DSpace Angular :: Browsing by Author "Quintanilla, Rodrigo A."

Browsing by Author "Quintanilla, Rodrigo A."

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Adolescent Binge Alcohol Exposure Affects the Brain Function Through Mitochondrial Impairment
(2018) Tapia-Rojas, Cheril; Carvajal Cachaña, Francisco Javier; Mira, Rodrigo G.; Arce, Camila; Manuel Lerma-Cabrera, Jose; Orellana Roca, Juan Andrés; Cerpa Nebott, Waldo Francisco; Quintanilla, Rodrigo A.
Alcohol consumption during adolescence alters the hippocampal response to traumatic brain injury
(2020) Mira, Rodrigo G.; Lira, Matías; Quintanilla, Rodrigo A.; Cerpa Nebott, Waldo Francisco
Binge drinking is the consumption of large volumes of alcohol in short periods and exerts its effects on the central nervous system, including the hippocampus. We have previously shown that binge drinking alters mitochondrial dynamics and induces neuroinflammation in the hippocampus of adolescent rats. Mild traumatic brain injury (mTBI), is regularly linked to alcohol consumption and share mechanisms of brain damage. In this context, we hypothesized that adolescent binge drinking could prime the development of brain damage generated by mTBI. We found that alcohol binge drinking induced by the “drinking in the dark” (DID) paradigm increases oxidative damage and astrocyte activation in the hippocampus of adolescent mice. Interestingly, adolescent animals submitted to DID showed decreased levels of mitofusin 2 that controls mitochondrial dynamics. When mTBI was evaluated as a second challenge, hippocampi from animals previously submitted to DID showed a reduction in dendritic spine number and a different spine profile. Mitochondrial performance could be compromised by alterations in mitochondrial fission in DID-mTBI animals. These data suggest that adolescent alcohol consumption can modify the progression of mTBI pathophysiology. We propose that mitochondrial impairment and oxidative damage could act as priming factors, modifying predisposition against mTBI effects.
Alcohol impairshippocampal function:FromNMDAreceptorsynaptic transmissiontomitochondrial function
(2019) Mira, Rodrigo G.; Tapia Rojas, Cheril; Pérez, María José; Jara, Claudia; Vergara, Erick H.; Quintanilla, Rodrigo A.; Cerpa Nebott, Waldo Francisco
Many studies have reported that alcohol produces harmful effects on several brain structures, including the hippocampus, in both rodents and humans. The hippocampus is one of the most studied areas of the brain due to its function in learning and memory, and a lot of evidence suggests that hippocampal failure is responsible for the cognitive loss present in individuals with recurrent alcohol consumption. Mitochondria are organelles that generate the energy needed for the brain to maintain neuronal communication, and their functional failure is considered a mediator of the synaptic dysfunction induced by alcohol. In this review, we discuss the mechanisms of how alcohol exposure affects neuronal communication through the impairment of glutamate receptor (NMDAR) activity, neuroinflammatory events and oxidative damage observed after alcohol exposure, all processes under the umbrella of mitochondrial function. Finally, we discuss the direct role of mitochondrial dysfunction mediating cognitive and memory decline produced by alcohol exposure and their consequences associated with neurodegeneration.
Carbamylated form of human erythropoietin normalizes cardiorespiratory disorders triggered by intermittent hypoxia mimicking sleep apnea syndrome
(LIPPINCOTT WILLIAMS & WILKINS, 2021) Andrade, David C.; Toledo, Camilo; Diaz, Hugo S.; Pereyra, Katherin, V; Schwarz, Karla G.; Diaz Jara, Esteban; Melipillan, Claudia; Rios Gallardo, Angelica P.; Uribe Ojeda, Atenea; Alcayaga, Julio; Quintanilla, Rodrigo A.; Iturriaga, Rodrigo; Richalet, Jean Paul; Voituron, Nicolas; Del Rio, Rodrigo
Background and objective: Chronic intermittent hypoxia (CIH), one of the main features of obstructive sleep apnea (OSA), enhances carotid body-mediated chemoreflex and induces hypertension and breathing disorders. The carbamylated form of erythropoietin (cEpo) may have beneficial effects as it retains its antioxidant/anti-inflammatory and neuroprotective profile without increasing red blood cells number. However, no studies have evaluated the potential therapeutic effect of cEpo on CIH-related cardiorespiratory disorders. We aimed to determine whether cEpo normalized the CIH-enhanced carotid body ventilatory chemoreflex, the hypertension and ventilatory disorders in rats. Methods: Male Sprague-Dawley rats (250 g) were exposed to CIH (5% O-2, 12/h, 8 h/day) for 28 days. cEPO (20 mu g/kg, i.p) was administrated from day 21 every other day for one more week. Cardiovascular and respiratory function were assessed in freely moving animals. Results: Twenty-one days of CIH increased carotid body-mediated chemoreflex responses as evidenced by a significant increase in the hypoxic ventilatory response (FiO2 10%) and triggered irregular eupneic breathing, active expiration, and produced hypertension. cEpo treatment significantly reduced the carotid body--chemoreflex responses, normalizes breathing patterns and the hypertension in CIH. In addition, cEpo treatment effectively normalized carotid body chemosensory responses evoked by acute hypoxic stimulation in CIH rats. Conclusion: Present results strongly support beneficial cardiorespiratory therapeutic effects of cEpo during CIH exposure.
