ArticleScientific reports2016
Differential neuronal vulnerability identifies IGF-2 as a protective factor in ALS.
Article in Scientific reports, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 70 papers, 1 of them a synthesis that pooled it.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
70 citing papers in PubMed, 1 synthesis or guideline pooled it, 103 citations in OpenAlex.
- Meta-analysis of Genetic Modifiers Reveals Candidate Dysregulated Pathways in Amyotrophic Lateral Sclerosis.Neuroscience · 2019Pooled it
- Reevaluating the role of beta2-microglobulin: new insights on selective vulnerability in ALS pathology.Acta neuropathologica · 2026Article
- Review of the Pathology of Muscle in Amyotrophic Lateral Sclerosis.International journal of molecular sciences · 2026Review
- Type 2 diabetes mellitus, antidiabetics, and the risk of amyotrophic lateral sclerosis.Amyotrophic lateral sclerosis & frontotemporal degeneration · 2025Article
- Transcriptional modulation unique to vulnerable motor neurons predicts ALS across species and SOD1 mutations.Genome research · 2025Article
- Mitochondrial protein import stress augments α-synuclein aggregation and neural damage independent of bioenergetics.Research square · 2025Article
- Insulin-like growth factor 2 reduces Huntington's disease aggregates via AKT and NF-κB signaling in huntington's disease.Cell & bioscience · 2025Article
- Intrinsic neuronal resilience as a tool for therapeutic discovery.Brain : a journal of neurology · 2025Article
- Diversity of Microglia-Derived Molecules with Neurotrophic Properties That Support Neurons in the Central Nervous System and Other Tissues.Molecules (Basel, Switzerland) · 2024Review
- Revealing the potential role of hsa-miR-663a in modulating the PI3K-Akt signaling pathway via miRNA microarray in spinal muscular atrophy patient fibroblast-derived iPSCs.Journal of neuropathology and experimental neurology · 2024Article
- Effects of Short-Term Treatment of Rabbit Extraocular Muscle With Ciliary Neurotrophic Factor.Investigative ophthalmology & visual science · 2024Article
- Spinal inhibitory neurons degenerate before motor neurons and excitatory neurons in a mouse model of ALS.Science advances · 2024Article
- Molecular and cellular mechanisms of selective vulnerability in neurodegenerative diseases.Nature reviews. Neuroscience · 2024Review
- VEGF expression disparities in brainstem motor neurons of the SOD1Neurotherapeutics : the journal of the American Society for Experimental NeuroTherapeutics · 2024Article
- Motor neurons and endothelial cells additively promote development and fusion of human iPSC-derived skeletal myocytes.Skeletal muscle · 2024Article
- Iron-inhibited autophagy via transcription factor ZFP27 in Parkinson's disease.Journal of cellular and molecular medicine · 2023Article
- Intrathecal delivery of AAV-NDNF ameliorates disease progression of ALS mice.Molecular therapy : the journal of the American Society of Gene Therapy · 2023Article
- IGF2 in memory, neurodevelopmental disorders, and neurodegenerative diseases.Trends in neurosciences · 2023Review
- Insulin-like growth factor-2 is a promising candidate for the treatment and prevention of Alzheimer's disease.CNS neuroscience & therapeutics · 2023Review
- Neuroprotective effects of insulin-like growth factor-2 in 6-hydroxydopamine-induced cellular and mouse models of Parkinson's disease.Neural regeneration research · 2023Article
10 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
9 authors at 2 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The fatal disease amyotrophic lateral sclerosis (ALS) is characterized by the loss of somatic motor neurons leading to muscle wasting and paralysis. However, motor neurons in the oculomotor nucleus, controlling eye movement, are for unknown reasons spared. We found that insulin-like growth factor 2 (IGF-2) was maintained in oculomotor neurons in ALS and thus could play a role in oculomotor resistance in this disease. We also showed that IGF-1 receptor (IGF-1R), which mediates survival pathways upon IGF binding, was highly expressed in oculomotor neurons and on extraocular muscle endplate. The addition of IGF-2 induced Akt phosphorylation, glycogen synthase kinase-3β phosphorylation and β-catenin levels while protecting ALS patient motor neurons. IGF-2 also rescued motor neurons derived from spinal muscular atrophy (SMA) patients from degeneration. Finally, AAV9::IGF-2 delivery to muscles of SOD1(G93A) ALS mice extended life-span by 10%, while preserving motor neurons and inducing motor axon regeneration. Thus, our studies demonstrate that oculomotor-specific expression can be utilized to identify candidates that protect vulnerable motor neurons from degeneration.
Indexed as
Identifiers
What OpenQuestion holds
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.