Evidence map›Paper›PMID 39396064›Full record

ArticleMolecular psychiatry2025

Cannabidiol ameliorates cognitive decline in 5×FAD mouse model of Alzheimer's disease through potentiating the function of extrasynaptic glycine receptors.

Jin Jin, Chonglei Fu, Jing Xia, Heyi Luo, Xianglian Wang, Si Chen, Huanhuan Mao, Kai Yuan, Lin Lu, Wei Xiong and 1 more

Abstract read
PubMed Publisher
In one paragraph

Article in Molecular psychiatry, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
7citing papers in PubMed, 1 pooled it
–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

7 citing papers in PubMed, 1 synthesis or guideline pooled it.

  1. Pooled it
  2. Article
  3. Review
  4. Review
  5. Review
  6. Review
  7. Review
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.

Jin Jin *Department of neurology, The First Affiliated Hospital of USTC, Division of Life Sciences and Medicine, University of Science and Technology of China, Hefei, 230026, China.
Chonglei Fu *Institute of Brain Science and Brain-inspired Research, Shandong First Medical University & Shandong Academy of Medical Sciences, Jinan, 250117, China.ORCID 0000-0002-1082-2783
Jing Xia *Department of neurology, The First Affiliated Hospital of USTC, Division of Life Sciences and Medicine, University of Science and Technology of China, Hefei, 230026, China.
Heyi Luo *Department of neurology, The First Affiliated Hospital of USTC, Division of Life Sciences and Medicine, University of Science and Technology of China, Hefei, 230026, China.
Xianglian WangDepartment of neurology, The First Affiliated Hospital of USTC, Division of Life Sciences and Medicine, University of Science and Technology of China, Hefei, 230026, China.
Si ChenInstitute of Brain Science and Brain-inspired Research, Shandong First Medical University & Shandong Academy of Medical Sciences, Jinan, 250117, China.
Huanhuan MaoDepartment of neurology, The First Affiliated Hospital of USTC, Division of Life Sciences and Medicine, University of Science and Technology of China, Hefei, 230026, China.
Kai YuanPeking University Sixth Hospital, Peking University Institute of Mental Health, NHC Key Laboratory of Mental Health (Peking University), National Clinical Research Center for Mental Disorders (Peking University Sixth Hospital), Chinese Academy of Medical Sciences Research Unit (No.2018RU006), Peking University, 100191, Beijing, China.ORCID 0000-0002-3498-8163
Lin LuInstitute of Brain Science and Brain-inspired Research, Shandong First Medical University & Shandong Academy of Medical Sciences, Jinan, 250117, China. linlu@bjmu.edu.cn.ORCID 0000-0003-0742-9072
Wei XiongDepartment of neurology, The First Affiliated Hospital of USTC, Division of Life Sciences and Medicine, University of Science and Technology of China, Hefei, 230026, China. wxiong@ustc.edu.cn.ORCID 0000-0002-1585-3749
Guichang ZouInstitute of Brain Science and Brain-inspired Research, Shandong First Medical University & Shandong Academy of Medical Sciences, Jinan, 250117, China. guicz@sdfmu.edu.cn.

Funding

National Natural Science Foundation of China (National Science Foundation of China) 32225020, 91849206, 91942315, 92049304, 32121002National Natural Science Foundation of China (National Science Foundation of China) 32225020, 91849206, 91942315, 92049304, 32121002, 81901157, 82241032
6 · The paper itself

Abstract

Emerging evidence supports the therapeutic potential of cannabinoids in Alzheimer's disease (AD), but the underlying mechanism upon how cannabinoids impact brain cognition and AD pathology remains unclear. Here we show that chronic cannabidiol (CBD) administration significantly mitigates cognitive deficiency and hippocampal β-amyloid (Aβ) pathology in 5×FAD mouse model of AD. CBD achieves its curative effect mainly through potentiating the function of inhibitory extrasynaptic glycine receptor (GlyR) in hippocampal dentate gyrus (DG). Based on the in vitro and in vivo electrophysiological recording and calcium imaging, CBD mediated anti-AD effects via GlyR are mainly accomplished by decreasing neuronal hyperactivity of granule cells in the DG of AD mice. Furthermore, the AAV-mediated ablation of DG GlyRα1, or the GlyRα1

Indexed as

Alzheimer DiseaseCannabidiolCognitive DysfunctionReceptors, GlycineAmyloid beta-PeptidesAnimalsCognitionDentate GyrusDisease Models, AnimalHippocampusHumansMaleMiceMice, Inbred C57BLMice, TransgenicNeuronsAmyloid beta-PeptidesCannabidiolReceptors, Glycine

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Registered trials

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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.