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Item type:Publication, NTS-Polyplex: a potential nanocarrier for neurotrophic therapy of Parkinson's disease(2012) ;Daniel Martinez-Fong ;Michael J. Bannon ;Louis-Eric Trudeau ;Juan A. Gonzalez-BarriosMartha L. Arango-Rodriguez3Scopus© Citations 56 - Some of the metrics are blocked by yourconsent settings
Item type:Publication, Neonatal Mesenchymal Stem Cell Treatment Improves Myelination Impaired by Global Perinatal Asphyxia in Rats(2021) ;Andrea Tapia-Bustos ;Carolyne Lespay-Rebolledo ;Valentina Vío ;Ronald Pérez-LobosEmmanuel Casanova-Ortiz<jats:p>The effect of perinatal asphyxia (PA) on oligodendrocyte (OL), neuroinflammation, and cell viability was evaluated in telencephalon of rats at postnatal day (P)1, 7, and 14, a period characterized by a spur of neuronal networking, evaluating the effect of mesenchymal stem cell (MSCs)-treatment. The issue was investigated with a rat model of global PA, mimicking a clinical risk occurring under labor. PA was induced by immersing fetus-containing uterine horns into a water bath for 21 min (AS), using sibling-caesarean-delivered fetuses (CS) as controls. Two hours after delivery, AS and CS neonates were injected with either 5 μL of vehicle (10% plasma) or 5 × 104 MSCs into the lateral ventricle. Samples were assayed for myelin-basic protein (MBP) levels; Olig-1/Olig-2 transcriptional factors; Gglial phenotype; neuroinflammation, and delayed cell death. The main effects were observed at P7, including: (i) A decrease of MBP-immunoreactivity in external capsule, corpus callosum, cingulum, but not in fimbriae of hippocampus; (ii) an increase of Olig-1-mRNA levels; (iii) an increase of IL-6-mRNA, but not in protein levels; (iv) an increase in cell death, including OLs; and (v) MSCs treatment prevented the effect of PA on myelination, OLs number, and cell death. The present findings show that PA induces regional- and developmental-dependent changes on myelination and OLs maturation. Neonatal MSCs treatment improves survival of mature OLs and myelination in telencephalic white matter.</jats:p>Scopus© Citations 7 2 - Some of the metrics are blocked by yourconsent settings
Item type:Publication, Scopus© Citations 8 10 - Some of the metrics are blocked by yourconsent settings
Item type:Publication, Small molecules to perform big roles: The search for Parkinson's and Huntington's disease therapeutics(2023) ;Rodrigo Pérez-Arancibia ;Marisol Cisternas-Olmedo ;Denisse Sepúlveda ;Paulina Troncoso-EscuderoRene L. Vidal<jats:p>Neurological motor disorders (NMDs) such as Parkinson's disease and Huntington's disease are characterized by the accumulation and aggregation of misfolded proteins that trigger cell death of specific neuronal populations in the central nervous system. Differential neuronal loss initiates the impaired motor control and cognitive function in the affected patients. Although major advances have been carried out to understand the molecular basis of these diseases, to date there are no treatments that can prevent, cure, or significantly delay the progression of the disease. In this context, strategies such as gene editing, cellular therapy, among others, have gained attention as they effectively reduce the load of toxic protein aggregates in different models of neurodegeneration. Nevertheless, these strategies are expensive and difficult to deliver into the patients' nervous system. Thus, small molecules and natural products that reduce protein aggregation levels are highly sought after. Numerous drug discovery efforts have analyzed large libraries of synthetic compounds for the treatment of different NMDs, with a few candidates reaching clinical trials. Moreover, the recognition of new druggable targets for NMDs has allowed the discovery of new small molecules that have demonstrated their efficacy in pre-clinical studies. It is also important to recognize the contribution of natural products to the discovery of new candidates that can prevent or cure NMDs. Additionally, the repurposing of drugs for the treatment of NMDs has gained huge attention as they have already been through clinical trials confirming their safety in humans, which can accelerate the development of new treatment. In this review, we will focus on the new advances in the discovery of small molecules for the treatment of Parkinson's and Huntington's disease. We will begin by discussing the available pharmacological treatments to modulate the progression of neurodegeneration and to alleviate the motor symptoms in these diseases. Then, we will analyze those small molecules that have reached or are currently under clinical trials, including natural products and repurposed drugs.</jats:p>3Scopus© Citations 21 - Some of the metrics are blocked by yourconsent settings
Item type:Publication, Default Mode Network, Meditation, and Age-Associated Brain Changes: What Can We Learn from the Impact of Mental Training on Well-Being as a Psychotherapeutic Approach?(2019) ;Ricardo Ramírez-Barrantes ;Marcelo Arancibia ;Jana Stojanova; Claudio CórdovaAging is a physiological process accompanied by cognitive decline, principally in memory and executive functions. Alterations in the connectivity of the default mode network (DMN) have been found to participate in cognitive decline, as well as in several neurocognitive disorders. The DMN has antisynchronic activity with attentional networks (task-positive networks (TPN)), which are critical to executive function and memory. Findings pointing to the regulation of the DMN via activation of TPN suggest that it can be used as a strategy for neuroprotection. Meditation is a noninvasive and nonpharmacological technique proven to increase meta-awareness, a cognitive ability which involves the control of both networks. In this review, we discuss the possibility of facilitating healthy aging through the regulation of networks through meditation. We propose that by practicing specific types of meditation, cognitive decline could be slowed, promoting a healthy lifestyle, which may enhance the quality of life for the elderly.Scopus© Citations 38 1 - Some of the metrics are blocked by yourconsent settings
