Evidence map›Paper›PMID 39240280›Full record

ReviewMolecular neurobiology2025

Insulin-Like Growth Factor Signaling in Alzheimer's Disease: Pathophysiology and Therapeutic Strategies.

Jie Miao, Yanli Zhang, Chen Su, Qiandan Zheng, Junhong Guo

Abstract readReview
In one paragraph

Review in Molecular neurobiology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 30 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
30citing papers in PubMed, 1 pooled it
–field-weighted citation impact
1 · What the graph read from 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.

2 · The registry

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.

3 · Its place in the literature

Who cites it

30 citing papers in PubMed, 1 synthesis or guideline pooled it.

  1. Pooled it
  2. Gm26550 Modulates Learning and Memory by Increasing IGF1 mRNA Expression and Stability in Nrf2Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026
    Article
  3. Insulin-like growth factor receptor signaling in physiology and disease.Signal transduction and targeted therapy · 2026
    Review
  4. Article
  5. Review
  6. Review
  7. Review
  8. Vitamin DInternational journal of molecular sciences · 2026
    Article
  9. Review
  10. Article
  11. Article
  12. Article
  13. Review
  14. Review
  15. Article
  16. Article
  17. Article
  18. Advancing global dementia research through equity and inclusion.Alzheimer's & dementia : the journal of the Alzheimer's Association · 2026
    Article
  19. Article
  20. Article
4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

5 authors.

Jie MiaoDepartment of Neurology, First Hospital of Shanxi Medical University, Taiyuan, 030001, Shanxi, China.
Yanli ZhangDepartment of Neurology, First Hospital of Shanxi Medical University, Taiyuan, 030001, Shanxi, China.
Chen SuDepartment of Neurology, First Hospital of Shanxi Medical University, Taiyuan, 030001, Shanxi, China.
Qiandan ZhengDepartment of Neurology, First Hospital of Shanxi Medical University, Taiyuan, 030001, Shanxi, China.
Junhong GuoDepartment of Neurology, First Hospital of Shanxi Medical University, Taiyuan, 030001, Shanxi, China. neuroguo@163.com.

Funding

National Key Research and Development Program of China 2023YFC3605400Shanxi Province Basic Research Program 202303021212373Shanxi Province Basic Research Program 202303021221212Shanxi Province Basic Research Program 202303021222348STI2030-Major Projects 2021ZD 0201801
6 · The paper itself

Abstract

Alzheimer's disease (AD) is the leading cause of dementia among the elderly population, posing a significant public health challenge due to limited therapeutic options that merely delay cognitive decline. AD is associated with impaired energy metabolism and reduced neurotrophic signaling. The insulin-like growth factor (IGF) signaling pathway, crucial for central nervous system (CNS) development, metabolism, repair, cognition, and emotion regulation, includes IGF-1, IGF-2, IGF-1R, IGF-2R, insulin receptor (IR), and six insulin-like growth factor binding proteins (IGFBPs). Research has identified abnormalities in IGF signaling in individuals with AD and AD models. Dysregulated expression of IGFs, receptors, IGFBPs, and disruptions in downstream phosphoinositide 3-kinase-protein kinase B (PI3K/AKT) and mitogen-activated protein kinase (MAPK) pathways collectively increase AD susceptibility. Studies suggest modulating the IGF pathway may ameliorate AD pathology and cognitive decline. This review explores the CNS pathophysiology of IGF signaling in AD progression and assesses the potential of targeting the IGF system as a novel therapeutic strategy. Further research is essential to elucidate how aberrant IGF signaling contributes to AD development, understand underlying molecular mechanisms, and evaluate the safety and efficacy of IGF-based treatments.

Indexed as

Alzheimer DiseaseBrainInsulin-Like Growth Factor IInsulin-Like Growth Factor IIAnimalsDisease Models, AnimalDisease ProgressionHumansInsulin-Like Growth Factor Binding ProteinsNeuronal PlasticityNeuroprotectionOxidative StressReceptor, IGF Type 1Receptor, IGF Type 2Signal TransductionInsulin-Like Growth Factor Binding ProteinsInsulin-Like Growth Factor IInsulin-Like Growth Factor IIReceptor, IGF Type 1Receptor, IGF Type 2Alzheimer’s diseaseCentral nervous systemInsulin-like growth factor binding proteinsInsulin-like growth factor receptorsInsulin-like growth factorsTreatment

Identifiers

PMID39240280
PMCPMC11790777

What OpenQuestion holds

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Registered trials

None linked

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.