General Information:
Id: | 1,588 |
Diseases: |
Alzheimer disease
- [OMIM]
Multiple sclerosis - [OMIM] Parkinson disease |
Mammalia | |
review | |
Reference: | Di Filippo M et al.(2010) Mitochondria and the link between neuroinflammation and neurodegeneration J. Alzheimers Dis. 20: S369-S379 [PMID: 20463396] |
Interaction Information:
Comment | Neuroinflammation and neurodegeneration represent a ubiquitous pathological finding during the course of several different neurological diseases like AD, PD, and MS. |
Formal Description Interaction-ID: 11446 |
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Comment | Neuroinflammation and neurodegeneration represent a ubiquitous pathological finding during the course of several different neurological diseases like AD, PD, and MS. |
Formal Description Interaction-ID: 11447 |
disease Parkinson disease increases_activity of phenotype neuroinflammation |
Comment | Neuroinflammation and neurodegeneration represent a ubiquitous pathological finding during the course of several different neurological diseases like AD, PD, and MS. |
Formal Description Interaction-ID: 11448 |
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Comment | Neuroinflammation and neurodegeneration represent a ubiquitous pathological finding during the course of several different neurological diseases like AD, PD, and MS. |
Formal Description Interaction-ID: 11450 |
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Comment | Neuroinflammation and neurodegeneration represent a ubiquitous pathological finding during the course of several different neurological diseases like AD, PD, and MS. |
Formal Description Interaction-ID: 11451 |
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Comment | The innate immune response can promote repair and remyelination and trigger the production of neurotrophic factors in response to injury, but many potentially harmful mediators such as cytokines, reactive oxygen species (ROS), and nitric oxide (NO) are also released. |
Formal Description Interaction-ID: 11452 |
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Comment | The innate immune response can promote repair and remyelination and trigger the production of neurotrophic factors in response to injury, but many potentially harmful mediators such as cytokines, reactive oxygen species (ROS), and nitric oxide (NO) are also released. |
Formal Description Interaction-ID: 11453 |
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Comment | The innate immune response can promote repair and remyelination and trigger the production of neurotrophic factors in response to injury, but many potentially harmful mediators such as cytokines, reactive oxygen species (ROS), and nitric oxide (NO) are also released. |
Formal Description Interaction-ID: 11454 |
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Comment | The innate immune response can promote repair and remyelination and trigger the production of neurotrophic factors in response to injury, but many potentially harmful mediators such as cytokines, reactive oxygen species (ROS), and nitric oxide (NO) are also released. |
Formal Description Interaction-ID: 11455 |
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Comment | The innate immune response can promote repair and remyelination and trigger the production of neurotrophic factors in response to injury, but many potentially harmful mediators such as cytokines, reactive oxygen species (ROS), and nitric oxide (NO) are also released. |
Formal Description Interaction-ID: 11456 |
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Comment | Molecules of the innate immune response can promote repair and remyelination and trigger the production of neurotrophic factors in response to injury, but many potentially harmful mediators such as cytokines, reactive oxygen species (ROS), and nitric oxide (NO) are also released. |
Formal Description Interaction-ID: 11457 |
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Comment | Molecules of the innate immune response can promote repair and remyelination and trigger the production of neurotrophic factors in response to injury, but many potentially harmful mediators such as cytokines, reactive oxygen species (ROS), and nitric oxide (NO) are also released. |
Formal Description Interaction-ID: 11458 |
process affects_activity of |
Comment | Microglial cells are the main cell type of the innate immune system in the brain. The acute response of microglial cells to neuroinflammatory stimuli involves changes in cell phenotype and gene expression, including the de novo expression of the inducible isoform of nitric oxide synthase (iNOS) and cytokines such as tumor necrosis factor alpha (TNF-alpha) and interleukin-1beta (IL-1beta). |
