Evidence map›Paper›PMID 25820815›Full record

ArticleScientific reports2015

Spatial training preserves associative memory capacity with augmentation of dendrite ramification and spine generation in Tg2576 mice.

Xia Jiang, Gao-Shang Chai, Zhi-Hao Wang, Yu Hu, Xiao-Guang Li, Zhi-Wei Ma, Qun Wang, Jian-Zhi Wang, Gong-Ping Liu

Abstract read
In one paragraph

Article in Scientific reports, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 26 papers.

0numbers the graph read from it
0cells of the map it votes in
26citing 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

26 citing papers in PubMed.

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  15. Spatial Training Ameliorates Long-Term Alzheimer's Disease-Like Pathological Deficits by Reducing NLRP3 Inflammasomes in PR5 Mice.Neurotherapeutics : the journal of the American Society for Experimental NeuroTherapeutics · 2019
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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

9 authors.

Xia Jiang1] Department of Pathophysiology, Key Laboratory of Ministry of Education for Neurological Disorders, the School of Basal Medicine, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, 430030. P. R. China [2] Department of Pathology, Hubei University of Chinese Medicine, Wuhan, 430065. P. R. China.
Gao-Shang Chai1] Department of Pathophysiology, Key Laboratory of Ministry of Education for Neurological Disorders, the School of Basal Medicine, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, 430030. P. R. China [2] Department of Basic Medicine, Wuxi Medical School, Jiangnan University, Wuxi, Jiangsu Province, 214122, P. R. China.
Zhi-Hao WangDepartment of Pathophysiology, Key Laboratory of Ministry of Education for Neurological Disorders, the School of Basal Medicine, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, 430030. P. R. China.
Yu HuDepartment of Pathophysiology, Key Laboratory of Ministry of Education for Neurological Disorders, the School of Basal Medicine, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, 430030. P. R. China.
Xiao-Guang LiDepartment of Pathophysiology, Key Laboratory of Ministry of Education for Neurological Disorders, the School of Basal Medicine, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, 430030. P. R. China.
Zhi-Wei MaDepartment of Pathophysiology, Key Laboratory of Ministry of Education for Neurological Disorders, the School of Basal Medicine, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, 430030. P. R. China.
Qun WangDepartment of Pathophysiology, Key Laboratory of Ministry of Education for Neurological Disorders, the School of Basal Medicine, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, 430030. P. R. China.
Jian-Zhi Wang1] Department of Pathophysiology, Key Laboratory of Ministry of Education for Neurological Disorders, the School of Basal Medicine, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, 430030. P. R. China [2] Co-innovation Center of Neuroregeneration, Nantong University, Nantong, JS 226001, China.
Gong-Ping Liu1] Department of Pathophysiology, Key Laboratory of Ministry of Education for Neurological Disorders, the School of Basal Medicine, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, 430030. P. R. China [2] Co-innovation Center of Neuroregeneration, Nantong University, Nantong, JS 226001, China.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Alzheimer's disease (AD) is the most common neurodegenerative disorder and there is currently no efficient cure for this devastating disease. Cognitive stimulation can delay memory loss during aging and in patients with mild cognitive impairment. In 3 × Tg-AD mice, training decreased the neuropathologies with transient amelioration of memory decline. However, the neurobiological mechanisms underlying the learning-improved memory capacity are poorly understood. Here, we found in Tg2576 mice spatial training in Morris water maze (MWM) remarkably improved the subsequent associative memory acquisition detected by contextual fear conditioning. We also found that spatial training enhanced long term potentiation, dendrite ramification and spine generation in hippocampal dentate gyrus (DG) and CA1 neurons at 24 h after the training. In the molecular level, the MWM training remarkably activated calcium/calmodulin-dependent protein kinase II (CaMKII) with elevation of glutamate AMPA receptor GluA1 subunit (GluA1), postsynaptic density protein 93 (PSD93) and postsynaptic density protein 95 (PSD95) in the hippocampus. Finally, the training also significantly ameliorated AD-like tau and amyloid pathologies. We conclude that spatial training in MWM preserves associative memory capacity in Tg2576 mice, and the mechanisms involve augmentation of dendrite ramification and spine generation in hippocampus.

Indexed as

MemorySpatial LearningAlzheimer DiseaseAmyloid beta-PeptidesAnimalsCalcium-Calmodulin-Dependent Protein Kinase Type 2DendritesDentate GyrusDisease Models, AnimalDisks Large Homolog 4 ProteinGuanylate KinasesHippocampusHumansLong-Term PotentiationMembrane ProteinsMiceAmyloid beta-PeptidesCalcium-Calmodulin-Dependent Protein Kinase Type 2Disks Large Homolog 4 ProteinDlg4 protein, mouseGuanylate KinasesMembrane ProteinsReceptors, AMPAtau Proteins

Identifiers

PMID25820815
PMCPMC4377552

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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.