Evidence map›Paper›PMID 25268773›Full record

ArticlePloS one2014

Magnesium protects cognitive functions and synaptic plasticity in streptozotocin-induced sporadic Alzheimer's model.

Zhi-Peng Xu, Li Li, Jian Bao, Zhi-Hao Wang, Juan Zeng, En-Jie Liu, Xiao-Guang Li, Rong-Xi Huang, Di Gao, Meng-Zhu Li and 3 more

Open access · goldAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in PloS one, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 65 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
65citing papers in PubMed, 2 pooled it
7.7field-weighted citation impact, top 2% 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

65 citing papers in PubMed, 2 syntheses or guidelines pooled it, 131 citations in OpenAlex.

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  14. Two novel variants inFrontiers in genetics · 2025
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5 more citing papers are in PubMed but not listed here.

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

13 authors at 1 institution in 1 country.

Zhi-Peng XuDepartment of Pathophysiology, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, China; Key Laboratory of Neurological Disease of National Education Ministry, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, China.
Li LiDepartment of Pathophysiology, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, China; Key Laboratory of Neurological Disease of National Education Ministry, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, China.
Jian BaoDepartment of Pathophysiology, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, China; Key Laboratory of Neurological Disease of National Education Ministry, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, China.
Zhi-Hao WangDepartment of Pathophysiology, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, China; Key Laboratory of Neurological Disease of National Education Ministry, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, China.
Juan ZengDepartment of Pathophysiology, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, China; Key Laboratory of Neurological Disease of National Education Ministry, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, China.
En-Jie LiuDepartment of Pathophysiology, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, China; Key Laboratory of Neurological Disease of National Education Ministry, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, China.
Xiao-Guang LiDepartment of Pathophysiology, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, China; Key Laboratory of Neurological Disease of National Education Ministry, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, China.
Rong-Xi HuangDepartment of Pathophysiology, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, China; Key Laboratory of Neurological Disease of National Education Ministry, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, China.
Di GaoDepartment of Pathophysiology, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, China; Key Laboratory of Neurological Disease of National Education Ministry, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, China.
Meng-Zhu LiDepartment of Pathophysiology, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, China; Key Laboratory of Neurological Disease of National Education Ministry, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, China.
Yao ZhangDepartment of Pathophysiology, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, China; Li Yuan Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, China.
Gong-Ping LiuDepartment of Pathophysiology, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, China; Key Laboratory of Neurological Disease of National Education Ministry, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, China.
Jian-Zhi WangDepartment of Pathophysiology, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, China; Key Laboratory of Neurological Disease of National Education Ministry, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, China.
Huazhong University of Science and Technology · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Alzheimer's disease (AD) is characterized by profound synapse loss and impairments of learning and memory. Magnesium affects many biochemical mechanisms that are vital for neuronal properties and synaptic plasticity. Recent studies have demonstrated that the serum and brain magnesium levels are decreased in AD patients; however, the exact role of magnesium in AD pathogenesis remains unclear. Here, we found that the intraperitoneal administration of magnesium sulfate increased the brain magnesium levels and protected learning and memory capacities in streptozotocin-induced sporadic AD model rats. We also found that magnesium sulfate reversed impairments in long-term potentiation (LTP), dendritic abnormalities, and the impaired recruitment of synaptic proteins. Magnesium sulfate treatment also decreased tau hyperphosphorylation by increasing the inhibitory phosphorylation of GSK-3β at serine 9, thereby increasing the activity of Akt at Ser473 and PI3K at Tyr458/199, and improving insulin sensitivity. We conclude that magnesium treatment protects cognitive function and synaptic plasticity by inhibiting GSK-3β in sporadic AD model rats, which suggests a potential role for magnesium in AD therapy.

Indexed as

Alzheimer DiseaseAnimalsCognitionDisease Models, AnimalGene Expression RegulationGlycogen Synthase Kinase 3Glycogen Synthase Kinase 3 betaHumansInjections, IntraperitonealInsulin ResistanceLong-Term PotentiationMagnesium SulfateMaleMaze LearningMemoryNeuroprotective AgentsGlycogen Synthase Kinase 3Glycogen Synthase Kinase 3 betaGSK3B protein, humanGsk3b protein, ratMagnesium SulfateNeuroprotective AgentsProto-Oncogene Proteins c-aktStreptozocintau Proteins

Identifiers

PMID25268773
PMCPMC4182554
OpenAlexW2048711819

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.