Effect of Alcohol on Hippocampal-Dependent Plasticity and Behavior: Role of Glutamatergic Synaptic Transmission
(Frontiers Media S.A., 2020) Mira, Rodrigo G.; Lira, Matias; Cerpa Nebott Waldo Francisco; Tapia-Rojas, Cheril; Rebolledo, Daniela; Quintanilla, Rodrigo A.
© Copyright © 2020 Mira, Lira, Tapia-Rojas, Rebolledo, Quintanilla and Cerpa. Problematic alcohol drinking and alcohol dependence are an increasing health problem worldwide. Alcohol abuse is responsible for approximately 5% of the total deaths in the world, but addictive consumption of it has a substantial impact on neurological and memory disabilities throughout the population. One of the better-studied brain areas involved in cognitive functions is the hippocampus, which is also an essential brain region targeted by ethanol. Accumulated evidence in several rodent models has shown that ethanol treatment produces cognitive impairment in hippocampal-dependent tasks. These adverse effects may be related to the fact that ethanol impairs the cellular and synaptic plasticity mechanisms, including adverse changes in neuronal morphology, spine architecture, neuronal communication, and finally an increase in neuronal death. There is evidence that the damage that occurs in the different brain structures is varied according to the stage of development during which the subjects are exposed to ethanol, and even much earlier exposure to it would cause damage in the adult stage. Studies on the cellular and cognitive deficiencies produced by alcohol in the brain are needed in order to search for new strategies to reduce alcohol neuronal toxicity and to understand its consequences on memory and cognitive performance with emphasis on the crucial stages of development, including prenatal events to adulthood.
Evidence for TGF-β1/Nrf2 Signaling Crosstalk in a Cuprizone Model of Multiple Sclerosis
(2024) Guevara, Coram; Vicencio, Sinay C.; Pizarro, Ignacio S.; Villavicencio-Tejo, Francisca; Quintanilla, Rodrigo A.; Astudillo, Pablo; Ampuero, Estibaliz; Varas, Rodrigo; Orellana, Juan A.; Ortiz, Fernando C.
Multiple sclerosis (MS) is a chronic and degenerative disease that impacts central nervous system (CNS) function. One of the major characteristics of the disease is the presence of regions lacking myelin and an oxidative and inflammatory environment. TGF-beta 1 and Nrf2 proteins play a fundamental role in different oxidative/inflammatory processes linked to neurodegenerative diseases such as MS. The evidence from different experimental settings has demonstrated a TGF-beta 1-Nrf2 signaling crosstalk under pathological conditions. However, this possibility has not been explored in experimental models of MS. Here, by using the cuprizone-induced demyelination model of MS, we report that the in vivo pharmacological blockage of the TGF-beta 1 receptor reduced Nrf2, catalase, and TGF beta-1 protein levels in the demyelination phase of cuprizone administration. In addition, ATP production, locomotor function and cognitive performance were diminished by the treatment. Altogether, our results provide evidence for a crosstalk between TGF-beta 1 and Nrf2 signaling pathways under CNS demyelination, highlighting the importance of the antioxidant cellular response of neurodegenerative diseases such as MS.
Genetic ablation of tau improves mitochondrial function and cognitive abilities in the hippocampus
(2018) Jara, Claudia; Aránguiz, Alejandra; Cerpa Nebott, Waldo Francisco; Tapia-Rojas, Cheril; Quintanilla, Rodrigo A.
