alzheimer’s disease (AD). AD is characterized by chronic neuroinflammation, neurodegeneration, tau tangles and β-amyloid (Aβ) deposition. Systemic inflammation has been implicated in contributing to the progression of AD. Multiple reports have demonstrated unique microglial signatures in AD mouse models and patients. However, the proteomic profiles of microglia modified by IIM have not been well-documented in an AD model. Therefore, in the present study, we investigate whether lipopolysaccharide (LPS)-induced IIM in the pre-clinical stage of AD alters the microglial responses and shapes the neuropathology. We accomplished this by priming 5xFAD and wild-type (WT) mice with an LPS injection at 6 weeks (before the robust development of plaques). 140 days later, we evaluated microglial morphology, activation, the microglial barrier around Aβ, and Aβ deposition in both 5xFAD primed and unprimed mice. Priming induced decreased soma size of microglia and reduced colocalization of PSD95 and Synaptophysin in the retrosplenial cortex. Priming appeared to increase phagocytosis of Aβ, resulting in fewer Thioflavin S+ Aβ fibrils in the dentate gyrus. RIPA-soluble Aβ 40 and 42 were significantly reduced in Primed-5xFAD mice leading to a smaller size of MOAB2+ Aβ plaques in the prefrontal cortex. We also found that Aβ-associated microglia in the Primed-5xFAD mice were less activated and fewer in number. After priming, we also observed improved memory performance in 5xFAD. To further elucidate the molecular mechanism underlying these changes, we performed quantitative proteomic analysis of microglia and bone marrow monocytes. A specific pattern in the microglial proteome was revealed in primed 5xFAD mice. These results suggest that the imprint signatures of primed microglia display a distinctive phenotype and highlight the potential for a beneficial adaption of microglia when intervention occurs in the pre-clinical stage of AD.
  • Microglial Caspase-3 is essential for modulating hippocampal neurogenesis
    Isabel M. Alonso Bellido, Mercedes Posada-Pérez, Francisco Hernández-Rasco, Sandra Vázquez-Reyes, María Cabanillas, Antonio J. Herrera, Sara Bachiller, Jesús Soldán-Hidalgo, Ana M. Espinosa-Oliva, Bertrand Joseph, Rocío M. de Pablos, José L. Venero, Rocío Ruiz
    Brain Behavior and Immunity, 2023
  • A metagenome-wide association study of HIV disease progression in HIV controllers
    Luis Miguel Real, María E. Sáez, Anais Corma-Gómez, Antonio Gonzalez-Pérez, Christian Thorball, Rocío Ruiz, María Reyes Jimenez-Leon, Alejandro Gonzalez-Serna, Carmen Gasca-Capote, María José Bravo, José Luis Royo, Alberto Perez-Gomez, María Inés Camacho-Sojo, Isabel Gallego, Joana Vitalle, Sara Bachiller, Alicia Gutierrez-Valencia, Francisco Vidal, Jacques Fellay, Mathias Lichterfeld, Ezequiel Ruiz-Mateos
    Iscience, 2023
  • Toll-like receptor agonists enhance HIV-specific T cell response mediated by plasmacytoid dendritic cells in diverse HIV-1 disease progression phenotypes
    Maria R. Jimenez-Leon, Carmen Gasca-Capote, Laura Tarancon-Diez, Beatriz Dominguez-Molina, Macarena Lopez-Verdugo, Ryan Ritraj, Isabel Gallego, Ana I. Alvarez-Rios, Joana Vitalle, Sara Bachiller, María Inés Camacho-Sojo, Alberto Perez-Gomez, Nuria Espinosa, Cristina Roca-Oporto, Mohamed Rafii-El-Idrissi Benhnia, Alicia Gutierrez-Valencia, Luis F. Lopez-Cortes, Ezequiel Ruiz-Mateos
    Ebiomedicine, 2023
  • The HERC proteins and the nervous system
    Eva M. Pérez-Villegas, Rocío Ruiz, Sara Bachiller, Francesc Ventura, Jose A. Armengol, Jose Luis Rosa
    Seminars in Cell and Developmental Biology, 2022
  • Early-life stress elicits peripheral and brain immune activation differently in wild type and 5xFAD mice in a sex-specific manner
    S. Bachiller, I. Hidalgo, M. G. Garcia, A. Boza-Serrano, A. Paulus, Q. Denis, C. Haikal, O. Manouchehrian, O. Klementieva, J. Y. Li, C. J. Pronk, G. K. Gouras, T. Deierborg