Formal Description Interaction-ID: 11459 |
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Comment | Microglial cells are the main cell type of the innate immune system in the brain. The acute response of microglial cells to neuroinflammatory stimuli involves changes in cell phenotype and gene expression, including the de novo expression of the inducible isoform of nitric oxide synthase (iNOS) and cytokines such as tumor necrosis factor alpha (TNF-alpha) and interleukin-1beta (IL-1beta). |
Formal Description Interaction-ID: 11646 |
process increases_activity of process |
Comment | Microglial cells are the main cell type of the innate immune system in the brain. The acute response of microglial cells to neuroinflammatory stimuli involves changes in cell phenotype and gene expression, including the de novo expression of the inducible isoform of nitric oxide synthase (iNOS) and cytokines such as tumor necrosis factor alpha (TNF-alpha) and interleukin-1beta (IL-1beta). |
Formal Description Interaction-ID: 11647 |
process increases_activity of process |
Comment | The acute response of microglial cells to neuroinflammatory stimuli involves changes in cell phenotype and gene expression, including the de novo expression of the inducible isoform of nitric oxide synthase (iNOS) and cytokines such as tumor necrosis factor alpha (TNFalpha) and interleukin-1beta (IL-1beta). |
Formal Description Interaction-ID: 11648 |
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Drugbank entries | Show/Hide entries for TNF |
Comment | The acute response of microglial cells to neuroinflammatory stimuli involves changes in cell phenotype and gene expression, including the de novo expression of the inducible isoform of nitric oxide synthase (iNOS) and cytokines such as tumor necrosis factor alpha (TNFalpha) and interleukin-1beta (IL-1beta). |
Formal Description Interaction-ID: 11650 |
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Drugbank entries | Show/Hide entries for IL1B |
Comment | The acute response of microglial cells to neuroinflammatory stimuli involves changes in cell phenotype and gene expression, including the de novo expression of the inducible isoform of nitric oxide synthase (iNOS) and cytokines such as tumor necrosis factor alpha (TNFalpha) and interleukin-1beta (IL-1beta). |
Formal Description Interaction-ID: 11651 |
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Drugbank entries | Show/Hide entries for NOS2 |
Comment | This acute microglial neuroinflammatory response involves the release of several inflammatory mediators such as cytokines and chemokines and is capable to trigger oxidative and nitrosative stress. |
Formal Description Interaction-ID: 11652 |
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Comment | This acute microglial neuroinflammatory response involves the release of several inflammatory mediators such as cytokines and chemokines and is capable to trigger oxidative and nitrosative stress. |
Formal Description Interaction-ID: 11653 |
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Comment | This acute microglial neuroinflammatory response involves the release of several inflammatory mediators such as cytokines and chemokines and is capable to trigger oxidative and nitrosative stress. |
Formal Description Interaction-ID: 11654 |
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Comment | Microglial cells are the main cell type of the innate immune system in the brain. The acute response of microglial cells to neuroinflammatory stimuli involves changes in cell phenotype and gene expression, including the de novo expression of the inducible isoform of nitric oxide synthase (iNOS) and cytokines such as tumor necrosis factor alpha (TNF-alpha) and interleukin-1beta (IL-1beta). |
Formal Description Interaction-ID: 11655 |
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Comment | Mitochondria represent a particularly vulnerable target of oxidative and nitrosative stress. |
Formal Description Interaction-ID: 11656 |
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Comment | Mitochondria represent a particularly vulnerable target of oxidative and nitrosative stress. |
Formal Description Interaction-ID: 11657 |
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Comment | Activated microglia can produce and release both ROS and nitrogen species (RNS). ROS and RNS can cause damage to essential components of the mitochondria such as mitochondrial DNA. |
Formal Description Interaction-ID: 11658 |
