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Neuroinflammation in motor neuron disease.

Komine O, Yamanaka K - Nagoya J Med Sci (2015)

Bottom Line: These findings led to the concept of non-cell autonomous neurodegeneration.Neuroinflammation, which is mediated by activated glial cells and infiltrated lymphocytes and accompanied by the subsequent production of proinflammatory cytokines and neurotoxic or neuroprotective molecules, is characteristic to the pathology in ALS and is a key component for non-cell autonomous neurodegeneration.Based on the cell-type specific pathomechanisms of motor neuron disease, targeting of neuroinflammation could lead to future therapeutic strategies for ALS and could be potentially applied to other neurodegenerative diseases.

View Article: PubMed Central - PubMed

Affiliation: Department of Neuroscience and Pathobiology, Research Institute of Environmental Medicine, Nagoya University, Nagoya, Japan.

ABSTRACT
Increasing evidence suggests that the pathogenesis of neurodegenerative diseases including amyotrophic lateral sclerosis (ALS) is not restricted to the neurons but attributed to the abnormal interactions of neurons and surrounding glial and lymphoid cells. These findings led to the concept of non-cell autonomous neurodegeneration. Neuroinflammation, which is mediated by activated glial cells and infiltrated lymphocytes and accompanied by the subsequent production of proinflammatory cytokines and neurotoxic or neuroprotective molecules, is characteristic to the pathology in ALS and is a key component for non-cell autonomous neurodegeneration. This review covers the involvement of microglia and astrocytes in the ALS mouse models and human ALS, and it also covers the deregulated pathways in motor neurons, which are involved in initiating the disease. Based on the cell-type specific pathomechanisms of motor neuron disease, targeting of neuroinflammation could lead to future therapeutic strategies for ALS and could be potentially applied to other neurodegenerative diseases.

No MeSH data available.


Related in: MedlinePlus

Activated microglia and astrocytes in the lumbar spinal cord of mutant SOD1 mice.Lumbar spinal cord sections from SOD1G93A mice at pre-onset (A), symptomatic stage (B), and end-stage (C) were stained with antibodies for ChAT (cholinergic motor neuron, blue), GFAP (astrocytes, green), and Iba-1 (microglia, red). Anterior horn regions were shown. Prominent activation of microglia and astrocytes with motor neuron loss were observed (B and C). Scale bar: 100μm.
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fig1: Activated microglia and astrocytes in the lumbar spinal cord of mutant SOD1 mice.Lumbar spinal cord sections from SOD1G93A mice at pre-onset (A), symptomatic stage (B), and end-stage (C) were stained with antibodies for ChAT (cholinergic motor neuron, blue), GFAP (astrocytes, green), and Iba-1 (microglia, red). Anterior horn regions were shown. Prominent activation of microglia and astrocytes with motor neuron loss were observed (B and C). Scale bar: 100μm.

Mentions: Astrogliosis and microgliosis are pathological hallmarks of neuroinflammation in ALS.21, 22) (Figure 1). Below, we have summarized the roles of microglia and astrocytes in the pathology of ALS as reported in studies of rodent models and humans with ALS.


Neuroinflammation in motor neuron disease.

Komine O, Yamanaka K - Nagoya J Med Sci (2015)

Activated microglia and astrocytes in the lumbar spinal cord of mutant SOD1 mice.Lumbar spinal cord sections from SOD1G93A mice at pre-onset (A), symptomatic stage (B), and end-stage (C) were stained with antibodies for ChAT (cholinergic motor neuron, blue), GFAP (astrocytes, green), and Iba-1 (microglia, red). Anterior horn regions were shown. Prominent activation of microglia and astrocytes with motor neuron loss were observed (B and C). Scale bar: 100μm.
© Copyright Policy - open-access
Related In: Results  -  Collection

License
Show All Figures
getmorefigures.php?uid=PMC4664586&req=5

fig1: Activated microglia and astrocytes in the lumbar spinal cord of mutant SOD1 mice.Lumbar spinal cord sections from SOD1G93A mice at pre-onset (A), symptomatic stage (B), and end-stage (C) were stained with antibodies for ChAT (cholinergic motor neuron, blue), GFAP (astrocytes, green), and Iba-1 (microglia, red). Anterior horn regions were shown. Prominent activation of microglia and astrocytes with motor neuron loss were observed (B and C). Scale bar: 100μm.
Mentions: Astrogliosis and microgliosis are pathological hallmarks of neuroinflammation in ALS.21, 22) (Figure 1). Below, we have summarized the roles of microglia and astrocytes in the pathology of ALS as reported in studies of rodent models and humans with ALS.

Bottom Line: These findings led to the concept of non-cell autonomous neurodegeneration.Neuroinflammation, which is mediated by activated glial cells and infiltrated lymphocytes and accompanied by the subsequent production of proinflammatory cytokines and neurotoxic or neuroprotective molecules, is characteristic to the pathology in ALS and is a key component for non-cell autonomous neurodegeneration.Based on the cell-type specific pathomechanisms of motor neuron disease, targeting of neuroinflammation could lead to future therapeutic strategies for ALS and could be potentially applied to other neurodegenerative diseases.

View Article: PubMed Central - PubMed

Affiliation: Department of Neuroscience and Pathobiology, Research Institute of Environmental Medicine, Nagoya University, Nagoya, Japan.

ABSTRACT
Increasing evidence suggests that the pathogenesis of neurodegenerative diseases including amyotrophic lateral sclerosis (ALS) is not restricted to the neurons but attributed to the abnormal interactions of neurons and surrounding glial and lymphoid cells. These findings led to the concept of non-cell autonomous neurodegeneration. Neuroinflammation, which is mediated by activated glial cells and infiltrated lymphocytes and accompanied by the subsequent production of proinflammatory cytokines and neurotoxic or neuroprotective molecules, is characteristic to the pathology in ALS and is a key component for non-cell autonomous neurodegeneration. This review covers the involvement of microglia and astrocytes in the ALS mouse models and human ALS, and it also covers the deregulated pathways in motor neurons, which are involved in initiating the disease. Based on the cell-type specific pathomechanisms of motor neuron disease, targeting of neuroinflammation could lead to future therapeutic strategies for ALS and could be potentially applied to other neurodegenerative diseases.

No MeSH data available.


Related in: MedlinePlus