    Journal of Neuroinflammation, 2022
  • Immune defects associated with lower SARS-CoV-2 BNT162b2 mRNA vaccine response in aged people
    Joana Vitallé, Alberto Pérez-Gómez, Francisco José Ostos, Carmen Gasca-Capote, María Reyes Jiménez-León, Sara Bachiller, Inmaculada Rivas-Jeremías, Maria del Mar Silva-Sánchez, Anabel M. Ruiz-Mateos, María Ángeles Martín-Sánchez, Luis Fernando López-Cortes, Mohammed Rafii-El-Idrissi Benhnia, Ezequiel Ruiz-Mateos
    Jci Insight, 2022
  • Acute systemic LPS-exposure impairs perivascular CSF distribution in mice
    Oscar Manouchehrian, Marta Ramos, Sara Bachiller, Iben Lundgaard, Tomas Deierborg
    Journal of Neuroinflammation, 2021
  • The effect of electroconvulsive therapy on neuroinflammation, behavior and amyloid plaques in the 5xFAD mouse model of Alzheimer’s disease
    Martina Svensson, Gustaf Olsson, Yiyi Yang, Sara Bachiller, Maria Ekemohn, Joakim Ekstrand, Tomas Deierborg
    Scientific Reports, 2021
  • The Other Side of SARS-CoV-2 Infection: Neurological Sequelae in Patients
    Isabel M. Alonso-Bellido, Sara Bachiller, Guillermo Vázquez, Luis Cruz-Hernández, Emilio Martínez, Ezequiel Ruiz-Mateos, Tomas Deierborg, José L. Venero, Luis M. Real, Rocío Ruiz
    Frontiers in Aging Neuroscience, 2021
  • Amyloid structural changes studied by infrared microspectroscopy in bigenic cellular models of alzheimer’s disease
    Agnes Paulus, Anders Engdahl, Yiyi Yang, Antonio Boza-Serrano, Sara Bachiller, Laura Torres-Garcia, Alexander Svanbergsson, Megg G. Garcia, Gunnar K. Gouras, Jia-Yi Li, Tomas Deierborg, Oxana Klementieva
    International Journal of Molecular Sciences, 2021
  • Maternal separation leads to regional hippocampal microglial activation and alters the behavior in the adolescence in a sex-specific manner
    S. Bachiller, A. Paulus, S. Vázquez-Reyes, I. García-Domínguez, T. Deierborg
    Brain Behavior and Immunity Health, 2020
  • The ubiquitin proteasome system in neuromuscular disorders: Moving beyond movement
    Sara Bachiller, Isabel M. Alonso-Bellido, Luis Miguel Real, Eva María Pérez-Villegas, José Luis Venero, Tomas Deierborg, José Ángel Armengol, Rocío Ruiz
    International Journal of Molecular Sciences, 2020
  • Microglia in neurological diseases: A road map to brain-disease dependent-inflammatory response
    Sara Bachiller, Itzia Jiménez-Ferrer, Agnes Paulus, Yiyi Yang, Maria Swanberg, Tomas Deierborg, Antonio Boza-Serrano
    Frontiers in Cellular Neuroscience, 2018
  • HERC1 Ubiquitin Ligase Is Required for Normal Axonal Myelination in the Peripheral Nervous System
    Sara Bachiller, María Angustias Roca-Ceballos, Irene García-Domínguez, Eva María Pérez-Villegas, David Martos-Carmona, Miguel Ángel Pérez-Castro, Luis Miguel Real, José Luis Rosa, Lucía Tabares, José Luis Venero, José Ángel Armengol, Ángel Manuel Carrión, Rocío Ruiz
    Molecular Neurobiology, 2018
  • Bidirectional Microglia–Neuron Communication in Health and Disease
    Zsuzsanna Szepesi, Oscar Manouchehrian, Sara Bachiller, Tomas Deierborg
    Frontiers in Cellular Neuroscience, 2018
  • L1 retrotransposition alters the hippocampal genomic landscape enabling memory formation
    Sara Bachiller, Yaiza del-Pozo-Martín, Ángel Manuel Carrión
    Brain Behavior and Immunity, 2017
  • HERC 1 ubiquitin ligase mutation affects neocortical, CA3 hippocampal and spinal cord projection neurons: An ultrastructural study
    Rocío Ruiz, Eva María Pérez-Villegas, Sara Bachiller, José Luis Rosa, José Angel Armengol
    Frontiers in Neuroanatomy, 2016
  • The HERC1 E3 Ubiquitin Ligase is essential for normal development and for neurotransmission at the mouse neuromuscular junction
    S. Bachiller, T. Rybkina, E. Porras-García, E. Pérez-Villegas, L. Tabares, J. A. Armengol, A. M. Carrión, R. Ruiz
    Cellular and Molecular Life Sciences, 2015