process increases_quantity of drug/chemical compound Reactive oxygen species |
Comment | Activated microglia can produce and release both ROS and nitrogen species (RNS). ROS and RNS can cause damage to essential components of the mitochondria such as mitochondrial DNA. |
Formal Description Interaction-ID: 11675 |
process increases_quantity of drug/chemical compound Reactive nitrogen species |
Comment | Activated microglia can produce and release both ROS and nitrogen species (RNS). ROS and RNS can cause damage to essential components of the mitochondria such as mitochondrial DNA. |
Formal Description Interaction-ID: 11678 |
drug/chemical compound Reactive nitrogen species increases_activity of |
Comment | Activated microglia can produce and release both ROS and nitrogen species (RNS). ROS and RNS can cause damage to essential components of the mitochondria such as mitochondrial DNA. |
Formal Description Interaction-ID: 11681 |
drug/chemical compound Reactive oxygen species increases_activity of |
Comment | Activated microglia can produce and release both ROS and nitrogen species (RNS). ROS and RNS can cause damage to essential components of the mitochondria such as mitochondrial DNA. |
Formal Description Interaction-ID: 11682 |
drug/chemical compound Reactive nitrogen species decreases_activity of cellular component |
Comment | Activated microglia can produce and release both ROS and nitrogen species (RNS). ROS and RNS can cause damage to essential components of the mitochondria such as mitochondrial DNA. |
Formal Description Interaction-ID: 11683 |
drug/chemical compound Reactive oxygen species decreases_activity of cellular component |
Comment | Nitrosative stress is involved in the pathogenesis of neurodegenerative and neuroinflammatory disorders. |
Formal Description Interaction-ID: 11688 |
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Comment | Nitrosative stress is involved in the pathogenesis of neurodegenerative and neuroinflammatory disorders. |
Formal Description Interaction-ID: 11690 |
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Comment | As AD progresses, both declarative and nondeclarative memory become profoundly impaired, the capacity for reasoning, abstraction, and language are progressively lost. |
Formal Description Interaction-ID: 11761 |
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Comment | Inflammatory responses in AD include changes in microglia morphology and astrogliosis. |
Formal Description Interaction-ID: 11762 |
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Comment | Inflammatory responses in AD include changes in microglia morphology and astrogliosis. |
Formal Description Interaction-ID: 11763 |
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Comment | In postmortem AD brains and in the cerebrospinal fluid and peripheral blood of AD patients elevated levels of expression of molecules associated with immune cells activation can be found such as the cytokines IL-1, IL-6, and TNF-alpha. |
Formal Description Interaction-ID: 11764 |
disease increases_quantity of gene/protein |
Drugbank entries | Show/Hide entries for IL1B |
Comment | In postmortem AD brains and in the cerebrospinal fluid and peripheral blood of AD patients elevated levels of expression of molecules associated with immune cells activation can be found such as the cytokines IL-1, IL-6, and TNF-alpha. |
Formal Description Interaction-ID: 11773 |
disease increases_quantity of gene/protein |
Drugbank entries | Show/Hide entries for IL6 |
Comment | In postmortem AD brains and in the cerebrospinal fluid and peripheral blood of AD patients elevated levels of expression of molecules associated with immune cells activation can be found such as the cytokines IL-1, IL-6, and TNF-alpha. |
Formal Description Interaction-ID: 11774 |
disease increases_quantity of gene/protein |
Drugbank entries | Show/Hide entries for TNF |
Comment | TNF-alpha is able to promote Abeta peptide accumulation potentially triggering a vicious cycle leading to enhanced inflammation and disease progression. |
Formal Description Interaction-ID: 11775 |
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Drugbank entries | Show/Hide entries for TNF |
Comment | Neuroinflammation and neurodegeneration represent a ubiquitous pathological finding during the course of several different neurological diseases like AD, PD, and MS. |
Formal Description Interaction-ID: 47326 |
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Comment | Nitrosative stress is involved in the pathogenesis of neurodegenerative and neuroinflammatory disorders. |
Formal Description Interaction-ID: 47327 |
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