Evidence map›Paper›PMID 39587077›Full record

ArticleCell death & disease2024

Microglial cannabinoid receptor type II stimulation improves cognitive impairment and neuroinflammation in Alzheimer's disease mice by controlling astrocyte activation.

Akira Sobue, Okiru Komine, Fumito Endo, Chihiro Kakimi, Yuka Miyoshi, Noe Kawade, Seiji Watanabe, Yuko Saito, Shigeo Murayama, Takaomi C Saido and 2 more

Abstract read
In one paragraph

Article in Cell death & disease, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.

0numbers the graph read from it
0cells of the map it votes in
18citing 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

18 citing papers in PubMed.

  1. Trial
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  6. Article
  7. Neurotransmitter Systems in Alzheimer's Disease.Current issues in molecular biology · 2026
    Review
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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

12 authors.

Akira SobueDepartment of Neuroscience and Pathobiology, Research Institute of Environmental Medicine, Nagoya University, Aichi, 464-8601, Japan.
Okiru KomineDepartment of Neuroscience and Pathobiology, Research Institute of Environmental Medicine, Nagoya University, Aichi, 464-8601, Japan.ORCID 0000-0003-0845-7358
Fumito EndoDepartment of Neuroscience and Pathobiology, Research Institute of Environmental Medicine, Nagoya University, Aichi, 464-8601, Japan.
Chihiro KakimiDepartment of Neuroscience and Pathobiology, Research Institute of Environmental Medicine, Nagoya University, Aichi, 464-8601, Japan.
Yuka MiyoshiDepartment of Neuroscience and Pathobiology, Research Institute of Environmental Medicine, Nagoya University, Aichi, 464-8601, Japan.
Noe KawadeDepartment of Neuroscience and Pathobiology, Research Institute of Environmental Medicine, Nagoya University, Aichi, 464-8601, Japan.
Seiji WatanabeDepartment of Neuroscience and Pathobiology, Research Institute of Environmental Medicine, Nagoya University, Aichi, 464-8601, Japan.ORCID 0000-0001-8038-7919
Yuko SaitoBrain Bank for Aging Research (Neuropathology), Tokyo Metropolitan Geriatric Hospital and Institute of Gerontology, Tokyo, 173-0015, Japan.
Shigeo MurayamaBrain Bank for Aging Research (Neuropathology), Tokyo Metropolitan Geriatric Hospital and Institute of Gerontology, Tokyo, 173-0015, Japan.
Takaomi C SaidoLaboratory for Proteolytic Neuroscience, RIKEN Center for Brain Science, Saitama, 351-0198, Japan.ORCID 0000-0003-1970-6903
Takashi SaitoDepartment of Neuroscience and Pathobiology, Research Institute of Environmental Medicine, Nagoya University, Aichi, 464-8601, Japan.ORCID 0000-0002-9659-9251
Koji YamanakaDepartment of Neuroscience and Pathobiology, Research Institute of Environmental Medicine, Nagoya University, Aichi, 464-8601, Japan. yamanaka.koji.p4@f.mail.nagoya-u.ac.jp.ORCID 0000-0003-4655-0035

Funding

Hori Sciences and Arts Foundation (Hori Sciences & Arts Foundation) NoneJapan Agency for Medical Research and Development (AMED) JP21wm0425019Japan Agency for Medical Research and Development (AMED) JP24wm0425014MEXT | Japan Science and Technology Agency (JST) JPMJM2024MEXT | Japan Society for the Promotion of Science (JSPS) JP22H04923MEXT | Japan Society for the Promotion of Science (JSPS) JP23K14687Takeda Science Foundation None
6 · The paper itself

Abstract

Alzheimer's disease (AD) is the most common form of dementia and is characterized by the accumulation of amyloid β (Aβ) and phosphorylated tau. Neuroinflammation, mainly mediated by glial activation, plays an important role in AD progression. Although there is growing evidence for the anti-neuroinflammatory and neuroprotective effects of the cannabinoid system modulation, the detailed mechanism remains unclear. To address these issues, we analyzed the expression levels of cannabinoid receptor type II (Cnr2/Cb2) in App

Indexed as

Alzheimer DiseaseAstrocytesCannabinoidsCognitive DysfunctionMice, TransgenicMicrogliaReceptor, Cannabinoid, CB2Amyloid beta-PeptidesAnimalsDisease Models, AnimalHumansMaleMiceNeuroinflammatory Diseases1,1-dimethylbutyl-1-deoxy-Delta(9)-THCAmyloid beta-PeptidesCannabinoidsReceptor, Cannabinoid, CB2

Identifiers

PMID39587077
PMCPMC11589152

What Socratic 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 Socratic graph.