ReviewCellular and molecular life sciences : CMLS2014
Cellular therapy to target neuroinflammation in amyotrophic lateral sclerosis.
Review in Cellular and molecular life sciences : CMLS, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 53 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
53 citing papers in PubMed, 93 citations in OpenAlex.
- Plasma exchange with albumin replacement and disease progression in amyotrophic lateral sclerosis: a pilot study.Neurological sciences : official journal of the Italian Neurological Society and of the Italian Society of Clinical Neurophysiology · 2022Trial
- Case Report: Autologous bone marrow mononuclear cell transplantation improved motor function in a patient with amyotrophic lateral sclerosis.Frontiers in medicine · 2026Article
- Cortical Stimulation-Based Transcriptome Shifts on Parkinson's Disease Animal Model.ASN neuro · 2025Article
- Evaluating the causal association between microRNAs and amyotrophic lateral sclerosis.Neurological sciences : official journal of the Italian Neurological Society and of the Italian Society of Clinical Neurophysiology · 2023Article
- Early Signs of Neuroinflammation in the Postnatal Wobbler Mouse Model of Amyotrophic Lateral Sclerosis.Cellular and molecular neurobiology · 2023Article
- Potential Applications for Growth Hormone Secretagogues Treatment of Amyotrophic Lateral Sclerosis.Current neuropharmacology · 2023Article
- APOE in the bullseye of neurodegenerative diseases: impact of the APOE genotype in Alzheimer's disease pathology and brain diseases.Molecular neurodegeneration · 2022Review
- Significance of intercellular communication for neurodegenerative diseases.Neural regeneration research · 2022Article
- Muscle cells of sporadic amyotrophic lateral sclerosis patients secrete neurotoxic vesicles.Journal of cachexia, sarcopenia and muscle · 2022Article
- Dying by fire: noncanonical functions of autophagy proteins in neuroinflammation and neurodegeneration.Neural regeneration research · 2022Review
- Bone Marrow Stromal Cell Antigen 2: Is a Potential Neuroinflammation Biomarker of SOD1Frontiers in neuroscience · 2021Article
- Molecular and Cellular Mechanisms Affected in ALS.Journal of personalized medicine · 2020Review
- Single-cell RNA-seq analysis of the brainstem of mutant SOD1 mice reveals perturbed cell types and pathways of amyotrophic lateral sclerosis.Neurobiology of disease · 2020Article
- Advances in nanotechnology-based strategies for the treatments of amyotrophic lateral sclerosis.Materials today. Bio · 2020Review
- Generation of Cellular Reactive Oxygen Species by Activation of the EP2 Receptor Contributes to Prostaglandin E2-Induced Cytotoxicity in Motor Neuron-Like NSC-34 Cells.Oxidative medicine and cellular longevity · 2020Article
- Advances, Challenges, and Perspectives in Translational Stem Cell Therapy for Amyotrophic Lateral Sclerosis.Molecular neurobiology · 2019Review
- Microglial activation in an amyotrophic lateral sclerosis-like model caused by Ranbp2 loss and nucleocytoplasmic transport impairment in retinal ganglion neurons.Cellular and molecular life sciences : CMLS · 2019Article
- Article
- Thymosin Alpha-1 Inhibits Complete Freund's Adjuvant-Induced Pain and Production of Microglia-Mediated Pro-inflammatory Cytokines in Spinal Cord.Neuroscience bulletin · 2019Article
- The coming-of-age of nucleocytoplasmic transport in motor neuron disease and neurodegeneration.Cellular and molecular life sciences : CMLS · 2019Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
7 authors at 4 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Neurodegenerative disorders are characterized by the selective vulnerability and progressive loss of discrete neuronal populations. Non-neuronal cells appear to significantly contribute to neuronal loss in diseases such as amyotrophic lateral sclerosis (ALS), Parkinson, and Alzheimer's disease. In ALS, there is deterioration of motor neurons in the cortex, brainstem, and spinal cord, which control voluntary muscle groups. This results in muscle wasting, paralysis, and death. Neuroinflammation, characterized by the appearance of reactive astrocytes and microglia as well as macrophage and T-lymphocyte infiltration, appears to be highly involved in the disease pathogenesis, highlighting the involvement of non-neuronal cells in neurodegeneration. There appears to be cross-talk between motor neurons, astrocytes, and immune cells, including microglia and T-lymphocytes, which are subsequently activated. Currently, effective therapies for ALS are lacking; however, the non-cell autonomous nature of ALS may indicate potential therapeutic targets. Here, we review the mechanisms of action of astrocytes, microglia, and T-lymphocytes in the nervous system in health and during the pathogenesis of ALS. We also evaluate the therapeutic potential of these cellular populations, after transplantation into ALS patients and animal models of the disease, in modulating the environment surrounding motor neurons from pro-inflammatory to neuroprotective. We also thoroughly discuss the recent advances made in the field and caveats that need to be overcome for clinical translation of cell therapies aimed at modulating non-cell autonomous events to preserve remaining motor neurons in patients.
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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.