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

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: 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

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: 11450

increases_activity of

phenotype

neurodegeneration

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

disease

Parkinson disease

increases_activity of

phenotype

neurodegeneration

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

affects_activity of

gene/protein

Cytokine

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

affects_activity of

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

affects_activity of

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

increases_quantity of

gene/protein

Proinflammatory cytokine

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

increases_quantity of

drug/chemical compound

Reactive oxygen species

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

increases_quantity of

drug/chemical compound

NO

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

affects_activity of

exactly: remyelination
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

tissue/cell line

microglia

increases_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: 11646

increases_activity of

in form of acute response of microglial cells
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

increases_activity of

process

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)
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

increases_expression of

gene/protein

TNF

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

increases_expression of

gene/protein

IL1B

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

increases_expression of

gene/protein

NOS2

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

increases_quantity of

gene/protein

Proinflammatory cytokine

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

affects_activity of

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

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: 11655

affects_activity of

tissue/cell line

microglia

Comment Mitochondria represent a particularly vulnerable target of oxidative and nitrosative stress.
Formal Description
Interaction-ID: 11656

affects_activity of

cellular component

mitochondrion

Comment Mitochondria represent a particularly vulnerable target of oxidative and nitrosative stress.
Formal Description
Interaction-ID: 11657

affects_activity of

cellular component

mitochondrion

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

increases_quantity of

drug/chemical compound

Reactive oxygen species

Activated microglia can produce and release ROS.
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

increases_quantity of

drug/chemical compound

Reactive nitrogen species

Activated microglia can produce and release RNS.
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

in mitochondria; RNS can cause damage to essential components of the mitochondria such as mitochondrial DNA.
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

in mitochondria; ROS can cause damage to essential components of the mitochondria such as mitochondrial DNA.
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

mitochondrion

RNS can cause damage to essential components of the mitochondria such as mitochondrial DNA.
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

mitochondrion

ROS can cause damage to essential components of the mitochondria such as mitochondrial DNA.
Comment Hypothesis: ROS, generated from oxidative phosphorylation, may cause mutations in the mtDNA, which in turn leads to mitochondrial oxidative phosphorylation dysfunction and to an increased production of ROS, potentially triggering a vicious cycle.
Formal Description
Interaction-ID: 11685

none selected

Drugbank entries Show/Hide entries for or
Comment Nitrosative stress is involved in the pathogenesis of neurodegenerative and neuroinflammatory disorders.
Formal Description
Interaction-ID: 11688

affects_activity of

Comment Nitrosative stress is involved in the pathogenesis of neurodegenerative and neuroinflammatory disorders.
Formal Description
Interaction-ID: 11690

affects_activity of

phenotype

neurodegeneration

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

decreases_activity of

Comment Inflammatory responses in AD include changes in microglia morphology and astrogliosis.
Formal Description
Interaction-ID: 11762

increases_activity of

Comment Inflammatory responses in AD include changes in microglia morphology and astrogliosis.
Formal Description
Interaction-ID: 11763

affects_activity of

phenotype

astrocytosis

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

increases_quantity of

gene/protein

IL1B

in postmortem AD brain and in the cerebrospinal fluid and peripheral blood; of AD patients
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

increases_quantity of

gene/protein

IL6

in postmortem AD brain and in the cerebrospinal fluid and peripheral blood; of AD patients
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

increases_quantity of

gene/protein

TNF

in postmortem AD brain and in the cerebrospinal fluid and peripheral blood; of AD patients
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

gene/protein

TNF

increases_quantity of

gene/protein

Amyloid beta peptide

Drugbank entries Show/Hide entries for TNF
Comment Hypothesis: A current hypothesis is that accumulation of misfolded proteins may result in oxidative and inflammatory damage, which in turn leads to energy failure, synaptic and neuronal dysfunction, and degeneration in AD brains.
Formal Description
Interaction-ID: 11776

none selected

Drugbank entries Show/Hide entries for or
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

increases_activity of

phenotype

neurodegeneration

Comment Nitrosative stress is involved in the pathogenesis of neurodegenerative and neuroinflammatory disorders.
Formal Description
Interaction-ID: 47327

affects_activity of

phenotype

neuroinflammation