Publications by authors named "Marina Sanz-Sancristobal"
Article Synopsis
- Parkinson's disease (PD) is a neurodegenerative disorder linked to the loss of dopamine-producing neurons, and current treatments only manage symptoms, highlighting the need for new therapeutic targets.
- The transcription factor CCAAT/Enhancer Binding Protein β (C/EBPβ) shows altered levels in various neurodegenerative diseases, indicating its potential as a therapeutic target for PD, particularly in regulating genes like mitochondrial transcription factor A (TFAM).
- Research showed that overexpressing C/EBPβ enhances TFAM activity, while reducing C/EBPβ levels led to increased TFAM and other mitochondrial markers, suggesting a role of C/EBPβ in mitochondrial function and autophagy processes in PD.
Article Synopsis
- Parkinson's disease (PD) is the second most common neurodegenerative disorder, characterized by the loss of dopamine-producing neurons and various cellular issues like oxidative stress and mitochondrial problems.
- Recent research suggests that changes in lipid metabolism could be linked to PD, prompting investigations into linoleic acid (LA) as a potential treatment.
- In tests on a PD cell line and mouse model, LA was found to be neuroprotective and anti-inflammatory, enhancing lipid droplet formation and improving cellular processes like autophagy, offering new insights into its protective mechanisms against PD.
Article Synopsis
- * Research shows that DMT stimulates the subgranular zone in the hippocampus, increasing the production of new neurons and improving memory performance in mice.
- * The neurogenic effects of DMT may be linked to the activation of the sigma-1 receptor, as inhibiting this receptor blocks the generation of new neurons, highlighting its role in enhancing brain health and cognitive abilities.
Article Synopsis
- C/EBPβ is a transcription factor linked to various brain conditions, but its role in neurodegenerative diseases, like Parkinson's, is not well understood.
- This study investigates how reducing C/EBPβ levels affects dopaminergic cell death and inflammation in a Parkinson's disease model, revealing that its interference protects these cells and reduces inflammation.
- Results suggest that targeting C/EBPβ could be a new strategy for treating neurodegenerative diseases by mitigating inflammatory brain damage.
Background: The CCAAT/enhancer-binding protein β (C/EBPβ) is a transcription factor implicated in the control of proliferation, differentiation, and inflammatory processes mainly in adipose tissue and liver; although more recent results have revealed an important role for this transcription factor in the brain. Previous studies from our laboratory indicated that CCAAT/enhancer-binding protein β is implicated in inflammatory process and brain injury, since mice lacking this gene were less susceptible to kainic acid-induced injury. More recently, we have shown that the complement component 3 gene (C3) is a downstream target of CCAAT/enhancer-binding protein β and it could be a mediator of the proinflammatory effects of this transcription factor in neural cells.
View Article and Find Full Text PDFThe phosphodiesterase 7 (PDE7) enzyme is one of the enzymes responsible for controlling intracellular levels of cyclic adenosine 3',5'-monophosphate in the immune and central nervous system. We have previously shown that inhibitors of this enzyme are potent neuroprotective and anti-inflammatory agents. In addition, we also demonstrated that PDE7 inhibition induces endogenous neuroregenerative processes toward a dopaminergic phenotype.
View Article and Find Full Text PDFGlycogen synthase kinase-3 (GSK-3) is a serine/threonine kinase originally identified as a regulator of glycogen metabolism but it also plays a pivotal role in numerous cellular functions, including differentiation, cell cycle regulation, and proliferation. The dentate gyrus of the hippocampus, together with the subventricular zone of the lateral ventricles, is one of the regions in which neurogenesis takes place in the adult brain. Here, using a chemical genetic approach that involves the use of several diverse inhibitors of GSK-3 as pharmacological tools, we show that inhibition of GSK-3 induces proliferation, migration, and differentiation of neural stem cells toward a neuronal phenotype in in vitro studies.
View Article and Find Full Text PDFArticle Synopsis
- Inhibition of glycogen synthase kinase-3 (GSK-3) and phosphodiesterase (PDE) enzymes is being explored for neuroprotection, as they can influence cAMP levels important for cellular health.
- Research demonstrated that a new compound, VP1.14, effectively reduced inflammation and neuronal loss in hippocampal regions after KA treatment, showcasing its potential as a neuroprotective and anti-inflammatory therapeutic agent.
Background: The dentate gyrus of the hippocampus is one of the regions in which neurogenesis takes place in the adult brain. We have previously demonstrated that CCAAT/enhancer binding protein β (C/EBPβ) is expressed in the granular layer of the dentate gyrus of the adult mouse hippocampus. Taking into account the important role of C/EBPβ in the consolidation of long term memory, the fact that newborn neurons in the hippocampus contribute to learning and memory processes, and the role of this transcription factor, previously demonstrated by our group, in regulating neuronal differentiation, we speculated that this transcription factor could regulate stem/progenitor cells in this region of the brain.
View Article and Find Full Text PDFBackground: Thiadiazolidinones (TDZD) are small heterocyclic compounds first described as non-ATP competitive inhibitors of glycogen synthase kinase 3β (GSK-3β). In this study, we analyzed the effects of 4-benzyl-2-methyl-1,2,4-thiadiazolidine-3,5-dione (TDZD-8), on murine GL261 cells growth in vitro and on the growth of established intracerebral murine gliomas in vivo.
Methodology/principal Findings: Our data show that TDZD-8 decreased proliferation and induced apoptosis of GL261 glioblastoma cells in vitro, delayed tumor growth in vivo, and augmented animal survival.
The CCAAT/enhancer-binding protein beta (C/EBPbeta, also known as CEBPB) was first identified as a regulator of differentiation and inflammatory processes in adipose tissue and liver. Although C/EBPbeta was initially implicated in synaptic plasticity, its function in the brain remains largely unknown. We have previously shown that C/EBPbeta regulates the expression of genes involved in inflammatory processes and brain injury.
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