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

**Authors:** Jae Min Lee, You Jung Choi, Da-Eun Sung, Tae Hyeok Sim, So Hee Kim, Seung Geun Yeo, Youn-Jung Kim

PMC · DOI: 10.3389/fphar.2025.1632640 · Frontiers in Pharmacology · 2025-07-23

## TL;DR

This study shows that NXP032, an antioxidant, reduces Alzheimer's disease markers in mice whether given orally or through injection.

## Contribution

The study demonstrates that oral NXP032 is as effective as intraperitoneal administration in reducing AD pathology in a mouse model.

## Key findings

- NXP032 reduced amyloid beta plaque accumulation in 5xFAD mice.
- Both oral and intraperitoneal NXP032 reduced neuroinflammation and neurodegeneration.
- Oral NXP032 improved cognitive function in the Alzheimer's disease model.

## Abstract

Alzheimer’s disease (AD) is a progressive neurodegenerative disorder characterized by cognitive impairment, amyloid beta (Aβ) plaque accumulation, neuroinflammation, and neurodegeneration. Excessive oxidative stress exacerbates these pathologies, potentially accelerating disease progression. Although antioxidants like vitamin C can mitigate neuroinflammation and offer neuroprotective effects, their efficacy is often limited due to rapid oxidation, particularly when administered orally. NXP032 has been developed to stabilize vitamin C and sustain its antioxidant effects over time.

This study evaluated the effects of NXP032 administered orally (PO) and intraperitoneally (IP) on AD pathology, specifically focusing on Aβ accumulation and neuroinflammation, using the 5xFAD mouse model over an 8-week period.

Both IP and PO administration of NXP032 significantly reduced Aβ plaque accumulation and thioflavin-S staining, while attenuating neuroinflammation in 5xFAD mice. This was associated with decreased neurodegeneration, evidenced by reduced Fluoro-Jade C staining in the hippocampus. Additionally, both administration routes resulted in significant cognitive function improvements.

NXP032 demonstrates potential as a therapeutic strategy to address multiple aspects of AD pathology and slow disease progression. The efficacy of oral administration is particularly notable, offering a practical method for clinical application.

## Linked entities

- **Chemicals:** vitamin C (PubChem CID 54670067)
- **Diseases:** Alzheimer’s disease (MONDO:0004975)

## Full-text entities

- **Genes:** App (amyloid beta precursor protein) [NCBI Gene 11820] {aka Abeta, Abpp, Adap, Ag, Cvap, E030013M08Rik}
- **Diseases:** cognitive impairment (MESH:D003072), neuroinflammation (MESH:D000090862), neurodegeneration (MESH:D019636), AD (MESH:D000544)
- **Chemicals:** thioflavin-S (MESH:C009462), 5xFAD (-), Fluoro-Jade C (MESH:C534582), vitamin C (MESH:D001205)
- **Species:** Mus musculus (house mouse, species) [taxon 10090]

## Full text

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## Figures

4 figures with captions in the complete paper: https://tomesphere.com/paper/PMC12325363/full.md

## References

43 references — full list in the complete paper: https://tomesphere.com/paper/PMC12325363/full.md

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Source: https://tomesphere.com/paper/PMC12325363