Heavy Alcohol Exposure Activates Astroglial Hemichannels and Pannexons in the Hippocampus of Adolescent Rats : Effects on Neuroinflammation and Astrocyte Arborization
(2018) Gomez, Gonzalo I.; Falcon, Romina V.; Maturana, Carola J.; Labra, Valeria C.; Salgado Cortés, Nicole Andrea; Rojas Vidal, Consuelo Antonia; Oyarzun, Juan E.; Cerpa Nebott, Waldo Francisco; Quintanilla, Rodrigo A.; Orellana Roca, Juan Andrés
Hemichannels contribute to mitochondrial Ca²⁺ and morphology alterations evoked by ethanol in astrocytes
(2024) Alvear, Tanhia F.; Farias-Pasten, Arantza; Vergara, Sergio A.; Prieto-Villalobos, Juan; Silva-Contreras, Antonia; Fuenzalida, Fernando A.; Quintanilla, Rodrigo A.; Orellana, Juan A.
Alcohol, a toxic and psychoactive substance with addictive properties, severely impacts life quality, leading to significant health, societal, and economic consequences. Its rapid passage across the blood-brain barrier directly affects different brain cells, including astrocytes. Our recent findings revealed the involvement of pannexin-1 (Panx1) and connexin-43 (Cx43) hemichannels in ethanol-induced astrocyte dysfunction and death. However, whether ethanol influences mitochondrial function and morphology in astrocytes, and the potential role of hemichannels in this process remains poorly understood. Here, we found that ethanol reduced basal mitochondrial Ca2+ but exacerbated thapsigargin-induced mitochondrial Ca2+ dynamics in a concentration-dependent manner, as evidenced by Rhod-2 time-lapse recordings. Similarly, ethanol-treated astrocytes displayed increased mitochondrial superoxide production, as indicated by MitoSox labeling. These effects coincided with reduced mitochondrial membrane potential and increased mitochondrial fragmentation, as determined by MitoRed CMXRos and MitoGreen quantification, respectively. Crucially, inhibiting both Cx43 and Panx1 hemichannels effectively prevented all ethanol-induced mitochondrial abnormalities in astrocytes. We speculate that exacerbated hemichannel activity evoked by ethanol may impair intracellular Ca2+ homeostasis, stressing mitochondrial Ca2+ with potentially damaging consequences for mitochondrial fusion and fission dynamics and astroglial bioenergetics.
Mild Traumatic Brain Injury Induces Mitochondrial Calcium Overload and Triggers the Upregulation of NCLX in the Hippocampus
(2023) Mira, Rodrigo G.; Quintanilla, Rodrigo A.; Cerpa Nebott, Waldo Francisco
Traumatic brain injury (TBI) is brain damage due to external forces. Mild TBI (mTBI) is the most common form of TBI, and repeated mTBI is a risk factor for developing neurodegenerative diseases. Several mechanisms of neuronal damage have been described in the cortex and hippocampus, including mitochondrial dysfunction. However, up until now, there have been no studies evaluating mitochondrial calcium dynamics. Here, we evaluated mitochondrial calcium dynamics in an mTBI model in mice using isolated hippocampal mitochondria for biochemical studies. We observed that 24 h after mTBI, there is a decrease in mitochondrial membrane potential and an increase in basal matrix calcium levels. These findings are accompanied by increased mitochondrial calcium efflux and no changes in mitochondrial calcium uptake. We also observed an increase in NCLX protein levels and calcium retention capacity. Our results suggest that under mTBI, the hippocampal cells respond by incrementing NCLX levels to restore mitochondrial function.
Mitochondrial permeability transition pore induces mitochondria injury in Huntington disease
(2013) Quintanilla, Rodrigo A.; Jin, Youngnam N.; Bernhardi Montgomery, Rommy von; Johnson, Gail V.
