Evidence map›Paper›PMID 39037560›Full record

ArticleNeurochemical research2024

NMN Synbiotics: A Multifaceted Therapeutic Approach for Alzheimer's Disease.

Caifeng Li, Xiaodong Zhao, Huilian Xu, Xiaoyong Liu, Yan He, Jinsong Gu

Abstract read
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In one paragraph

Article in Neurochemical research, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.

0numbers the graph read from it
0cells of the map it votes in
7citing papers in PubMed
–field-weighted citation impact
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

7 citing papers in PubMed.

  1. 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

6 authors.

Caifeng Li *College of Biological Science and Technology, University of Jinan, Jinan, 250022, China.
Xiaodong Zhao *College of Biological Science and Technology, University of Jinan, Jinan, 250022, China.
Huilian XuCollege of Biological Science and Technology, University of Jinan, Jinan, 250022, China.
Xiaoyong LiuCollege of Biological Science and Technology, University of Jinan, Jinan, 250022, China.
Yan HeDepartment of Neurology, The First Affiliated Hospital of Shandong First Medical University, Jinan, 250014, China.
Jinsong GuCollege of Biological Science and Technology, University of Jinan, Jinan, 250022, China. gujingsong222@163.com.

Funding

Clinical Medical Science and Technology Innovation Program of Jinan 202019191Cultivation Fund for the First Affiliated Hospital of Shandong First Medical University QYPY2020NSFC0601Nature Science Joint Foundation of Shandong Province ZR2021LSW022Technological SMEs' innovation ability improvement project 2021TSGC1279
6 · The paper itself

Abstract

With the aging global population, Alzheimer's disease (AD) has become a significant social and economic burden, necessitating the development of novel therapeutic strategies. This study investigates the therapeutic potential of nicotinamide mononucleotide (NMN) synbiotics, a combination of NMN, Lactiplantibacillus plantarum CGMCC 1.16089, and lactulose, in mitigating AD pathology. APP/PS1 mice were supplemented with NMN synbiotics and compared against control groups. The effects on amyloid-β (Aβ) deposition, intestinal histopathology, tight junction proteins, inflammatory cytokines, and reactive oxygen species (ROS) levels were assessed. NMN synbiotics intervention significantly reduced Aβ deposition in the cerebral cortex and hippocampus by 67% and 60%, respectively. It also ameliorated histopathological changes in the colon, reducing crypt depth and restoring goblet cell numbers. The expression of tight junction proteins Claudin-1 and ZO-1 was significantly upregulated, enhancing intestinal barrier integrity. Furthermore, NMN synbiotics decreased the expression of proinflammatory cytokines IL-1β, IL-6, and TNF-α, and reduced ROS levels, indicative of attenuated oxidative stress. The reduction in Aβ deposition, enhancement of intestinal barrier function, decrease in neuroinflammation, and alleviation of oxidative stress suggest that NMN synbiotics present a promising therapeutic intervention for AD by modulating multiple pathological pathways. Further research is required to elucidate the precise mechanisms, particularly the role of the NLRP3 inflammasome pathway, which may offer a novel target for AD treatment.

Indexed as

Alzheimer DiseaseSynbioticsAmyloid beta-PeptidesAnimalsCytokinesMaleMiceMice, TransgenicNicotinamide MononucleotideOxidative StressReactive Oxygen SpeciesAmyloid beta-PeptidesCytokinesNicotinamide MononucleotideReactive Oxygen SpeciesAlzheimer’s diseaseAmyloid-β depositionAPP/PS1 miceNMN synbioticsReactive oxygen species

Identifiers

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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.