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ORIGINAL RESEARCH article

Front. Pharmacol.

Sec. Neuropharmacology

Volume 16 - 2025 | doi: 10.3389/fphar.2025.1632640

The effect of oral administration of NXP032 equivalent to intraperitoneal administration in an Alzheimer's disease model

Provisionally accepted
Youn-Jung  KimYoun-Jung Kim1*Jae  Min LeeJae Min Lee1You  Jung ChoiYou Jung Choi2Da-Eun  SungDa-Eun Sung2Tae  Hyeok SimTae Hyeok Sim2So  Hee KimSo Hee Kim2
  • 1College of Nursing Science, Kyung Hee University, Seoul, Republic of Korea
  • 2Department of Nursing, Graduate School, Kyung Hee University, Seoul, Republic of Korea

The final, formatted version of the article will be published soon.

Alzheimer's disease (AD) is a progressive neurodegenerative disorder characterized by cognitive impairment, amyloid beta (Aβ) plaque accumulation, neuroinflammation, and neurodegeneration.Excessive oxidative stress in AD exacerbates neurological pathology and may play a crucial role in disease progression by enhancing Aβ plaques and promoting neuroinflammation and neuronal cell death. Although antioxidants like vitamin C can reduce neuroinflammation and exert neuroprotective effects, their efficacy is often limited due to rapid oxidation especially when taken orally. NXP032 is designed to stabilize vitamin C and sustain its antioxidant effects over time. This study aimed to evaluate the effects of oral (PO) administration of NXP032 on AD pathology, focusing on Aβ accumulation and neuroinflammation, and comparing its efficacy to intraperitoneal (IP) administration using the 5xFAD mouse model. Our results demonstrated that both IP and PO administration of NXP032 for 8 weeks significantly reduced Aβ plaque accumulation, thioflavin-S staining, and attenuated hyperactive neuroinflammation in 5xFAD mice. This reduction in Aβ plaques was associated with decreased neurodegeneration, evidenced by reduced Fluoro-Jade C staining in the hippocampus. Furthermore, NXP032 administration via both routes led to significant improvements in cognitive function, highlighting its potential to alleviate AD-related cognitive impairment. These findings suggest that NXP032 offers a promising therapeutic strategy to effectively address multiple aspects of AD pathology and slow disease progression, with the efficacy of oral administration providing a method that can be easily applied in clinical practice.

Keywords: Alzheimer's disease, 5xFAD, Amyloid beta plaques, Neuroinflammation, NXP032

Received: 21 May 2025; Accepted: 04 Jul 2025.

Copyright: © 2025 Kim, Lee, Choi, Sung, Sim and Kim. This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) or licensor are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms.

* Correspondence: Youn-Jung Kim, College of Nursing Science, Kyung Hee University, Seoul, Republic of Korea

Disclaimer: All claims expressed in this article are solely those of the authors and do not necessarily represent those of their affiliated organizations, or those of the publisher, the editors and the reviewers. Any product that may be evaluated in this article or claim that may be made by its manufacturer is not guaranteed or endorsed by the publisher.