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Microglial Activation Correlates with Disease Progression and Upper Motor Neuron Clinical Symptoms in Amyotrophic Lateral Sclerosis
Open accessAbstract
BACKGROUND/AIMS: We evaluated clinicopathological correlates of upper motor neuron (UMN) damage in amyotrophic lateral sclerosis (ALS), and analyzed if the presence of the C9ORF72 repeat expansion was associated with alterations in microglial inflammatory activity. METHODS: Microglial pathology was assessed by IHC with 2 different antibodies (CD68, Iba1), myelin loss by Kluver-Barrera staining and myelin basic protein (MBP) IHC, and axonal loss by neurofilament protein (TA51) IHC, performed on 59 autopsy cases of ALS including 9 cases with C9ORF72 repeat expansion. RESULTS: Microglial pathology as depicted by CD68 and Iba1 was significantly more extensive in the corticospinal tract (CST) of ALS cases with a rapid progression of disease. Cases with C9ORF72 repeat expansion showed more extensive microglial pathology in the medulla and motor cortex which persisted after adjusting for disease duration in a logistic regression model. Higher scores on the clinical UMN scale correlated with increasing microglial pathology in the cervical CST. TDP-43 pathology was more extensive in the motor cortex of cases with rapid progression of disease. CONCLUSIONS: This study demonstrates that microglial pathology in the CST of ALS correlates with disease progression and is linked to severity of UMN deficits.
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“Neuroinflammation has also been observed in patients with ALS, in which inflammatory microglial hyperactivity in these patients has been linked to disease progression [50,54].”
From Head Injury and Amyotrophic Lateral Sclerosis: Population-Based Study from the National ALS Registry (2025) · cites this paper as [54]
In the citing paper
“ALS patients carrying C9orf72 mutations display microglial activation that correlates with disease progression [438].”
From Autophagy and ALS: mechanistic insights and therapeutic implications (2022) · cites this paper as [438]
In the citing paper
“Postmortem studies308–310 and in vivo PET studies311–313 revealed widespread cerebral microglial activation in patients with ALS,308–312 and even in pre-symptomatic ALS-related mutation carriers.309,313”
From Microglia in neurodegenerative diseases: mechanism and potential therapeutic targets (2023) · cites this paper as [309]
In the citing paper
“Microglial activation in the corticospinal tract of ALS correlated with neuronal and axonal loss and more severe upper motor neuron symptoms.309”
From Microglia in neurodegenerative diseases: mechanism and potential therapeutic targets (2023) · cites this paper as [309]
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“Transcriptome and histologic analyses of postmortem tissue from patients with ALS carrying the C9orf72 expansion (C9-ALS) found that decreased C9orf72 expression in C9-ALS led to altered microglial function and increased microglial activation.309,361”
From Microglia in neurodegenerative diseases: mechanism and potential therapeutic targets (2023) · cites this paper as [309]
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Metadata
- Authors
- Brettschneider, J., Toledo, J. B., Van Deerlin, V. M., Elman, L., McCluskey, L., Lee, V. M.-Y., & Trojanowski, J. Q.
- Affiliations
- Universität Ulm (DE)
- University of Pennsylvania (US)
- Corresponding author
- Brettschneider, Johannes
- Venue
- PLoS ONE
- Publisher
- Public Library of Science (PLoS)
- Published
- 2012-06-14
- Volume
- 7
- Issue
- 6
- Pages
- e39216
- ISSN
- 1932-6203 (ISSN-L)
- PMC
- PMC3375234
- OpenAlex
- W1974485241
- Cited by
- 268
- References
- 68
- Citations by year
- 2026: 16 · 2025: 18 · 2024: 23 · 2023: 27 · 2022: 24 · 2021: 25 · 2020: 24 · 2019: 24 · 2018: 15 · 2017: 22 · 2016: 10 · 2015: 13 · 2014: 12 · 2013: 13 · 2012: 2
- FWCI
- 8.26
- Type
- journal article
- Language
- en
- Open access
- gold
- doi.org
- Locations
- PLoS ONE (publishedVersion, cc-by)
- PubMed Central (publishedVersion, cc-by)
- PubMed (publishedVersion)
- DOAJ (DOAJ: Directory of Open Access Journals) (submittedVersion, cc-by-sa)
- Figshare (submittedVersion, cc-by)
- Funders
- Deutsche Forschungsgemeinschaft (AG10124)
- National Institutes of Health (AG 10 124, AG 17586)
- National Institute on Aging (AG033101, AG-32953, P30AG010124, P01AG017586, AG17586, AG-10124, K08AG033101, P01AG032953)
- Topics
- Health Sciences › Medicine › Clinical Neurology › Amyotrophic Lateral Sclerosis Research
- Life Sciences › Neuroscience › Neurology › Neuroinflammation and Neurodegeneration Mechanisms
- Life Sciences › Neuroscience › Cellular and Molecular Neuroscience › Alzheimer's disease research and treatments
- Keywords
- amyotrophic lateral sclerosis, microglial activation, upper motor neuron lesion, corticospinal tract, C9orf72 repeat expansion, disease progression, TDP-43 pathology, demyelination, axonal loss, neuroinflammation, motor cortex, medulla
- MeSH terms
- Aged, Amyotrophic Lateral Sclerosis, Axons, Base Sequence, Female, Humans, Male, Middle Aged, Motor Neurons, Cohort Studies, Polymerase Chain Reaction, Open Reading Frames, Microglia, DNA Primers, Disease Progression
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