ArticleExperimental brain research2012
Intranasal deferoxamine improves performance in radial arm water maze, stabilizes HIF-1α, and phosphorylates GSK3β in P301L tau transgenic mice.
Article in Experimental brain research, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 40 papers.
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Who cites it
40 citing papers in PubMed, 74 citations in OpenAlex.
- Targeting hypoxia-related pathobiology in Alzheimer's disease: strategies for prevention and treatment.Molecular biology reports · 2025Review
- Brain Glucose Hypometabolism and Brain Iron Accumulation as Therapeutic Targets for Alzheimer's Disease and Other CNS Disorders.Pharmaceuticals (Basel, Switzerland) · 2025Review
- Homeostasis and metabolism of iron and other metal ions in neurodegenerative diseases.Signal transduction and targeted therapy · 2025Review
- Interleukin-6 related signaling pathways as the intersection between chronic diseases and sepsis.Molecular medicine (Cambridge, Mass.) · 2025Review
- The role of protein phosphorylation modifications mediated by iron metabolism regulatory networks in the pathogenesis of Alzheimer's disease.Frontiers in aging neuroscience · 2025Review
- Intranasal delivery of iron chelators and management of central nervous system disease.Frontiers in pharmacology · 2025Review
- Potential Roles of Hypoxia-Inducible Factor-1 in Alzheimer's Disease: Beneficial or Detrimental?Antioxidants (Basel, Switzerland) · 2024Review
- Low-dose intranasal deferoxamine modulates memory, neuroinflammation, and the neuronal transcriptome in the streptozotocin rodent model of Alzheimer's disease.Frontiers in neuroscience · 2024Article
- Challenges and Opportunities of Metal Chelation Therapy in Trace Metals Overload-Induced Alzheimer's Disease.Neurotoxicity research · 2023Review
- Molecular and neural roles of sodium-glucose cotransporter 2 inhibitors in alleviating neurocognitive impairment in diabetic mice.Psychopharmacology · 2023Article
- APP Knock-In Mice Produce E22P-Aβ Exhibiting an Alzheimer's Disease-like Phenotype with Dysregulation of Hypoxia-Inducible Factor Expression.International journal of molecular sciences · 2022Article
- Intranasal neprilysin rapidly eliminates amyloid-beta plaques, but causes plaque compensations: the explanation why the amyloid-beta cascade may fail?Neural regeneration research · 2022Review
- Oxygen Sensing and Signaling in Alzheimer's Disease: A Breathtaking Story!Cellular and molecular neurobiology · 2022Review
- Iron Dyshomeostasis and Ferroptosis: A New Alzheimer's Disease Hypothesis?Frontiers in aging neuroscience · 2022Review
- Deferiprone Treatment in Aged Transgenic Tau Mice Improves Y-Maze Performance and Alters Tau Pathology.Neurotherapeutics : the journal of the American Society for Experimental NeuroTherapeutics · 2021Article
- Challenges and Opportunities of Deferoxamine Delivery for Treatment of Alzheimer's Disease, Parkinson's Disease, and Intracerebral Hemorrhage.Molecular pharmaceutics · 2021Review
- Mechanisms of Intranasal Deferoxamine in Neurodegenerative and Neurovascular Disease.Pharmaceuticals (Basel, Switzerland) · 2021Review
- Intranasal Delivery of Collagen-Loaded Neprilysin Clears Beta-Amyloid Plaques in a Transgenic Alzheimer Mouse Model.Frontiers in aging neuroscience · 2021Article
- The Potential of Ferroptosis-Targeting Therapies for Alzheimer's Disease: From Mechanism to Transcriptomic Analysis.Frontiers in aging neuroscience · 2021Review
- Novel Targets and Interventions for Cognitive Complications of Diabetes.Frontiers in physiology · 2021Review
Corrections and comments
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Authors and funding
12 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Deferoxamine (DFO), a metal chelator, has been previously reported to slow the loss of spatial memory in a mouse model of amyloid accumulation when delivered intranasally (IN). In this study, we determined whether IN DFO also has beneficial effects in the P301L mouse, which accumulates hyperphosphorylated tau. Mice were intranasally treated three times per week with either 10% DFO (2.4 mg) or saline for 5 months, and a battery of behavioral tests were conducted before tissue collection and biochemical analyses of brain tissue with Western blot and ELISA. Wild-type (WT) mice statistically outperformed transgenic (TG) saline mice in the radial arm water maze, while performance of TG-DFO mice was not different than WT mice, suggesting improved performance in the radial arm water maze. Other behavioral changes were not evident. Beneficial changes in brain biochemistry were evident in DFO-treated mice for several proteins. The TG mice had significantly less pGSK3β and HIF-1α, with more interleukin-1β and total protein oxidation than wild-type controls, and for each protein, DFO treatment significantly reduced these differences. There was not a significant decrease in phosphorylated tau in brain tissue of DFO-treated mice at the sites we measured. These data suggest that IN DFO is a potential treatment not only for Alzheimer's disease, but also for other neurodegenerative diseases and psychiatric disorders in which GSK3β and HIF-1α play a prominent role.
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