Item type:Publication, Intranasal Administration of Mesenchymal Stem Cell Secretome Reduces Hippocampal Oxidative Stress, Neuroinflammation and Cell Death, Improving the Behavioral Outcome Following Perinatal Asphyxia(2020) ;Nancy Farfán ;Jaime Carril ;Martina Redel ;Marta ZamoranoMaureen Araya<jats:p>Perinatal Asphyxia (PA) is a leading cause of motor and neuropsychiatric disability associated with sustained oxidative stress, neuroinflammation, and cell death, affecting brain development. Based on a rat model of global PA, we investigated the neuroprotective effect of intranasally administered secretome, derived from human adipose mesenchymal stem cells (MSC-S), preconditioned with either deferoxamine (an hypoxia-mimetic) or TNF-α+IFN-γ (pro-inflammatory cytokines). PA was generated by immersing fetus-containing uterine horns in a water bath at 37 °C for 21 min. Thereafter, 16 μL of MSC-S (containing 6 μg of protein derived from 2 × 105 preconditioned-MSC), or vehicle, were intranasally administered 2 h after birth to asphyxia-exposed and control rats, evaluated at postnatal day (P) 7. Alternatively, pups received a dose of either preconditioned MSC-S or vehicle, both at 2 h and P7, and were evaluated at P14, P30, and P60. The preconditioned MSC-S treatment (i) reversed asphyxia-induced oxidative stress in the hippocampus (oxidized/reduced glutathione); (ii) increased antioxidative Nuclear Erythroid 2-Related Factor 2 (NRF2) translocation; (iii) increased NQO1 antioxidant protein; (iv) reduced neuroinflammation (decreasing nuclearNF-κB/p65 levels and microglial reactivity); (v) decreased cleaved-caspase-3 cell-death; (vi) improved righting reflex, negative geotaxis, cliff aversion, locomotor activity, anxiety, motor coordination, and recognition memory. Overall, the study demonstrates that intranasal administration of preconditioned MSC-S is a novel therapeutic strategy that prevents the long-term effects of perinatal asphyxia.</jats:p>Scopus© Citations 28 9 - Some of the metrics are blocked by yourconsent settings
Item type:Publication, Estado actual de la Hipotermia Terapéutica en la Encefalopatía Hipóxico-Isquémica(2021) ;Juan Fasce ;José Manuel Novoa Pizarro ;Paulina TosoAlfredo García-Alix<jats:p>La hipotermia terapéutica (HT) es el tratamiento estándar de la Encefalopatía Hipóxico-Isqué- mica (EHI) neonatal desde hace más de una década. Esta terapia ha sido uno de los tratamientos mejor estudiados en la medicina neonatal, pasando desde modelos preclínicos a la aplicación en el paciente. Su implementación se ha acompañado del desarrollo de la neuromonitorización, la neurología neonatal como un área de conocimiento específico y de la intensa búsqueda de nuevas estrategias neuroprotectoras. Este artículo ofrece una actualización en los alcances clínicos de esta terapia, con énfasis en la problemática de nuestra región geográfica. Además, se revisan algunas estrategias adicionales que pueden mejorar la eficacia terapéutica de la HT, así como los aspectos controvertidos en su aplicación y algunas perspectivas de futuro en la atención de los neonatos con EHI.</jats:p>15Scopus© Citations 3 - Some of the metrics are blocked by yourconsent settings
Item type:Publication, N-Acetylcysteine and Acetylsalicylic Acid Inhibit Alcohol Consumption by Different Mechanisms: Combined Protection(2020) ;María Elena Quintanilla; ;Paola Morales; Scopus© Citations 21 1 - Some of the metrics are blocked by yourconsent settings
Item type:Publication, Complex Interaction between Resident Microbiota and Misfolded Proteins: Role in Neuroinflammation and Neurodegeneration(2020) ;Juliana González-Sanmiguel ;Christina M. A. P. Schuh ;Carola Muñoz-Montesino ;Pamina Contreras-KallensLuis G. Aguayo<jats:p>Neurodegenerative diseases such as Alzheimer’s disease (AD), Parkinson’s disease (PD) and Creutzfeldt–Jakob disease (CJD) are brain conditions affecting millions of people worldwide. These diseases are associated with the presence of amyloid-β (Aβ), alpha synuclein (α-Syn) and prion protein (PrP) depositions in the brain, respectively, which lead to synaptic disconnection and subsequent progressive neuronal death. Although considerable progress has been made in elucidating the pathogenesis of these diseases, the specific mechanisms of their origins remain largely unknown. A body of research suggests a potential association between host microbiota, neuroinflammation and dementia, either directly due to bacterial brain invasion because of barrier leakage and production of toxins and inflammation, or indirectly by modulating the immune response. In the present review, we focus on the emerging topics of neuroinflammation and the association between components of the human microbiota and the deposition of Aβ, α-Syn and PrP in the brain. Special focus is given to gut and oral bacteria and biofilms and to the potential mechanisms associating microbiome dysbiosis and toxin production with neurodegeneration. The roles of neuroinflammation, protein misfolding and cellular mediators in membrane damage and increased permeability are also discussed.</jats:p>3Scopus© Citations 34 - Some of the metrics are blocked by yourconsent settings
Item type:Publication, Intranasal delivery of mesenchymal stem cell-derived exosomes reduces oxidative stress and markedly inhibits ethanol consumption and post-deprivation relapse drinking(2019); ;María Elena Quintanilla ;Paola Morales ;Daniela Santapau1Scopus© Citations 60 5