ArticleFrontiers in molecular neuroscience2023
GAP-43 closely interacts with BDNF in hippocampal neurons and is associated with Alzheimer's disease progression.
Article in Frontiers in molecular neuroscience, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.
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17 citing papers in PubMed, 28 citations in OpenAlex.
- Targeted muscle reinnervation surgery modulates apoptosis and synaptic plasticity to improve motor function following tibial nerve injury in rats.Annals of medicine · 2026Article
- Effects of GABAAR modulators CL218872 and MRK-016 on neural repair and synaptic plasticity in mice with Intracerebral hemorrhage.PloS one · 2026Article
- Artificial intelligence empowers gut microbiota research in neurodegenerative diseases molecular mechanisms and precision therapy.iScience · 2025Review
- Effect of regular treadmill exercise on astrocyte proliferation-related proteins in the motor cortex and hippocampus after traumatic brain injury.Journal of exercise rehabilitation · 2025Article
- From Amyloid to Synaptic Dysfunction: Biomarker-Driven Insights into Alzheimer's Disease.Current issues in molecular biology · 2025Review
- Electroacupuncture treatment enhances synaptic plasticity in middle cerebral artery occlusion mice via the miR-670-3p/HMGB1 axis.Journal of the Chinese Medical Association : JCMA · 2025Article
- Aberrance of GAP43/p-GAP43 Closely Associates with the Pathology of Neuron Loss in Prion-Infected Rodent Models.Molecular neurobiology · 2025Article
- The Role of Brain-Derived Neurotrophic Factor as an Essential Mediator in Neuronal Functions and the Therapeutic Potential of Its Mimetics for Neuroprotection in Neurologic and Psychiatric Disorders.Molecules (Basel, Switzerland) · 2025Review
- Varenicline Attenuates Memory Impairment in Amyloid-Beta-Induced Rat Model of Alzheimer's Disease.Neurochemical research · 2025Article
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- Comparative Genomics of the World's Smallest Mammals Reveals Links to Echolocation, Metabolism, and Body Size Plasticity.Genome biology and evolution · 2024Article
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- Environmental Toxins and Alzheimer's Disease: a Comprehensive Analysis of Pathogenic Mechanisms and Therapeutic Modulation.Molecular neurobiology · 2024Review
- An Interaction between Brain-Derived Neurotrophic Factor and Stress-Related Glucocorticoids in the Pathophysiology of Alzheimer's Disease.International journal of molecular sciences · 2024Review
- Association between Plasma Brain-derived Neurotrophic Factor Level and Alzheimer's Disease: A Mendelian Randomization Study.Current neurovascular research · 2024Article
- Intranasal CEPO-FC prevents attention deficits in streptozotocin-induced rat model of Alzheimer's disease: Focus on synaptic plasticity-related factors.EXCLI journal · 2024Article
- Involvement of brain-derived neurotrophic factor signaling in the pathogenesis of stress-related brain diseases.Frontiers in molecular neuroscience · 2023Review
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Authors and funding
9 authors at 2 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Introduction: Growth-associated protein 43 (GAP-43) is known as a neuronal plasticity protein because it is widely expressed at high levels in neuronal growth cones during axonal regeneration. GAP-43 expressed in mature adult neurons is functionally important for the neuronal communication of synapses in learning and memory. Brain-derived neurotrophic factor (BDNF) is closely related to neurodegeneration and synaptic plasticity during the aging process. However, the molecular mechanisms regulating neurodegeneration and synaptic plasticity underlying the pathogenesis and progression of Alzheimer's disease (AD) still remain incompletely understood. Methods: Remarkably, the expressions of GAP-43 and BDNF perfectly match in various neurons in the Human Brain Atlas database. Moreover, GAP-43 and BDNF are highly expressed in a healthy adults' hippocampus brain region and are inversely correlated with the amyloid beta (Aβ), which is the pathological peptide of amyloid plaques found in the brains of patients with AD. Results: These data led us to investigate the impact of the direct molecular interaction between GAP-43 and BDNF in hippocampal neuron fate. In this study, we show that GAP-43 and BDNF are inversely associated with pathological molecules for AD (Tau and Aβ). In addition, we define the three-dimensional protein structure for GAP-43 and BDNF, including the predictive direct binding sites Conclusion: These results show that GAP-43 and BDNF are direct binding partners in hippocampal neurons and that their molecular signaling might be potential therapeutic targets for AD.
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