MCP1-CCR2 and neuroinflammation in the ALS motor cortex with TDP-43 pathology.


Journal

Journal of neuroinflammation
ISSN: 1742-2094
Titre abrégé: J Neuroinflammation
Pays: England
ID NLM: 101222974

Informations de publication

Date de publication:
30 Oct 2019
Historique:
received: 07 05 2019
accepted: 13 09 2019
entrez: 1 11 2019
pubmed: 2 11 2019
medline: 31 3 2020
Statut: epublish

Résumé

The involvement of non-neuronal cells and the cells of innate immunity has been attributed to the initiation and progression of ALS. TDP-43 pathology is observed in a broad spectrum of ALS cases and is one of the most commonly shared pathologies. The potential involvement of the neuroimmune axis in the motor cortex of ALS patients with TDP-43 pathology needs to be revealed. This information is vital for building effective treatment strategies. We investigated the presence of astrogliosis and microgliosis in the motor cortex of ALS patients with TDP-43 pathology. prpTDP-43 We detected both activated astrocytes and microglia, especially rod-like microglia, in the motor cortex of patients and TDP-43 mouse model. Besides, CCR2+ TMEM119- infiltrating monocytes were detected as they penetrate the brain parenchyma. Interestingly, Betz cells, which normally do not express MCP1, were marked with high levels of MCP1 expression when diseased. There is an early contribution of a neuroinflammatory response for upper motor neuron (UMN) degeneration with respect to TDP-43 pathology, and MCP1-CCR2 signaling is important for the recognition of diseased upper motor neurons by infiltrating monocytes. The findings are conserved among species and are observed in both ALS and ALS-FTLD patients.

Sections du résumé

BACKGROUND BACKGROUND
The involvement of non-neuronal cells and the cells of innate immunity has been attributed to the initiation and progression of ALS. TDP-43 pathology is observed in a broad spectrum of ALS cases and is one of the most commonly shared pathologies. The potential involvement of the neuroimmune axis in the motor cortex of ALS patients with TDP-43 pathology needs to be revealed. This information is vital for building effective treatment strategies.
METHODS METHODS
We investigated the presence of astrogliosis and microgliosis in the motor cortex of ALS patients with TDP-43 pathology. prpTDP-43
RESULTS RESULTS
We detected both activated astrocytes and microglia, especially rod-like microglia, in the motor cortex of patients and TDP-43 mouse model. Besides, CCR2+ TMEM119- infiltrating monocytes were detected as they penetrate the brain parenchyma. Interestingly, Betz cells, which normally do not express MCP1, were marked with high levels of MCP1 expression when diseased.
CONCLUSIONS CONCLUSIONS
There is an early contribution of a neuroinflammatory response for upper motor neuron (UMN) degeneration with respect to TDP-43 pathology, and MCP1-CCR2 signaling is important for the recognition of diseased upper motor neurons by infiltrating monocytes. The findings are conserved among species and are observed in both ALS and ALS-FTLD patients.

Identifiants

pubmed: 31666087
doi: 10.1186/s12974-019-1589-y
pii: 10.1186/s12974-019-1589-y
pmc: PMC6822373
doi:

Substances chimiques

CCR2 protein, human 0
DNA-Binding Proteins 0
Receptors, CCR2 0
TARDBP protein, human 0

Types de publication

Journal Article

Langues

eng

Sous-ensembles de citation

IM

Pagination

196

Subventions

Organisme : NIA NIH HHS
ID : P30 AG013854
Pays : United States
Organisme : NINDS NIH HHS
ID : R21 NS085750
Pays : United States
Organisme : ALS Association
ID : Milton Safenowitz Postdoctoral Fellowship
Organisme : NIH HHS
ID : R21-NS085750
Pays : United States
Organisme : NIH/NIA
ID : AG13854

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Auteurs

Javier H Jara (JH)

Davee Department of Neurology and Clinical Neurological Sciences, Northwestern University Feinberg School of Medicine, Chicago, USA.
Les Turner ALS Center, Chicago, USA.

Mukesh Gautam (M)

Davee Department of Neurology and Clinical Neurological Sciences, Northwestern University Feinberg School of Medicine, Chicago, USA.
Les Turner ALS Center, Chicago, USA.

Nuran Kocak (N)

Davee Department of Neurology and Clinical Neurological Sciences, Northwestern University Feinberg School of Medicine, Chicago, USA.
Les Turner ALS Center, Chicago, USA.

Edward F Xie (EF)

Davee Department of Neurology and Clinical Neurological Sciences, Northwestern University Feinberg School of Medicine, Chicago, USA.
Les Turner ALS Center, Chicago, USA.

Qinwen Mao (Q)

Department of Pathology, Northwestern University, Chicago, USA.
Mesulam Center for Cognitive Neurology and Alzheimer's Disease, Northwestern University Feinberg School of Medicine, Chicago, USA.

Eileen H Bigio (EH)

Department of Pathology, Northwestern University, Chicago, USA.
Mesulam Center for Cognitive Neurology and Alzheimer's Disease, Northwestern University Feinberg School of Medicine, Chicago, USA.

P Hande Özdinler (PH)

Davee Department of Neurology and Clinical Neurological Sciences, Northwestern University Feinberg School of Medicine, Chicago, USA. ozdinler@northwestern.edu.
Les Turner ALS Center, Chicago, USA. ozdinler@northwestern.edu.
Mesulam Center for Cognitive Neurology and Alzheimer's Disease, Northwestern University Feinberg School of Medicine, Chicago, USA. ozdinler@northwestern.edu.
Robert H. Lurie Comprehensive Cancer Center, Northwestern University, Chicago, IL, 60611, USA. ozdinler@northwestern.edu.
Department of Neurology, 303 E Chicago Ave., Ward 10-015, Chicago, IL, 60611, USA. ozdinler@northwestern.edu.

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