ReviewMolecular neurobiology2025
Decoding the Role of Neurotrophins in Glycogen Synthase Kinase 3-Beta Regulation in Alzheimer's Disease.
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 4 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.
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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
4 citing papers in PubMed.
- Timosaponin B-II attenuates hemorrhagic transformation-driven acceleration of alzheimer disease-related pathology after ischemic stroke.Biochemistry and biophysics reports · 2026Article
- Metabolic reprogramming of neurons in alzheimer disease: a biochemical perspective.Metabolic brain disease · 2026Review
- Small molecule modulation of the p75 neurotrophin receptor promotes dendritic spine resilience to pathogenic tau species and reduces their accumulation.Acta neuropathologica communications · 2026Article
- From Synaptic Plasticity to Neurodegeneration: BDNF as a Transformative Target in Medicine.International journal of molecular sciences · 2025Review
Corrections and comments
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Authors and funding
2 authors.
Funding
Abstract
Alzheimer's disease (AD) is a progressive neurodegenerative disorder and the most prevalent contributor to dementia in elderly individuals. Numerous signalling pathways influencing AD pathophysiology, involving glycogen synthase kinase-3β (Gsk-3β), have been investigated extensively as potential therapeutic targets. Gsk-3β is a critical factor in AD pathogenesis that affects several key hallmarks of the disease notably tau phosphorylation, amyloid-β generation, cognition, neurogenesis, and synaptic integrity. Neurotrophins are small proteins that are critical for maintaining neuronal health and function and may be used to treat neurodegenerative diseases. Notably, the dysregulation of certain neurotrophins and their receptors is also linked with AD which is a major contributor to neurodegeneration. Studies indicated that neurotrophins and their modulators are capable of protecting neurons by blocking the Gsk-3β activity suggesting a potential link for neuroprotection. Neurotrophins support the survival of neurons by regulating Gsk-3β activity. Brain-derived neurotrophic factor (BDNF) and nerve growth factor (NGF) signalling pathways activate Trk receptors that trigger downstream signalling cascades that subsequently inhibit Gsk-3β activity and reduce AD-related neuropathology. We also explore the role of modulators including phosphatases, kinase cascades, and other regulatory proteins that cross paths with neurotrophin-Gsk-3β signalling. In conclusion, this manuscript summarizes both direct and indirect regulatory roles of neurotrophins and modulators on Gsk-3β to understand the intricate mechanisms driving neurodegeneration in AD.
Indexed as
Identifiers
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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.