A5073504340- Amyotrophic Lateral Sclerosis Research
- Neurogenetic and Muscular Disorders Research
- Parkinson's Disease Mechanisms and Treatments
- Biochemical Acid Research Studies
- Neuroscience and Neuropharmacology Research
- Spinal Cord Injury Research
- Neuroinflammation and Neurodegeneration Mechanisms
- Nerve injury and regeneration
- Nitric Oxide and Endothelin Effects
- Histone Deacetylase Inhibitors Research
- Mitochondrial Function and Pathology
- Alzheimer's disease research and treatments
- Heme Oxygenase-1 and Carbon Monoxide
- Neonatal and fetal brain pathology
- biodegradable polymer synthesis and properties
- Neurological Disease Mechanisms and Treatments
- Neurotransmitter Receptor Influence on Behavior
- Amino Acid Enzymes and Metabolism
- Neuroscience of respiration and sleep
- Sulfur Compounds in Biology
- Synthetic Organic Chemistry Methods
- Sirtuins and Resveratrol in Medicine
- Growth Hormone and Insulin-like Growth Factors
- Autophagy in Disease and Therapy
- Psychedelics and Drug Studies
Universidad de la República
2012-2025
Universidad Nacional Autónoma de México
2011
Instituto de Investigaciones Biológicas Clemente Estable
2009
Motoneuron loss and reactive astrocytosis are pathological hallmarks of amyotrophic lateral sclerosis (ALS), a paralytic neurodegenerative disease that can be triggered by mutations in Cu-Zn superoxide dismutase (SOD1). Dysfunctional astrocytes contribute to ALS pathogenesis, inducing motoneuron damage accelerating progression. However, it is unknown whether progression associated with the appearance specific astrocytic phenotype neurotoxic potential. Here, we report isolation aberrant...
In the SOD1(G93A) mutant rat model of amyotrophic lateral sclerosis (ALS), neuronal death and rapid paralysis progression are associated with emergence activated aberrant glial cells that proliferate in degenerating spinal cord. Whether pharmacological downregulation such will decrease motor neuron prolong survival is unknown. We hypothesized proliferation dependent on kinase receptor activation, therefore, tyrosine inhibitor masitinib (AB1010) could potentially control neuroinflammation...
Abstract Oxidative stress mediated by nitric oxide (NO) and its toxic metabolite peroxynitrite has previously been associated with motor neuron degeneration in amyotrophic lateral sclerosis (ALS). Degenerating spinal neurons familial sporadic ALS are typically surrounded reactive astrocytes expressing the inducible form of NO synthase (iNOS), suggesting that astroglia may have a pathogenic role ALS. We report here brief exposure cord astrocyte monolayers to (0.25–1 mM) provoked long‐lasting...
Fibroblast growth factor-1 (FGF-1) is highly expressed in motor neurons and can be released response to sublethal cell injury. Because FGF-1 potently activates astroglia exerts a direct neuroprotection after spinal cord injury or axotomy, we examined whether it regulated the expression of inducible cytoprotective heme oxygenase-1 (HO-1) enzyme astrocytes. induced HO-1 cultured rat astrocytes, which was dependent on FGF receptor activation prevented by cycloheximide. also Nrf2 mRNA protein...
Mitochondrial dysfunction is one of the pathogenic mechanisms that lead to neurodegeneration in Amyotrophic Lateral Sclerosis (ALS). Astrocytes expressing ALS-linked SOD1(G93A) mutation display a decreased mitochondrial respiratory capacity associated phenotypic changes cause them induce motor neuron death. Astrocyte-mediated toxicity can be prevented by mitochondria-targeted antioxidants, indicating critical role mitochondria neurotoxic phenotype. However, it presently unknown whether drugs...
Ibogaine is an atypical psychedelic alkaloid, which has been subject of research due to its reported ability attenuate drug-seeking behavior. Recent work suggested that ibogaine effects on alcohol self-administration in rats are related the release Glial cell Derived Neurotrophic Factor (GDNF) Ventral Tegmental Area (VTA), a mesencephalic region hosts soma dopaminergic neurons. Although previous reports have shown ibogaine´s induce GDNF expression rat midbrain, there no studies addressing...
Amyotrophic lateral sclerosis (ALS) is characterized by progressive motor neuron (MN) degeneration. Various studies using cellular and animal models of ALS indicate that there a complex interplay between MN neighboring non-neuronal cells, such as astrocytes, resulting in noncell autonomous neurodegeneration. Astrocytes exhibit lower ability to support survival than nondisease-associated ones, which strongly correlated with low-mitochondrial respiratory activity. Indeed, pharmacological...
We studied the subcellular distribution of mitochondria and superoxide dismutase-1 (SOD1) in whole mounts microdissected motor axons rats expressing ALS-linked SOD1-G93A mutation. The rationale was to determine whether physical interactions between enzyme were linked axonopathy fibers occurring amyotrophic lateral sclerosis (ALS). Mitochondria SOD1 displayed a homogeneous along both nontransgenic those overexpressing wild-type SOD1. In contrast, from (older than 35 days) showed accumulation...
The lack of current treatments for amyotrophic lateral sclerosis (ALS) highlights the need a comprehensive understanding biological mechanisms disease. A consistent neuropathological feature ALS is extensive inflammation around motor neurons and axonal degeneration, evidenced by accumulation reactive astrocytes activated microglia. Final products inflammatory processes may be detected as screening tool to identify treatment response. Herein, we focus on (a) detection arachidonic acid (AA)...
Abstract Peroxynitrite‐dependent tyrosine nitration has been postulated to be involved in motor neuron degeneration amyotrophic lateral sclerosis (ALS). Evidence supporting this supposition includes the appearance of both free and protein‐linked 3‐nitro‐ l ‐tyrosine (nitrotyrosine) sporadic familial ALS, as well increased nitrotyrosine levels spinal cord transgenic mice expressing ALS‐linked superoxide dismutase mutants at symptom onset. Here we demonstrate that incubation with clinically...
Abstract Cellular senescence is an endpoint of chemotherapy, and targeted therapies in melanoma the senescence-associated secretory phenotype (SASP) can affect tumor growth microenvironment, influencing treatment outcomes. Metabolic interventions modulate SASP, enhanced mitochondrial energy metabolism supports resistance to therapy cells. Herein, we assessed function therapy-induced senescent cells obtained after exposing temozolomide (TMZ), a methylating chemotherapeutic agent. Senescence...
Glial reactivity in the dorsal horn of spinal cord is a hallmark most chronic pain conditions. Neuroinflammation-associated reactive glia, particular astrocytes, have been shown to exhibit reduced mitochondrial respiratory function. Here, we studied function at lumbar tissue from complete Freund's adjuvant-induced inflammatory rat and constriction injury mouse models by high-resolution respirometry. A significant decrease bioenergetic parameters injury-related level coincided with highest...