Abstract Background Mitochondrial impairment has been implicated in the pathogenesis of Huntington’s disease (HD). However, how mutant huntingtin impairs mitochondrial function and thus contributes to HD has not been fully elucidated. In this study, we used striatal cells expressing wild type (STHdhQ7/Q7) or mutant (STHdhQ111/Q111) huntingtin protein, and cortical neurons expressing the exon 1 of the huntingtin protein with physiological or pathological polyglutamine domains, to examine the interrelationship among specific mitochondrial functions. Results Depolarization induced by KCl resulted in similar changes in calcium levels without compromising mitochondrial function, both in wild type and mutant cells. However, treatment of mutant cells with thapsigargin (a SERCA antagonist that raises cytosolic calcium levels), resulted in a pronounced decrease in mitochondrial calcium uptake, increased production of reactive oxygen species (ROS), mitochondrial depolarization and fragmentation, and cell viability loss. The mitochondrial dysfunction in mutant cells was also observed in cortical neurons expressing exon 1 of the huntingtin protein with 104 Gln residues (Q104-GFP) when they were exposed to calcium stress. In addition, calcium overload induced opening of the mitochondrial permeability transition pore (mPTP) in mutant striatal cells. The mitochondrial impairment observed in mutant cells and cortical neurons expressing Q104-GFP was prevented by pre-treatment with cyclosporine A (CsA) but not by FK506 (an inhibitor of calcineurin), indicating a potential role for mPTP opening in the mitochondrial dysfunction induced by calcium stress in mutant huntingtin cells. Conclusions Expression of mutant huntingtin alters mitochondrial and cell viability through mPTP opening in striatal cells and cortical neurons.
Neurodegeneration in Multiple Sclerosis: The Role of Nrf2-Dependent Pathways
(2022) Maldonado, Paloma P.; Guevara, Coram; Olesen, Margrethe A.; Orellana Roca, Juan Andrés; Quintanilla, Rodrigo A.; Ortiz, Fernando C.
Multiple sclerosis (MS) encompasses a chronic, irreversible, and predominantly immune-mediated disease of the central nervous system that leads to axonal degeneration, neuronal death, and several neurological symptoms. Although various immune therapies have reduced relapse rates and the severity of symptoms in relapsing-remitting MS, there is still no cure for this devastating disease. In this brief review, we discuss the role of mitochondria dysfunction in the progression of MS, focused on the possible role of Nrf2 signaling in orchestrating the impairment of critical cellular and molecular aspects such as reactive oxygen species (ROS) management, under neuroinflammation and neurodegeneration in MS. In this scenario, we propose a new potential downstream signaling of Nrf2 pathway, namely the opening of hemichannels and pannexons. These large-pore channels are known to modulate glial/neuronal function and ROS production as they are permeable to extracellular Ca2+ and release potentially harmful transmitters to the synaptic cleft. In this way, the Nrf2 dysfunction impairs not only the bioenergetics and metabolic properties of glial cells but also the proper antioxidant defense and energy supply that they provide to neurons.
Phosphorylated tau potentiates Aβ-induced mitochondrial damage in mature neurons
(2014) Quintanilla, Rodrigo A.; von Bernhardi, Rommy; Godoy, Juan A.; Inestrosa, Nibaldo C.; Johnson, Gail V. W.
Tau phosphorylated at the PHF-1 epitope (S396/S404) is likely involved in the pathogenesis of Alzheimer's disease (AD). However, the molecular mechanisms by which tau phosphorylated at these sites negatively impacts neuronal functions are still under scrutiny. Previously, we showed that expression of tau truncated at D421 enhances mitochondrial dysfunction induced by A beta in cortical neurons. To extend these findings, we expressed tau pseudo-phosphorylated at S396/404 (T42EC) in mature and young cortical neurons and evaluated different aspects of mitochondrial function in response to A beta. Expression of T42EC did not induce significant changes in mitochondrial morphology, mitochondrial length, or mitochondrial transport, compared to GFP and full-length tau. However, T42EC expression enhanced A beta-induced mitochondrial membrane potential loss and increased superoxide levels compared to what was observed in mature neurons expressing full-length tau. The same effect was observed in mature neurons that expressed both pseudo-phosphorylated and truncated tau when they were treated with AS. Interestingly, the mitochondrial failure induced by A beta in mature neurons that expressed T42EC, was not observed in young neurons expressing T42EC. These novel findings suggest that phosphorylated tau (PHF-1 epitope) enhances A beta-induced mitochondrial injury, which contributes to neuronal dysfunction and to the pathogenesis of AD. (C) 2014 Elsevier Inc All rights reserved.
Quercetin Exerts Differential Neuroprotective Effects Against H2O2 and A beta Aggregates in Hippocampal Neurons: the Role of Mitochondria
(2017) Godoy, Juan A.; Lindsay, Carolina B.; Quintanilla, Rodrigo A.; Carvajal Cachaña, Francisco Javier; Cerpa Nebott, Waldo Francisco; Inestrosa Cantín, Nibaldo
Revisiting the physiological effects of exercise training on autonomic regulation and chemoreflex control in heart failure : does ejection fraction matter?
