ArticleFrontiers in cellular neuroscience2013
Beta-2 microglobulin is important for disease progression in a murine model for amyotrophic lateral sclerosis.
Article in Frontiers in cellular neuroscience, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.
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Who cites it
18 citing papers in PubMed, 25 citations in OpenAlex.
- PAICS mediates DNA damage and cerebellar neuronal loss in C9orf72 amyotrophic lateral sclerosis.Brain : a journal of neurology · 2026Article
- Reevaluating the role of beta2-microglobulin: new insights on selective vulnerability in ALS pathology.Acta neuropathologica · 2026Article
- Transcriptional downregulation of rhodopsin is associated with desensitization of rods to light-induced damage in a murine model of retinitis pigmentosa.Human molecular genetics · 2025Article
- Review
- Early activation of cellular stress and death pathways caused by cytoplasmic TDP-43 in the rNLS8 mouse model of ALS and FTD.Molecular psychiatry · 2023Article
- Neuroprotection by upregulation of the major histocompatibility complex class I (MHC I) in SOD1Frontiers in cellular neuroscience · 2023Article
- Bioinformatics Approach to Identify Significant Biomarkers, Drug Targets Shared Between Parkinson's Disease and Bipolar Disorder: A Pilot Study.Bioinformatics and biology insights · 2022Article
- Cytotoxic CD8Proceedings of the National Academy of Sciences of the United States of America · 2019Article
- Counteracting roles of MHCI and CD8Molecular neurodegeneration · 2018Article
- Temporospatial Analysis and New Players in the Immunology of Amyotrophic Lateral Sclerosis.International journal of molecular sciences · 2018Review
- The Emerging Role of the Major Histocompatibility Complex Class I in Amyotrophic Lateral Sclerosis.International journal of molecular sciences · 2017Review
- Major histocompatibility complex class I molecules protect motor neurons from astrocyte-induced toxicity in amyotrophic lateral sclerosis.Nature medicine · 2016Article
- Major Histocompatibility Complex I Expression by Motor Neurons and Its Implication in Amyotrophic Lateral Sclerosis.Frontiers in neurology · 2016Review
- Bayesian graphical network analyses reveal complex biological interactions specific to Alzheimer's disease.Journal of Alzheimer's disease : JAD · 2015Article
- Functional deficiency of MHC class I enhances LTP and abolishes LTD in the nucleus accumbens of mice.PloS one · 2014Article
- Microglia centered pathogenesis in ALS: insights in cell interconnectivity.Frontiers in cellular neuroscience · 2014Review
- Cellular and molecular mechanisms of motor neuron death in amyotrophic lateral sclerosis: a perspective.Frontiers in cellular neuroscience · 2014Article
- Article
Corrections and comments
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Authors and funding
8 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Beta-2 microglobulin (β2m) is an essential component of the major histocompatibility complex (MHC) class I proteins and in the nervous system β2m is predominantly expressed in motor neurons. As β2m can promote nerve regeneration, we investigated its potential role in amyotrophic lateral sclerosis (ALS) by investigating its expression level as well as the effect of genetically removing β2m on the disease process in mutant superoxide dismutase 1 (SOD1 (G93A) ) mice, a model of ALS. We observed a strong upregulation of β2m in motor neurons during the disease process and ubiquitous removal of β2m dramatically shortens the disease duration indicating that β2m plays an essential and positive role during the disease process. We hypothesize that β2m contributes to plasticity that is essential for muscle reinnervation. Absence of this plasticity will lead to faster muscle denervation and counteracting this process could be a relevant therapeutic target.
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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.