Version 1
: Received: 13 April 2024 / Approved: 15 April 2024 / Online: 15 April 2024 (11:17:49 CEST)
How to cite:
Lu, H.; Chen, M.; Zhu, C. Intranasal Administration of Apelin-13 Ameliorates Cognitive Deficit in STZ-Induced Alzheimer’s Disease Model via Enhancement of Nrf2-HO1 Pathways. Preprints2024, 2024040959. https://doi.org/10.20944/preprints202404.0959.v1
Lu, H.; Chen, M.; Zhu, C. Intranasal Administration of Apelin-13 Ameliorates Cognitive Deficit in STZ-Induced Alzheimer’s Disease Model via Enhancement of Nrf2-HO1 Pathways. Preprints 2024, 2024040959. https://doi.org/10.20944/preprints202404.0959.v1
Lu, H.; Chen, M.; Zhu, C. Intranasal Administration of Apelin-13 Ameliorates Cognitive Deficit in STZ-Induced Alzheimer’s Disease Model via Enhancement of Nrf2-HO1 Pathways. Preprints2024, 2024040959. https://doi.org/10.20944/preprints202404.0959.v1
APA Style
Lu, H., Chen, M., & Zhu, C. (2024). Intranasal Administration of Apelin-13 Ameliorates Cognitive Deficit in STZ-Induced Alzheimer’s Disease Model via Enhancement of Nrf2-HO1 Pathways. Preprints. https://doi.org/10.20944/preprints202404.0959.v1
Chicago/Turabian Style
Lu, H., Ming Chen and Cuiqing Zhu. 2024 "Intranasal Administration of Apelin-13 Ameliorates Cognitive Deficit in STZ-Induced Alzheimer’s Disease Model via Enhancement of Nrf2-HO1 Pathways" Preprints. https://doi.org/10.20944/preprints202404.0959.v1
Abstract
(1) Background: Alzheimer’s disease (AD) presents a significant challenge in terms of discovering novel diagnostic methods and therapies. Previous research has shed light on the neuroprotective properties of Apelin-13 in neurodegenerative disorders. However, elucidating the mechanism underlying its efficacy in combating AD-related nerve injury is imperative. In this study, we aimed to investigate the mechanism of action of Apelin-13 in an in vivo model of AD induced by streptozocin (STZ); (2) Methods: We utilized an STZ-induced nerve injury model of AD in mice to investigate the effects of Apelin-13 administration. The Apelin-13 was administered intranasally, and cognitive impairment was assessed using standardized behavioral tests. The main methods included behavioral assessment, histological analysis, and biochemical assays to evaluate synaptic plasticity and oxidative stress signaling pathways; (3) Results: Our findings indicate that intranasal administration of Apelin-13 ameliorated cognitive impairment in the STZ-induced AD model. Furthermore, we observed that this effect was potentially mediated through the enhancement of synaptic plasticity and attenuation of oxidative stress signaling pathways; (4) Conclusions: The results of this study suggest that intranasal administration of Apelin-13 holds promise as a therapeutic strategy for preventing neurodegenerative diseases such as AD. By improving synaptic plasticity and mitigating oxidative stress, Apelin-13 may offer a novel approach to neuroprotection in AD and related conditions.
Biology and Life Sciences, Neuroscience and Neurology
Copyright:
This is an open access article distributed under the Creative Commons Attribution License which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.