(2018) Andrade Andrade, David Cristóbal; Arce Alvarez, Alexis; Toledo, Camilo; Díaz, Hugo S.; Lucero, Claudia; Quintanilla, Rodrigo A.; Schultz, Harold D.; Marcus, Noah J.; Amann, Markus; Del Río, Rodrigo
Rosiglitazone treatment prevents mitochondrial dysfunction in mutant huntingtin-expressing cells -: Possible role of peroxisome proliferator-activated receptor-γ (PPARγ) in the pathogenesis of Huntington disease
(2008) Quintanilla, Rodrigo A.; Jin, Youngnam N.; Fuenzalida, Karen; Bronfman, Miguel; Johnson, Gail V. W.
Peroxisome proliferator-activated receptor-gamma (PPAR gamma) is a member of the PPAR family of transcription factors. Synthetic PPAR gamma agonists are used as oral anti-hyperglycemic drugs for the treatment of non-insulin-dependent diabetes. However, emerging evidence indicates that PPAR gamma activators can also prevent or attenuate neurodegeneration. Given these previous findings, the focus of this report is on the potential neuroprotective role of PPAR gamma activation in preventing the loss of mitochondrial function in Huntington disease (HD). For these studies we used striatal cells that express wild-type (STHdh(Q7/Q7)) or mutant (STHdh(Q111/Q111)) huntingtin protein at physiological levels. Treatment of mutant cells with thapsigargin resulted in a significant decrease in mitochondrial calcium uptake, an increase in reactive oxygen species production, and a significant decrease in mitochondrial membrane potential. PPAR gamma activation by rosiglitazone prevented the mitochondrial dysfunction and oxidative stress that occurred when mutant striatal cells were challenged with pathological increases in calcium. The beneficial effects of rosiglitazone were likely mediated by activation of PPAR gamma, as all protective effects were prevented by the PPAR gamma antagonist GW9662. Additionally, the PPAR gamma signaling pathway was significantly impaired in the mutant striatal cells with decreases in PPAR gamma expression and reduced PPAR gamma transcriptional activity. Treatment with rosiglitazone increased mitochondrial mass levels, suggesting a role for the PPAR gamma pathway in mitochondrial function in striatal cells. Altogether, this evidence indicates that PPAR gamma activation by rosiglitazone attenuates mitochondrial dysfunction in mutant huntingtin-expressing striatal cells, and this could be an important therapeutic avenue to ameliorate the mitochondrial dysfunction that occurs in HD.
Superoxide dismutase 2 deficiency is associated with enhanced central chemoreception in mice: Implications for breathing regulation
(2024) Diaz-Jara, Esteban; Pereyra, Katherine; Vicencio, Sinay; Olesen, Margrethe A.; Schwarz, Karla G.; Toledo, Camilo; Diaz, Hugo S.; Quintanilla, Rodrigo A.; Del Rio, Rodrigo
Aims: In mammals, central chemoreception plays a crucial role in the regulation of breathing function in both health and disease conditions. Recently, a correlation between high levels of superoxide anion (O2.-) in the Retrotrapezoid nucleus (RTN), a main brain chemoreceptor area, and enhanced central chemoreception has been found in rodents. Interestingly, deficiency in superoxide dismutase 2 (SOD2) expression, a pivotal antioxidant enzyme, has been linked to the development/progression of several diseases. Despite, the contribution of SOD2 on O2.-regulation on central chemoreceptor function is unknown. Accordingly, we sought to determine the impact of partial deletion of SOD2 expression on i) O2.-accumulation in the RTN, ii) central ventilatory chemoreflex function, and iii) disordered-breathing. Finally, we study cellular localization of SOD2 in the RTN of healthy mice.Methods: Central chemoreflex drive and breathing function were assessed in freely moving heterozygous SOD2 knockout mice (SOD2+/-mice) and age-matched control wild type (WT) mice by whole-body plethysmography. O2.-levels were determined in RTN brainstem sections and brain isolated mitochondria, while SOD2 protein expression and tissue localization were determined by immunoblot, RNAseq and immunofluorescent staining, respectively.Results: Our results showed that SOD2+/-mice displayed reductions in SOD2 levels and high O2.-formation and mitochondrial dysfunction within the RTN compared to WT. Additionally, SOD2+/-mice displayed a heightened ventilatory response to hypercapnia and exhibited overt signs of altered breathing patterns. Both, RNAseq analysis and immunofluorescence co-localization studies showed that SOD2 expression was confined to RTN astrocytes but not to RTN chemoreceptor neurons. Finally, we found that SOD2+/-mice displayed alterations in RTN astrocyte morphology compared to RTN astrocytes from WT mice.Innovation & conclusion: These findings provide first evidence of the role of SOD2 in the regulation of O2.-levels in the RTN and its potential contribution on the regulation of central chemoreflex function. Our results suggest that reductions in the expression of SOD2 in the brain may contribute to increase O2.-levels in the RTN being the outcome a chronic surge in central chemoreflex drive and the development/maintenance of altered breathing patterns. Overall, dysregulation of SOD2 and the resulting increase in O2.-levels in brainstem respiratory areas can disrupt normal respiratory control mechanisms and contribute to breathing dysfunction seen in certain disease conditions characterized by high oxidative stress.
