Evidence map›Paper›PMID 34916926›Full record

ArticleFrontiers in aging neuroscience2021

Deficits in N-Methyl-D-Aspartate Receptor Function and Synaptic Plasticity in Hippocampal CA1 in APP/PS1 Mouse Model of Alzheimer's Disease.

Le Xu, Yiying Zhou, Linbo Hu, Hongde Jiang, Yibei Dong, Haowei Shen, Zhongze Lou, Siyu Yang, Yunxin Ji, Liemin Ruan and 1 more

Open access · goldAbstract read
In one paragraph

Article in Frontiers in aging neuroscience, 2021. 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
2.9field-weighted citation impact, top 8% 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

26 citing papers in PubMed, 39 citations in OpenAlex.

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  9. Synaptic and extrasynaptic distribution of NMDA receptors in the cortex of Alzheimer's disease patients.Alzheimer's & dementia : the journal of the Alzheimer's Association · 2024
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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 3 institutions in 1 country.

Le XuZhejiang Key Laboratory of Pathophysiology, Department of Pharmacology, School of Medicine, Ningbo University, Ningbo, China.
Yiying ZhouZhejiang Key Laboratory of Pathophysiology, Department of Pharmacology, School of Medicine, Ningbo University, Ningbo, China.
Linbo HuZhejiang Key Laboratory of Pathophysiology, Department of Pharmacology, School of Medicine, Ningbo University, Ningbo, China.
Hongde JiangZhejiang Key Laboratory of Pathophysiology, Department of Pharmacology, School of Medicine, Ningbo University, Ningbo, China.
Yibei DongZhejiang Key Laboratory of Pathophysiology, Department of Pharmacology, School of Medicine, Ningbo University, Ningbo, China.
Haowei ShenZhejiang Key Laboratory of Pathophysiology, Department of Pharmacology, School of Medicine, Ningbo University, Ningbo, China.
Zhongze LouDepartment of Psychosomatic Medicine, Ningbo First Hospital, Ningbo Hospital of Zhejiang University, Ningbo, China.
Siyu YangZhejiang Key Laboratory of Pathophysiology, Department of Pharmacology, School of Medicine, Ningbo University, Ningbo, China.
Yunxin JiDepartment of Psychosomatic Medicine, Ningbo First Hospital, Ningbo Hospital of Zhejiang University, Ningbo, China.
Liemin RuanDepartment of Psychosomatic Medicine, Ningbo First Hospital, Ningbo Hospital of Zhejiang University, Ningbo, China.
Xiaoqin ZhangZhejiang Key Laboratory of Pathophysiology, Department of Pharmacology, School of Medicine, Ningbo University, Ningbo, China.
Ningbo University · CNNingbo First Hospital · CNNingbo Kangning Hospital · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The N-methyl-D-aspartate receptor is a critical molecule for synaptic plasticity and cognitive function. Impaired synaptic plasticity is thought to contribute to the cognitive impairment associated with Alzheimer's disease (AD). However, the neuropathophysiological alterations of N-methyl-D-aspartate receptor (NMDAR) function and synaptic plasticity in hippocampal CA1 in transgenic rodent models of AD are still unclear. In the present study, APP/PS1 mice were utilized as a transgenic model of AD, which exhibited progressive cognitive impairment including defective working memory, recognition memory, and spatial memory starting at 6 months of age and more severe by 8 months of age. We found an impaired long-term potentiation (LTP) and reduced NMDAR-mediated spontaneous excitatory postsynaptic currents (sEPSCs) in the hippocampal CA1 of APP/PS1 mice with 8 months of age. Golgi staining revealed that dendrites of pyramidal neurons had shorter length, fewer intersections, and lower spine density in APP/PS1 mice compared to control mice. Further, the reduced expression levels of NMDAR subunits, PSD95 and SNAP25 were observed in the hippocampus of APP/PS1 mice. These results suggest that NMDAR dysfunction, impaired synaptic plasticity, and disrupted neuronal morphology constitute an important part of the neuropathophysiological alterations associated with cognitive impairment in APP/PS1 mice.

Indexed as

Alzheimer’s diseasecognitive behaviordendritic morphologyNMDARsynaptic plasticity

Identifiers

PMID34916926
PMCPMC8669806
OpenAlexW3216090061

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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.