Evidence map›Paper›PMID 37748061›Full record

ArticleProceedings of the National Academy of Sciences of the United States of America2023

Impairments in endogenous AMPA receptor dynamics correlates with learning deficits in Alzheimer's disease model mice.

Kongjie Lu, Chenyang Li, Jiao Liu, Jinpeng Wang, Yongfeng Li, Bin He, Junzhao Li, Xiaochen Zhang, Mengping Wei, Yonglu Tian and 3 more

Open access · greenAbstract read
In one paragraph

Article in Proceedings of the National Academy of Sciences of the United States of America, 2023. 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
1.9field-weighted citation impact, top 14% 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

7 citing papers in PubMed, 13 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

13 authors at 3 institutions in 1 country.

Kongjie LuNeuroscience Research Institute and Department of Neurobiology, School of Basic Medical Sciences, Peking University, Key Laboratory for Neuroscience, Ministry of Education of China and National Health Commission of the People's Republic of China, Beijing 100083, China.
Chenyang LiNeuroscience Research Institute and Department of Neurobiology, School of Basic Medical Sciences, Peking University, Key Laboratory for Neuroscience, Ministry of Education of China and National Health Commission of the People's Republic of China, Beijing 100083, China.
Jiao LiuCenter of Medical and Health Analysis, Peking University Health Science Center, Beijing 100083, China.
Jinpeng WangNeuroscience Research Institute and Department of Neurobiology, School of Basic Medical Sciences, Peking University, Key Laboratory for Neuroscience, Ministry of Education of China and National Health Commission of the People's Republic of China, Beijing 100083, China.
Yongfeng LiNeuroscience Research Institute and Department of Neurobiology, School of Basic Medical Sciences, Peking University, Key Laboratory for Neuroscience, Ministry of Education of China and National Health Commission of the People's Republic of China, Beijing 100083, China.
Bin HeNeuroscience Research Institute and Department of Neurobiology, School of Basic Medical Sciences, Peking University, Key Laboratory for Neuroscience, Ministry of Education of China and National Health Commission of the People's Republic of China, Beijing 100083, China.
Junzhao LiNeuroscience Research Institute and Department of Neurobiology, School of Basic Medical Sciences, Peking University, Key Laboratory for Neuroscience, Ministry of Education of China and National Health Commission of the People's Republic of China, Beijing 100083, China.
Xiaochen ZhangAcademy of Medical Engineering and Translational Medicine, Tianjin University, Tianjin 300072, China.
Mengping WeiSchool of Basic Medical Sciences, Beijing Key Laboratory of Neural Regeneration and Repair, Advanced Innovation Center for Human Brain Protection, Capital Medical University, Beijing 100069, China.
Yonglu TianPKU-IDG/McGovern Institute for Brain Research, Beijing 100871, China.ORCID 0000-0002-1036-767X
Rong ZhangNeuroscience Research Institute and Department of Neurobiology, School of Basic Medical Sciences, Peking University, Key Laboratory for Neuroscience, Ministry of Education of China and National Health Commission of the People's Republic of China, Beijing 100083, China.ORCID 0000-0002-6889-5571
Chen ZhangSchool of Basic Medical Sciences, Beijing Key Laboratory of Neural Regeneration and Repair, Advanced Innovation Center for Human Brain Protection, Capital Medical University, Beijing 100069, China.ORCID 0000-0002-7940-8054
Yong ZhangNeuroscience Research Institute and Department of Neurobiology, School of Basic Medical Sciences, Peking University, Key Laboratory for Neuroscience, Ministry of Education of China and National Health Commission of the People's Republic of China, Beijing 100083, China.ORCID 0000-0001-8765-7037
Peking University · CNCapital Medical University · CNTianjin University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

AMPA receptors (AMPARs) play a critical role in synaptic plasticity and learning and memory, and dysfunction or dysregulation of AMPARs could lead to various neurological and psychiatric disorders, such as Alzheimer's disease (AD). However, the dynamics and/or longitudinal changes of AMPARs in vivo during AD pathogenesis remain elusive. Here, employing 5xFAD SEP-GluA1 KI mice, we investigated endogenous AMPA receptor dynamics in a whisker deflection-associated Go/No-go learning paradigm. We found a significant increase in synaptosomal AMPA receptor subunits GluA1 in WT mice after learning, while no such changes were detected in 7-mo-old 5xFAD mice. Daily training led to an increase in endogenous spine surface GluA1 in Control mice, while this increase was absent in 5xFAD-KI mice which correlates with its learning defects in Go/No-go paradigm. Furthermore, we demonstrated that the onset of abnormal AMPAR dynamics corresponds temporally with microglia and astrocyte overactivation. Our results have shown that impairments in endogenous AMPA receptor dynamics play an important role in learning deficits in 5xFAD mice and AD pathogenesis.

Indexed as

Alzheimer DiseaseReceptors, AMPAAnimalsAstrocytesHumansLearningMiceMicrogliaReceptors, AMPAAlzheimer’s diseaseAMPA receptorsynaptic plasticitytwo-photon imaging

Identifiers

PMID37748061
PMCPMC10556575
OpenAlexW4387009915

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-ND
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.