ReviewJournal of molecular medicine (Berlin, Germany)2004
Role of insulin-like growth factor I signaling in neurodegenerative diseases.
Review in Journal of molecular medicine (Berlin, Germany), 2004. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 39 papers, 2 of them syntheses 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
39 citing papers in PubMed, 2 syntheses or guidelines pooled it, 110 citations in OpenAlex.
- The Insulin-like Growth Factor Family as a Potential Peripheral Biomarker in Psychiatric Disorders: A Systematic Review.International journal of molecular sciences · 2025Pooled it
- Pooled it
- Mechanistic insights into postoperative delirium using untargeted high-throughput proteomics in elderly patients - a case-control study.Scientific reports · 2026Observational
- Profile of Trofinetide in the Treatment of Rett Syndrome: Design, Development and Potential Place in Therapy.Drug design, development and therapy · 2024Review
- IGF2 prevents dopaminergic neuronal loss and decreases intracellular alpha-synuclein accumulation in Parkinson's disease models.Cell death discovery · 2023Article
- The neurobiology of insulin-like growth factor I: From neuroprotection to modulation of brain states.Molecular psychiatry · 2023Review
- Insulin resistance, cognition, and Alzheimer disease.Obesity (Silver Spring, Md.) · 2023Review
- Article
- Cell-penetrating peptide-conjugated Morpholino rescues SMA in a symptomatic preclinical model.Molecular therapy : the journal of the American Society of Gene Therapy · 2022Article
- (Neuro) Peptides, Physical Activity, and Cognition.Journal of clinical medicine · 2020Review
- The functional roles of IGF-1 variants in the susceptibility and clinical outcomes of mild traumatic brain injury.Journal of biomedical science · 2019Article
- Altered Insulin/Insulin-Like Growth Factor Signaling in a Comorbid Rat model of Ischemia and β-Amyloid Toxicity.Scientific reports · 2018Article
- Integrating insulin-like growth factor 1 and sex hormones into neuroprotection: Implications for diabetes.World journal of diabetes · 2017Review
- Amyloid-β transmission or unexamined bias?Nature · 2016Article
- Autophagy resolves early retinal inflammation in Igf1-deficient mice.Disease models & mechanisms · 2016Article
- Article
- Integrative neurobiology of metabolic diseases, neuroinflammation, and neurodegeneration.Frontiers in neuroscience · 2015Review
- Effect of sericin on diabetic hippocampal growth hormone/insulin-like growth factor 1 axis.Neural regeneration research · 2013Article
- Melatonin anticancer effects: review.International journal of molecular sciences · 2013Article
- Beta-amyloid monomer and insulin/IGF-1 signaling in Alzheimer's disease.Molecular neurobiology · 2012Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
4 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Disturbed trophic support to neurons has long been considered a potential mechanism in neurodegeneration. Recent evidence indicates that intracellular trophic signaling may be compromised in several neurodegenerative diseases. Changes in the levels of insulin-like growth factor I (IGF-I), a trophic hormone with multiple neuroprotective actions, have recently been observed in several human neurodegenerative illnesses. Therefore analysis of IGF-I pathways could help provide greater insight into trophic disturbances to neurons. However, neurodegenerative diseases with similar clinical manifestations show either high or low levels of circulating IGF-I. This apparently puzzling observation can be explained if we consider that IGF-I input to target neurons is disrupted by either lower IGF-I availability or by reduced cell sensitivity to IGF-I. The latter disturbance may be associated with high IGF-I levels. We hypothesize that in the majority of neurodegenerative diseases compromised IGF-I support to neurons emerges as part of the pathological cascade during the degenerative process and contributes to neuronal demise. In addition, loss of IGF-I input to specific neuronal populations might be the cause of a small group of neurodegenerative diseases.
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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.