A5033252117- Neuroscience and Neuropharmacology Research
- RNA regulation and disease
- Tryptophan and brain disorders
- Mitochondrial Function and Pathology
- Traumatic Brain Injury and Neurovascular Disturbances
- Neuroinflammation and Neurodegeneration Mechanisms
- Cell death mechanisms and regulation
- Nicotinic Acetylcholine Receptors Study
- Endoplasmic Reticulum Stress and Disease
- Stress Responses and Cortisol
- Immune Cell Function and Interaction
- Circadian rhythm and melatonin
- Cardiac Arrest and Resuscitation
- Cancer, Stress, Anesthesia, and Immune Response
- Lymphoma Diagnosis and Treatment
- Estrogen and related hormone effects
- interferon and immune responses
- Genetics, Aging, and Longevity in Model Organisms
- Chronic Lymphocytic Leukemia Research
- Genetics and Neurodevelopmental Disorders
- Alzheimer's disease research and treatments
- Adenosine and Purinergic Signaling
- Eosinophilic Esophagitis
- Adipose Tissue and Metabolism
- Traumatic Brain Injury Research
Fundación Ciencia and Vida
2016-2023
Universidad Andrés Bello
2017
Pfizer (United States)
2017
Treatments that promote protein synthesis in the brain may preserve cognition Alzheimer’s disease.
With increased life expectancy, age-associated cognitive decline becomes a growing concern, even in the absence of recognizable neurodegenerative disease. The integrated stress response (ISR) is activated during aging and contributes to age-related brain phenotypes. We demonstrate that treatment with drug-like small-molecule ISR inhibitor ISRIB reverses activation brain, as indicated by decreased levels activating transcription factor 4 (ATF4) phosphorylated eukaryotic translation initiation...
Age is the main risk factor for development of neurodegenerative diseases. In aged brain, axonal degeneration an early pathological event, preceding neuronal dysfunction, and cognitive disabilities in humans, primates, rodents, invertebrates. Necroptosis mediates injured axons, but whether necroptosis triggers neurodegeneration impairment along aging unknown. Here, we show that loss necroptotic effector Mlkl was sufficient to delay age-associated neuroinflammation, protecting against...
Mild repetitive traumatic brain injury (rTBI) induces chronic behavioral and cognitive alterations increases the risk for dementia. Currently, there are no therapeutic strategies to prevent or mitigate deficits associated with rTBI. Previously we developed an animal model of rTBI that recapitulates observed in humans. We now report results increase risk-taking behavior male but not female mice. This phenotype is activation integrated stress response cell-specific synaptic type A subtype...
T helper type 17 (Th17) lymphocytes, characterized by the production of interleukin-17 and other pro-inflammatory cytokines, are present in intestinal lamina propria have been described as important players driving inflammation. Recent evidence, supporting notion a functional phenotypic instability Th17 cells, has shown that differentiate into 1 regulatory (Tr1) cells during resolution Moreover, it suggested expression CD39 ectonucleotidase endows with immunosuppressive properties. However,...
Traumatic brain injury (TBI) is a leading cause of long-term neurological disability in the world and strongest environmental risk factor for development dementia. Even mild TBI (resulting from concussive injuries) associated with greater than twofold increase dementia onset. Little known about cellular mechanisms responsible progression long-lasting cognitive deficits. The integrated stress response (ISR), phylogenetically conserved pathway involved to stress, activated after TBI,...
Although new targeted therapies, such as ibrutinib and idelalisib, have made a large impact on non-Hodgkin's lymphoma (NHL) patients, the disease is often fatal because patients are initially resistant to these or they eventually develop resistance. New drugs treatments necessary for patients. One attractive approach inhibit multiple parallel pathways that drive growth of hematologic tumors, possibly prolonging duration response reducing Early clinical trials tested this by dosing two in...
ABSTRACT With increased life expectancy age-associated cognitive decline becomes a growing concern, even in the absence of recognizable neurodegenerative disease. The integrated stress response (ISR) is activated during aging and contributes to age-related brain phenotypes. We demonstrate that treatment with drug-like small-molecule ISR inhibitor ISRIB reverses activation brain, as indicated by decreased levels activating transcription factor 4 (ATF4) phosphorylated eukaryotic translation...
Abstract Traumatic brain injury (TBI) is a leading cause of long-term neurological disability in the world and strongest environmental risk factor for development dementia. Even mild TBI (resulting from concussive injuries) associated with >2-fold increase dementia onset. Little known about cellular mechanisms responsible progression long lasting cognitive deficits. The integrated stress response (ISR), phylogenetically conserved pathway involved to stress, activated after TBI, axsnd...
Abstract Neuronal protein synthesis is essential for long-term memory consolidation. Conversely, dysregulation of has been implicated in a number neurodegenerative disorders, including Alzheimer’s disease (AD). Several types cellular stress trigger the activation kinases that converge on phosphorylation eukaryotic translation initiation factor 2α (eIF2α-P). This leads to attenuation cap-dependent mRNA translation, component integrated response (ISR). We show AD brains exhibit increased...
Abstract Age is the main risk factor for development of neurodegenerative diseases. In aged brain, axonal degeneration an early pathological event, preceding neuronal dysfunction, and cognitive disabilities in humans, primates, rodents, invertebrates. Necroptosis mediates injured axons, but whether necroptosis triggers neurodegeneration impairment along aging unknown. Here we show that loss necroptotic effector Mlkl was sufficient to delay age-associated neuroinflammation, protecting against...