ArticleThe Journal of neuroscience : the official journal of the Society for Neuroscience2014
Deficiency of GDNF Receptor GFRα1 in Alzheimer's Neurons Results in Neuronal Death.
Article in The Journal of neuroscience : the official journal of the Society for Neuroscience, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 papers.
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Who cites it
25 citing papers in PubMed, 50 citations in OpenAlex.
- APOE-stratified genome-wide association analyses provide insights into the genetic etiology of Alzheimers's disease.Nature genetics · 2026Article
- NeuroFANN: identification of neuropathological subtypes in dementia with plasma proteins by using functionally annotated neural network.Briefings in bioinformatics · 2025Article
- GDNF overexpression in astrocytes enhances branching and partially preserves hippocampal function in an Alzheimer's rat model.Scientific reports · 2025Article
- Article
- The significance of glial cell line-derived neurotrophic factor analysis in Progressive Supranuclear Palsy.Scientific reports · 2024Article
- Proteomics analysis of plasma from middle-aged adults identifies protein markers of dementia risk in later life.Science translational medicine · 2023Article
- Neurotrophic factor-based pharmacological approaches in neurological disorders.Neural regeneration research · 2023Review
- Identification of risk genes for Alzheimer's disease by gene embedding.Cell genomics · 2022Article
- Do serum GDNF levels correlate with severity of Alzheimer's disease?Neurological sciences : official journal of the Italian Neurological Society and of the Italian Society of Clinical Neurophysiology · 2021Article
- Therapeutic Potential of AAV1-Rheb(S16H) Transduction against Neurodegenerative Diseases.International journal of molecular sciences · 2021Review
- Dysregulation of Exosome Cargo by Mutant Tau Expressed in Human-induced Pluripotent Stem Cell (iPSC) Neurons Revealed by Proteomics Analyses.Molecular & cellular proteomics : MCP · 2020Article
- Induction of GDNF and GFRα-1 Following AAV1-Rheb(S16H) Administration in the HippocampusExperimental neurobiology · 2020Article
- Upregulation of Neuronal Rheb(S16H) for Hippocampal Protection in the Adult Brain.International journal of molecular sciences · 2020Review
- Cholinergic Modulation of Glial Function During Aging and Chronic Neuroinflammation.Frontiers in cellular neuroscience · 2020Review
- Dl-3-n-Butylphthalide Reduces Cognitive Impairment Induced by Chronic Cerebral Hypoperfusion Through GDNF/GFRα1/Ret Signaling Preventing Hippocampal Neuron Apoptosis.Frontiers in cellular neuroscience · 2019Article
- Sensory and Motor Behavior Evidences Supporting the Usefulness of Conditioned Medium from Dental Pulp-Derived Stem Cells in Spinal Cord Injury in Rats.Asian spine journal · 2018Article
- GDNF/GFRα1 Complex Abrogates Self-Renewing Activity of Cortical Neural Precursors Inducing Their Differentiation.Stem cell reports · 2018Article
- Proteomic Dissection of Nanotopography-Sensitive Mechanotransductive Signaling Hubs that Foster Neuronal Differentiation in PC12 Cells.Frontiers in cellular neuroscience · 2017Article
- The Non-Survival Effects of Glial Cell Line-Derived Neurotrophic Factor on Neural Cells.Frontiers in molecular neuroscience · 2017Review
- Inhibitory Effect of Memantine on Streptozotocin-Induced Insulin Receptor Dysfunction, Neuroinflammation, Amyloidogenesis, and Neurotrophic Factor Decline in Astrocytes.Molecular neurobiology · 2016Article
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Authors and funding
7 authors at 4 institutions in 4 countries.
Funding
Abstract
We have recently developed aged cortical neuron cultures from autopsied human brains with Alzheimer's disease (AD). During the culturing process, we found that glutamatergic cortical neurons from the AD brain lacked a response to glial cell line-derived neurotrophic factor (GDNF), including no axonal regrowth, and were starting to undergo apoptosis. Here we showed that, in cortical neurons from age- and gender-matched cognitively normal control (NC) subjects (NC neurons), GDNF enhanced the expression of GDNF family receptor subtype α1 (GFRα1), but not the other three subtypes (GFRα2, GFRα3, and GFRα4), whereas GDNF failed to induce GFRα1 expression in cortical neurons from the AD brain (AD neurons). The exogenous introduction of GFRα1, but not of its binding partner α1-neural cell adhesion molecule, or RET into AD neurons restored the effect of GDNF on neuronal survival. Moreover, between NC and AD neurons, the AMPA receptor blocker CNQX and the NMDA receptor blocker AP-5 had opposite effects on the GFRα1 expression induced by GDNF. In NC neurons, the presence of glutamate receptors was necessary for GDNF-linked GFRα1 expression, while in AD neurons the absence of glutamate receptors was required for GFRα1 expression by GDNF stimulation. These results suggest that, in AD neurons, specific impairments of GFRα1, which may be linked to glutamatergic neurotransmission, shed light on developing potential therapeutic strategies for AD by upregulation of GFRα1 expression.
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