ArticleMolecular neurobiology2025
A Novel Neuroprotective Derived Peptide of Erythropoietin Improved Cognitive Function in Vascular Dementia Mice.
Article in Molecular neurobiology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 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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Who cites it
2 citing papers in PubMed.
- XKR8 Deletion Protects Against Noise-Induced Hearing Loss by Attenuating Apoptosis and Preserving Mitochondrial Bioenergetics in the Cochlea.Molecular neurobiology · 2026Article
- Erythropoietin in tissue engineering and beyond: a multifunctional macromolecule with emerging roles in organoids, immune modulation, and cancer research.Frontiers in bioengineering and biotechnology · 2026Review
Corrections and comments
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Authors and funding
8 authors.
Funding
Abstract
The effective therapeutics for vascular dementia are still lacking. Here, we designed a novel derived peptide of erythropoietin-DEPO and evaluated its safety, erythropoiesis effect, and neuroprotective effects in mice of vascular dementia. For evaluating the safety and erythropoiesis, DEPO was injected into naive C57BL6 mice (n = 5) for 4-8 weeks, and venous blood was collected at 1, 2, and 4 weeks after DEPO treatment. Neuroprotective effects of DEPO were studied in both cultured neurons and bilateral common carotid artery stenosis (BCAS) mice (n = 10/group). After 4-week DEPO administration, neurobehavioral tests and histology were applied to evaluate cognitive function and brain tissue damage of mice, respectively. Molecule docking, western blotting, pharmacological or genetic interference with EPOR, and JAK/STAT/AKT pathway were used to determine the mechanism of neuroprotective effects of DEPO. DEPO did not increase the hemoglobin concentration or red blood cell number in mice after 4-week treatment compared to the Vehicle group (p > 0.05). DEPO treatment alleviated spatial reference memory impairment and the anxiety level in mice (p < 0.05). Both gray and white matter injuries were significantly alleviated by DEPO treatment. DEPO activated JAK/STAT pathway in cultured neurons and protected neurons against chronic ischemia (p < 0.05). Pharmacological or genetic interference with JAK2 signaling or EPOR inhibited the pro-survival effect of DEPO on chronic ischemia neurons (p < 0.05). DEPO is a novel safe erythropoietin-derived peptide and exerted its neuroprotective effects in vascular dementia mice through activating EPOR and its downstream JAK/STAT signaling pathway. DEPO is a potential alternative agent for treatment of vascular dementia or chronic cerebral ischemia.
Indexed as
Identifiers
39702833What Socratic holds
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 Socratic graph.