Evidence map›Paper›PMID 33180247›Full record

ArticleNeurochemical research2021

Graphene Oxide Ameliorates the Cognitive Impairment Through Inhibiting PI3K/Akt/mTOR Pathway to Induce Autophagy in AD Mouse Model.

Fangxuan Chu, Kai Li, Xiaolin Li, Lanju Xu, Jie Huang, Zhuo Yang

Abstract read
PubMed Publisher
In one paragraph

Article in Neurochemical research, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers.

0numbers the graph read from it
0cells of the map it votes in
24citing papers in PubMed
2.5field-weighted citation impact, top 11% 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

24 citing papers in PubMed, 49 citations in OpenAlex.

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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 at 2 institutions in 2 countries.

Fangxuan Chu *Medical School, State Key Laboratory of Medicinal Chemical Biology, Key Laboratory of Bioactive Materials for Ministry of Education, College of Medicine, Nankai University, Tianjin, 300071, China.
Kai Li *Medical School, State Key Laboratory of Medicinal Chemical Biology, Key Laboratory of Bioactive Materials for Ministry of Education, College of Medicine, Nankai University, Tianjin, 300071, China.
Xiaolin LiMedical School, State Key Laboratory of Medicinal Chemical Biology, Key Laboratory of Bioactive Materials for Ministry of Education, College of Medicine, Nankai University, Tianjin, 300071, China.
Lanju XuMedical School, State Key Laboratory of Medicinal Chemical Biology, Key Laboratory of Bioactive Materials for Ministry of Education, College of Medicine, Nankai University, Tianjin, 300071, China.
Jie HuangDepartment of Mechanical Engineering, University College London, London, UK.
Zhuo YangMedical School, State Key Laboratory of Medicinal Chemical Biology, Key Laboratory of Bioactive Materials for Ministry of Education, College of Medicine, Nankai University, Tianjin, 300071, China. zhuoyang@nankai.edu.cn.ORCID http://orcid.org/0000-0001-5212-0053
Nankai University · CNUniversity College London · GB

Funding

National Natural Science Foundation of China 81771979
6 · The paper itself

Abstract

Alzheimer's disease (AD) is a neurodegenerative disease of the central nervous system characterised by cognitive impairment. Its major pathological feature is the deposition of β-amyloid (Aβ) peptide, which triggers a series of pathological cascades. Autophagy is a main pathway to eliminate abnormal aggregated proteins, and increasing autophagy represents a plausible treatment strategy against relative overproduction of neurotoxic Aβ. Graphene oxide (GO) is an emerging carbon-based nanomaterial. As a derivative of graphene with neuroprotective effects, it can effectively increase the clearance of abnormally aggregated protein. In this article, we investigated the protective function of GO in an AD mouse model. GO (30 mg/kg, intraperitoneal) was administered for 2 weeks. The results of the Morris water maze test and the novel object recognition test suggested that GO ameliorated learning and memory impairments in 5xFAD mice. The long-term potentiation and depotentiation from the perforant path to the dentate gyrus in the hippocampus were increased with GO treatment in 5xFAD mice. Furthermore, GO upregulated the expression of synapse-related proteins and increased the cell density in the hippocampus. Our results showed that GO up-regulated LC3II/LC3I and Beclin-1 and decreased p62 protein levels in 5xFAD mice. In addition, GO downregulated the PI3K/Akt/mTOR signalling pathway to induce autophagy. These results have revealed the protective potential of GO in AD.

Indexed as

Alzheimer DiseaseAmyloid beta-PeptidesAnimalsAutophagyCognitive DysfunctionDendritic SpinesFemaleGraphiteHippocampusMaleMiceMorris Water Maze TestNeuronal PlasticityNeuroprotective AgentsOpen Field TestSignal TransductionAmyloid beta-Peptidesgraphene oxideGraphiteNeuroprotective AgentsAlzheimer’s diseaseAutophagyCognitionGraphene oxideSynaptic plasticityβ-amyloid

Identifiers

PMID33180247
OpenAlexW3102381632

What OpenQuestion holds

Textmetadata
Read underepoch 390

Registered trials

None linked

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.