ArticlePloS one2012
Microglial activation correlates with disease progression and upper motor neuron clinical symptoms in amyotrophic lateral sclerosis.
Article in PloS one, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 169 papers, 1 of them a synthesis that pooled it.
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Who cites it
169 citing papers in PubMed, 1 synthesis or guideline pooled it, 260 citations in OpenAlex.
- The Current Potential Pathogenesis of Amyotrophic Lateral Sclerosis.Molecular neurobiology · 2025Pooled it
- Trial
- A PET/CT approach to spinal cord metabolism in amyotrophic lateral sclerosis.European journal of nuclear medicine and molecular imaging · 2016Trial
- Pathology of general proprioception in a canine disease model of amyotrophic lateral sclerosis.Journal of the neurological sciences · 2026Article
- Lateral sclerosis in amyotrophic lateral sclerosis is an upper motor neuron distal axonopathy ("dying back"): a clinical-neuropathological study.Acta neuropathologica · 2026Article
- Integrative ALS therapy: gene targeted therapy by base editing and potential exercise rehabilitation as synergistic strategies for functional recovery.Physical activity and nutrition · 2026Article
- Neurodegenerative diseases and immune system: From pathogenic mechanism to therapy.Neural regeneration research · 2026Article
- Multi-regional transcriptomic profiling reveals divergent molecular mechanisms in ALS-related neurodegeneration.PLoS genetics · 2026Article
- Intrathecal (GActa neuropathologica communications · 2026Article
- Caspase-4 transgenic mice exhibit cytoplasmic TDP-43 accumulation and age-dependent neuropathology.Nature communications · 2026Article
- PU.1 restores microglial dysfunction caused by C9ORF72 repeat expansions in neural organoids.Brain : a journal of neurology · 2026Article
- Microglial HVCN1 Deficiency Improves Movement and Survival of SOD1Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Article
- C9orf72 in myeloid cells prevents an inflammatory response to microbial glycogen.Cell reports · 2026Article
- Progressive neurodegeneration, motor decline, and premature mortality in aging Ngly1 deficient rats.Orphanet journal of rare diseases · 2026Article
- Intrathecal (GbioRxiv : the preprint server for biology · 2026Article
- Brain metabolic imaging with 18 F-PET-CT and machine-learning clustering analysis reveal divergent metabolic phenotypes in patients with amyotrophic lateral sclerosis.European journal of nuclear medicine and molecular imaging · 2026Article
- Spatiotemporal Dynamics and Cellular States of Neuroinflammation in Amyotrophic Lateral Sclerosis: Implications for Stage‑Specific Therapeutics.ASN neuro · 2026Review
- Human amyotrophic lateral sclerosis/motor neuron disease: The disease-associated microglial pathway is upregulated while APOE genotype governs risk and survival.Brain pathology (Zurich, Switzerland) · 2025Article
- Employing nullclines to balance treatment efficacy and neurotoxicity for sustained tumor control.Mathematical biosciences · 2025Article
- Inflammation in Neuronal Intranuclear Inclusion Disease (NIID): mechanisms, biomarkers, and therapeutic implications.Journal of neuroinflammation · 2025Review
109 more citing papers are in PubMed but not listed here.
Corrections and comments
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Authors and funding
7 authors at 2 institutions in 2 countries.
Funding
Abstract
BACKGROUND/
aimsWe 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.
methodsMicroglial 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.
resultsMicroglial 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.
conclusionsThis 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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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.