Evidence map›Paper›PMID 38277298›Full record

ArticleJournal of Alzheimer's disease : JAD2024

Transcriptomic Profiling Reveals Neuroinflammation in the Corpus Callosum of a Transgenic Mouse Model of Alzheimer's Disease.

Hajime Takase, Gen Hamanaka, Tomonori Hoshino, Ryo Ohtomo, Shuzhen Guo, Emiri T Mandeville, Eng H Lo, Ken Arai

Open access · greenAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Journal of Alzheimer's disease : JAD, 2024. 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
2.0field-weighted citation impact, top 15% 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, 8 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

8 authors at 2 institutions in 2 countries.

Hajime TakaseDepartments of Radiology and Neurology, Neuroprotection Research Laboratory, Massachusetts General Hospital and Harvard Medical School, Charlestown, MA, USA.
Gen HamanakaDepartments of Radiology and Neurology, Neuroprotection Research Laboratory, Massachusetts General Hospital and Harvard Medical School, Charlestown, MA, USA.
Tomonori HoshinoDepartments of Radiology and Neurology, Neuroprotection Research Laboratory, Massachusetts General Hospital and Harvard Medical School, Charlestown, MA, USA.
Ryo OhtomoDepartments of Radiology and Neurology, Neuroprotection Research Laboratory, Massachusetts General Hospital and Harvard Medical School, Charlestown, MA, USA.
Shuzhen GuoDepartments of Radiology and Neurology, Neuroprotection Research Laboratory, Massachusetts General Hospital and Harvard Medical School, Charlestown, MA, USA.
Emiri T MandevilleDepartments of Radiology and Neurology, Neuroprotection Research Laboratory, Massachusetts General Hospital and Harvard Medical School, Charlestown, MA, USA.
Eng H LoDepartments of Radiology and Neurology, Neuroprotection Research Laboratory, Massachusetts General Hospital and Harvard Medical School, Charlestown, MA, USA.
Ken AraiDepartments of Radiology and Neurology, Neuroprotection Research Laboratory, Massachusetts General Hospital and Harvard Medical School, Charlestown, MA, USA.
Harvard University · USMassachusetts General Hospital · US

Funding

The effect of circadian rhythm disruptions on the angiogenic response to hypoperfusion in the AD brainR01AG081841 · NIA · MASSACHUSETTS GENERAL HOSPITAL · PI Ken Arai, Eng H. Lo · 2023 to 2026
$3.0M
Effects of Hypertension and Hypoperfusion on the Brain VasculomeR01NS110818 · NINDS · MASSACHUSETTS GENERAL HOSPITAL · PI ARAI, KEN, LO, ENG H. · 2019 to 2019
$2.4M
Oligodendrocyte Precursor Cells Regulate White Matter Remodeling in Vascular Cognitive Impairment and DementiaR01NS113556 · NINDS · MASSACHUSETTS GENERAL HOSPITAL · PI ARAI, KEN · 2019 to 2023
$2.4M
NIA NIH HHS R01 AG081841NINDS NIH HHS R01 NS110818NINDS NIH HHS R01 NS113556
6 · The paper itself

Abstract

backgroundAlzheimer's disease (AD) is a widespread neurodegenerative disorder characterized by progressive cognitive decline, affecting a significant portion of the aging population. While the cerebral cortex and hippocampus have been the primary focus of AD research, accumulating evidence suggests that white matter lesions in the brain, particularly in the corpus callosum, play an important role in the pathogenesis of the disease.

objectiveThis study aims to investigate the gene expression changes in the corpus callosum of 5xFAD transgenic mice, a widely used AD mouse model.

methodsWe conducted behavioral tests for spatial learning and memory in 5xFAD transgenic mice and performed RNA sequencing analyses on the corpus callosum to examine transcriptomic changes.

resultsOur results show cognitive decline and demyelination in the corpus callosum of 5xFAD transgenic mice. Transcriptomic analysis reveals a predominance of upregulated genes in AD mice, particularly those associated with immune cells, including microglia. Conversely, downregulation of genes related to chaperone function and clock genes such as Per1, Per2, and Cry1 is also observed.

conclusionsThis study suggests that activation of neuroinflammation, disruption of chaperone function, and circadian dysfunction are involved in the pathogenesis of white matter lesions in AD. The findings provide insights into potential therapeutic targets and highlight the importance of addressing white matter pathology and circadian dysfunction in AD treatment strategies.

Indexed as

Alzheimer DiseaseAnimalsCorpus CallosumDisease Models, AnimalGene Expression ProfilingMiceMice, TransgenicNeuroinflammatory DiseasesAlzheimer’s diseasecircadian rhythmcorpus callosummicrogliamolecular chaperonesneuroinflammationRNA-seq

Identifiers

PMID38277298
PMCPMC12939303
OpenAlexW4391131152

What Socratic holds

Textmetadata
LicenceTDM
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.