Tau Deletion Prevents Cognitive Impairment and Mitochondrial Dysfunction Age Associated by a Mechanism Dependent on Cyclophilin-D
(2021) Jara, Claudia; Cerpa, Waldo; Tapia-Rojas, Cheril; Quintanilla, Rodrigo A.
Aging is an irreversible process and the primary risk factor for the development of neurodegenerative diseases, such as Alzheimer's disease (AD). Mitochondrial impairment is a process that generates oxidative damage and ATP deficit; both factors are important in the memory decline showed during normal aging and AD. Tau is a microtubule-associated protein, with a strong influence on both the morphology and physiology of neurons. In AD, tau protein undergoes post-translational modifications, which could play a relevant role in the onset and progression of this disease. Also, these abnormal forms of tau could be present during the physiological aging that could be related to memory impairment present during this stage. We previously showed that tau ablation improves mitochondrial function and cognitive abilities in young wild-type mice. However, the possible contribution of tau during aging that could predispose to the development of AD is unclear. Here, we show that tau deletion prevents cognitive impairment and improves mitochondrial function during normal aging as indicated by a reduction in oxidative damage and increased ATP production. Notably, we observed a decrease in cyclophilin-D (CypD) levels in aged tau-/- mice, resulting in increased calcium buffering and reduced mitochondrial permeability transition pore (mPTP) opening. The mPTP is a mitochondrial structure, whose opening is dependent on CypD expression, and new evidence suggests that this could play an essential role in the neurodegenerative process showed during AD. In contrast, hippocampal CypD overexpression in aged tau-/- mice impairs mitochondrial function evidenced by an ATP deficit, increased mPTP opening, and memory loss; all effects were observed in the AD pathology. Our results indicate that the absence of tau prevents age-associated cognitive impairment by maintaining mitochondrial function and reducing mPTP opening through a CypD-dependent mechanism. These findings are novel and represent an important advance in the study of how tau contributes to the cognitive and mitochondrial failure present during aging and AD in the brain.
Understanding Risk Factors for Alzheimer's Disease: Interplay of Neuroinflammation, Connexin-based Communication and Oxidative Stress
(Elsevier Inc., 2012) Quintanilla, Rodrigo A.; Orellana Roca, Juan Andrés; Bernhardi Montgomery, Rommy von
Alzheimer's disease (AD) is an age-related neurodegenerative disease characterized by dementia and the presence of amyloid plaques and anomalous tau aggregates. Although pathophysiological mechanisms are still unclear, neuroinflammation and glial cell dysfunction have been identified as conspicuous components of AD. Glial cell dysfunction is associated with dysregulated production of inflammation mediators and generation of both reactive oxygen species (ROS) and reactive nitrogen species (RNS), which affect synapses and induce neuronal damage. Importantly, both increased neuroinflammation and ROS/RNS production by glia dysregulate communication mediated by connexin-based channels in brain cells, which could further affect oxidative balance and neuronal viability. Recent evidence suggests that connexin-based channels could be involved in AD pathogenesis. Here we discuss how aging affects neuroinflammation, oxidative stress, and connexin-based channels and the potential relevance of these changes for AD. Understanding how they cooperate as pathogenic mechanisms of AD is promising for the discovery of new therapeutic strategies against neurodegenerative disorders.
Ventilatory and Autonomic Regulation in Sleep Apnea Syndrome: A Potential Protective Role for Erythropoietin?
(2018) Andrade Andrade, David Cristóbal; Haine, Liasmine; Toledo, Camilo; Diaz, Hugo S.; Quintanilla, Rodrigo A.; Marcus, Noah J.; Iturriaga Agüera, Rodrigo; Richalet, Jean-Paul; Voituron, Nicolas; Del Rio, Rodrigo

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