salubrinal and Nerve-Degeneration

salubrinal has been researched along with Nerve-Degeneration* in 2 studies

Other Studies

2 other study(ies) available for salubrinal and Nerve-Degeneration

Article	Year
Rescue of ATXN3 neuronal toxicity in Disease models & mechanisms, 2017, 12-19, Volume: 10, Issue:12 Polyglutamine expansion diseases are a group of hereditary neurodegenerative disorders that develop when a CAG repeat in the causative genes is unstably expanded above a certain threshold. The expansion of trinucleotide CAG repeats causes hereditary adult-onset neurodegenerative disorders, such as Huntington's disease, dentatorubral-pallidoluysian atrophy, spinobulbar muscular atrophy and multiple forms of spinocerebellar ataxia (SCA). The most common dominantly inherited SCA is the type 3 (SCA3), also known as Machado-Joseph disease (MJD), which is an autosomal dominant, progressive neurological disorder. The gene causatively associated with MJD is Topics: Animals; Animals, Genetically Modified; Ataxin-3; Caenorhabditis elegans; Caenorhabditis elegans Proteins; Cinnamates; Endoplasmic Reticulum Stress; Guanabenz; Humans; Longevity; Methylene Blue; Motor Neurons; Mutation; Nerve Degeneration; Oxidative Stress; Paralysis; Phenotype; Protein Aggregates; Repressor Proteins; Small Molecule Libraries; Thiourea; Transgenes; Unfolded Protein Response	2017
Salubrinal attenuates β-amyloid-induced neuronal death and microglial activation by inhibition of the NF-κB pathway. Neurobiology of aging, 2012, Volume: 33, Issue:5 Alzheimer's disease (AD) is characterized by the deposition of β-amyloid (Aβ) peptides in the brain, inducing neuronal cell death and microglial activation. Endoplasmic reticulum (ER) stress has been proposed to be a mediator of Aβ neurotoxicity. In this study, we test whether salubrinal, an ER stress inhibitor, can protect against Aβ-mediated neurotoxicity. We show in rat primary cortical neurons and mouse microglial BV-2 cells that short-term treatment with salubrinal attenuates Aβ-induced neuronal death and microglial activation. Remarkably, our results show that salubrinal's neuroprotective effects are not due to inhibition of ER stress. Rather, we demonstrate that salubrinal exerts its effects through the inhibition of IκB kinase (IKK) activation, IκB degradation, and the subsequent nuclear factor-kappa B (NF-κB) activation. These results elucidate inhibition of the NF-κB pathway as a new mechanism responsible for the protective effects of salubrinal against Aβ neurotoxicity. This study also suggests that modulation of Aβ-induced NF-κB activation could be a potential therapeutic strategy for Alzheimer's disease. Topics: Alzheimer Disease; Amyloid beta-Peptides; Animals; Cell Death; Cell Line; Cinnamates; Mice; Microglia; Nerve Degeneration; Neurons; Neuroprotective Agents; NF-kappa B; Primary Cell Culture; Rats; Thiourea	2012

Article

Year

Disease models & mechanisms, 2017, 12-19, Volume: 10, Issue:12

Polyglutamine expansion diseases are a group of hereditary neurodegenerative disorders that develop when a CAG repeat in the causative genes is unstably expanded above a certain threshold. The expansion of trinucleotide CAG repeats causes hereditary adult-onset neurodegenerative disorders, such as Huntington's disease, dentatorubral-pallidoluysian atrophy, spinobulbar muscular atrophy and multiple forms of spinocerebellar ataxia (SCA). The most common dominantly inherited SCA is the type 3 (SCA3), also known as Machado-Joseph disease (MJD), which is an autosomal dominant, progressive neurological disorder. The gene causatively associated with MJD is

Topics: Animals; Animals, Genetically Modified; Ataxin-3; Caenorhabditis elegans; Caenorhabditis elegans Proteins; Cinnamates; Endoplasmic Reticulum Stress; Guanabenz; Humans; Longevity; Methylene Blue; Motor Neurons; Mutation; Nerve Degeneration; Oxidative Stress; Paralysis; Phenotype; Protein Aggregates; Repressor Proteins; Small Molecule Libraries; Thiourea; Transgenes; Unfolded Protein Response

2017

Salubrinal attenuates β-amyloid-induced neuronal death and microglial activation by inhibition of the NF-κB pathway.

Neurobiology of aging, 2012, Volume: 33, Issue:5

Alzheimer's disease (AD) is characterized by the deposition of β-amyloid (Aβ) peptides in the brain, inducing neuronal cell death and microglial activation. Endoplasmic reticulum (ER) stress has been proposed to be a mediator of Aβ neurotoxicity. In this study, we test whether salubrinal, an ER stress inhibitor, can protect against Aβ-mediated neurotoxicity. We show in rat primary cortical neurons and mouse microglial BV-2 cells that short-term treatment with salubrinal attenuates Aβ-induced neuronal death and microglial activation. Remarkably, our results show that salubrinal's neuroprotective effects are not due to inhibition of ER stress. Rather, we demonstrate that salubrinal exerts its effects through the inhibition of IκB kinase (IKK) activation, IκB degradation, and the subsequent nuclear factor-kappa B (NF-κB) activation. These results elucidate inhibition of the NF-κB pathway as a new mechanism responsible for the protective effects of salubrinal against Aβ neurotoxicity. This study also suggests that modulation of Aβ-induced NF-κB activation could be a potential therapeutic strategy for Alzheimer's disease.

Topics: Alzheimer Disease; Amyloid beta-Peptides; Animals; Cell Death; Cell Line; Cinnamates; Mice; Microglia; Nerve Degeneration; Neurons; Neuroprotective Agents; NF-kappa B; Primary Cell Culture; Rats; Thiourea

2012