Evidence map›Paper›PMID 31293402›Full record

ArticleFrontiers in behavioral neuroscience2019

Neuropeptide S Ameliorates Cognitive Impairment of APP/PS1 Transgenic Mice by Promoting Synaptic Plasticity and Reducing Aβ Deposition.

Peng Zhao, Xiaohang Qian, Yunjuan Nie, Na Sun, Zhongxuan Wang, Jiajun Wu, Chen Wei, Ruikun Ma, Zhe Wang, Gaoshang Chai and 1 more

Open access · goldAbstract read
In one paragraph

Article in Frontiers in behavioral neuroscience, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.

0numbers the graph read from it
0cells of the map it votes in
21citing papers in PubMed
2.2field-weighted citation impact, top 13% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

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.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

21 citing papers in PubMed, 33 citations in OpenAlex.

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  5. A pH-responsive and self-healing CEC/PEG-(CHO)Frontiers in neuroscience · 2026
    Article
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  15. Roles of Neuropeptide S in Anesthesia, Analgesia, and Sleep.Pharmaceuticals (Basel, Switzerland) · 2021
    Review
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4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

11 authors at 1 institution in 2 countries.

Peng ZhaoWuxi Medical School, Jiangnan University, Wuxi, China.
Xiaohang QianWuxi Medical School, Jiangnan University, Wuxi, China.
Yunjuan NieWuxi Medical School, Jiangnan University, Wuxi, China.
Na SunWuxi Medical School, Jiangnan University, Wuxi, China.
Zhongxuan WangWuxi Medical School, Jiangnan University, Wuxi, China.
Jiajun WuWuxi Medical School, Jiangnan University, Wuxi, China.
Chen WeiWuxi Medical School, Jiangnan University, Wuxi, China.
Ruikun MaWuxi Medical School, Jiangnan University, Wuxi, China.
Zhe WangWuxi Medical School, Jiangnan University, Wuxi, China.
Gaoshang ChaiWuxi Medical School, Jiangnan University, Wuxi, China.
Yuqing LiWuxi Medical School, Jiangnan University, Wuxi, China.
Jiangnan University · CN

Funding

Restless Legs Syndrome: Pathophysiology using Btbd9 Conditional Knockout MiceR01NS082244 · NINDS · UNIVERSITY OF FLORIDA · PI LI, YUQING · 2014 to 2018
$1.6M
NINDS NIH HHS R01 NS082244
6 · The paper itself

Abstract

Alzheimer's disease (AD) is a devastating disease in the elderly with no known effective treatment. It is characterized by progressive deterioration of memory and cognition. Many new potential targets are being investigated to develop effective therapeutic strategies for AD. Neuropeptide S (NPS) is an endogenous peptide in the central nervous system, which has been shown to play a beneficial role in learning and memory. However, whether NPS can ameliorate cognitive deficits in AD remains unclear. In this study, we examined the effects of NPS treatment on the cognitive behaviors and pathological hallmarks in 8-month-old APPswe/PS1dE9 (APP/PS1) AD mice. We found that the APP/PS1 mice exhibited lower levels of NPS receptors (NPSRs) in the hippocampal area, and NPS administration increased c-Fos expression in the hippocampus and cortex, which suggests the NPS/NPSR system may contribute to the pathogenesis of AD. After an intracerebroventricular injection of NPS (1 nmol) for 2 weeks, we found NPS treatment ameliorated spatial memory deficits and promoted dendrite ramification and spine generation in hippocampal CA1 neurons, which was accompanied by the upregulation of postsynaptic density protein 95 (PSD95) and synapsin1. We also demonstrated that the injection of NPS decreased Aβ plaque deposits by decreasing the γ-secretase activity and the phosphorylation of APP at Thr668. Furthermore, application of NPS reversed the deficits in hippocampal late-phase long-term potentiation (LTP). These findings suggest NPS attenuated cognitive deficits by reducing pathological features in APP/PS1 mice, and NPS might be a potential therapeutic agent for AD.

Indexed as

Alzheimer’s diseaseAβcognitive deficitsNeuropeptide Ssynaptic plasticity

Identifiers

PMID31293402
PMCPMC6603143
OpenAlexW2954770304

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LicenceCC BY
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Registered trials

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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 OpenQuestion graph.