RETRACTED: Pharmacologic Inhibition of 5-Lipoxygenase Improves Memory, Rescues Synaptic Dysfunction, and Ameliorates Tau Pathology in a Transgenic Model of Tauopathy
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Background 5-Lipoxygenase (5-LO) is a protein widely distributed in the central nervous system where it modulates amyloidosis and memory impairments in transgenic mouse models of Alzheimer's disease. However, no data are available as to whether 5-LO is elevated in human tauopathy or if it directly influences tau pathology in a relevant model of the disease.Methods We assayed 5-LO levels in brain samples from patients with tauopathy and transgenic tau mice, and we evaluated the effect of 5-LO pharmacologic inhibition on the phenotype of these mice.Results The 5-LO protein is upregulated in human tauopathy and transgenic tau mice brains. Pharmacologic blockade of 5-LO in tau mice resulted in significant memory improvement, rescue of synaptic integrity and dysfunction, and reduction of tau pathology via a cdk5-dependent mechanism.Conclusions These results establish a key role of 5-LO in the development of the tau pathology phenotype and demonstrate it to be a novel viable therapeutic target for the pharmacologic treatment of human tauopathy.
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5-LO levels were significantly higher in the frontal cortex of the brains of PSP patients than in controls.
“5-LO levels were significantly higher in the frontal cortex of the brains of PSP patients than in controls.512”
From Microglia in neurodegenerative diseases: mechanism and potential therapeutic targets (2023) · cites this paper as [512]
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References 27 · Cited by 48
- Authors
- Giannopoulos, P. F., Chu, J., Sperow, M., Li, J.-G., Yu, W. H., Kirby, L. G., Abood, M., & Praticò, D.
- Affiliations
- Center for Translational Medicine (PL)
- Columbia University (US)
- Temple University (US)
- Corresponding author
- Praticò, Domenico
- Venue
- Biological Psychiatry
- Publisher
- Elsevier BV
- Published
- 2015-11
- Volume
- 78
- Issue
- 10
- Pages
- 693-701
- ISSN
- 0006-3223 (ISSN-L)
- PMC
- PMC4529386
- OpenAlex
- W2022352869
- Cited by
- 48
- References
- 27
- Citations by year
- 2026: 2 · 2025: 1 · 2024: 4 · 2023: 2 · 2022: 3 · 2021: 5 · 2020: 5 · 2019: 6 · 2018: 8 · 2017: 10 · 2015: 2
- FWCI
- 4.91
- Type
- journal article
- Language
- en
- Status
- Retracted
- Open access
- green
- www.ncbi.nlm.nih.gov
- Locations
- Biological Psychiatry (publishedVersion)
- PubMed (publishedVersion)
- Europe PMC (PubMed Central) (acceptedVersion)
- PubMed Central (acceptedVersion)
- Funders
- National Institutes of Health
- U.S. Food and Drug Administration
- National Institute on Aging (AG033568, R01AG033568)
- National Institute on Drug Abuse (P30-DA13429, P30DA013429, T32DA 07237, T32DA007237)
- Topics
- Health Sciences › Medicine › Physiology › Alzheimer's disease research and treatments
- Life Sciences › Neuroscience › Neurology › Neuroinflammation and Neurodegeneration Mechanisms
- Health Sciences › Medicine › Psychiatry and Mental health › Dementia and Cognitive Impairment Research
- Keywords
- 5-lipoxygenase, tauopathy, tau pathology, memory impairment, synaptic dysfunction, cyclin-dependent kinase 5, Alzheimer's disease, pharmacological inhibition, therapeutic target
- MeSH terms
- Animals, Arachidonate 5-Lipoxygenase, Brain, Cerebellum, Cerebral Cortex, Disease Models, Animal, Encephalitis, Humans, Hydroxyurea, Memory, Mice, Inbred C57BL, Mice, Transgenic, Neurons, Phenotype, Phosphorylation, Synapses, Lipoxygenase Inhibitors, tau Proteins, Excitatory Postsynaptic Potentials, Tauopathies, Cyclin-Dependent Kinase 5, Mice
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