Evidence map›Paper›PMID 32967251›Full record

ArticleInternational journal of molecular sciences2020

Characterization of Tauopathy in a Rat Model of Post-Stroke Dementia Combining Acute Infarct and Chronic Cerebral Hypoperfusion.

Dong Bin Back, Bo-Ryoung Choi, Jung-Soo Han, Kyoung Ja Kwon, Dong-Hee Choi, Chan Young Shin, Jongmin Lee, Hahn Young Kim

Open access · goldAbstract read
In one paragraph

Article in International journal of molecular sciences, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
23citing papers in PubMed, 1 pooled it
1.5field-weighted citation impact, top 20% 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

23 citing papers in PubMed, 1 synthesis or guideline pooled it, 33 citations in OpenAlex.

  1. Pooled it
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  14. Research progress in the evaluation of glymphatic system function by the DTI-ALPS method.Zhong nan da xue xue bao. Yi xue ban = Journal of Central South University. Medical sciences · 2023
    Article
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  16. Rodent Models of Post-Stroke Dementia.International journal of molecular sciences · 2022
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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 1 institution in 1 country.

Dong Bin BackDepartment of Neurology, Research Institute of Medical Science, Konkuk University School of Medicine, Seoul 05029, Korea.
Bo-Ryoung ChoiDepartment of Neurology, Research Institute of Medical Science, Konkuk University School of Medicine, Seoul 05029, Korea.
Jung-Soo HanDepartment of Biological Sciences, Konkuk University, Seoul 05029, Korea.ORCID 0000-0001-8447-4518
Kyoung Ja KwonDepartment of Neurology, Research Institute of Medical Science, Konkuk University School of Medicine, Seoul 05029, Korea.
Dong-Hee ChoiDepartment of Medicine, Konkuk University School of Medicine, Seoul 05029, Korea.
Chan Young ShinDepartment of Pharmacology, Konkuk University School of Medicine, Seoul 05029, Korea.
Jongmin LeeDepartment of Rehabilitation Medicine, Konkuk University School of Medicine, Seoul 05029, Korea.ORCID 0000-0001-8718-0099
Hahn Young KimDepartment of Neurology, Research Institute of Medical Science, Konkuk University School of Medicine, Seoul 05029, Korea.ORCID 0000-0001-9591-4005
Konkuk University · KR

Funding

Korea Health Industry Development Institute HI17C0368National Research Foundation of Korea 2017R1D1A1B03030906 and 2020R1F1A1076085
6 · The paper itself

Abstract

Post-stroke dementia (PSD) is a major neurodegenerative consequence of stroke. Tauopathy has been reported in diverse neurodegenerative diseases. We investigated the cognitive impairment and pathomechanism associated with tauopathy in a rat model of PSD by modeling acute ischemic stroke and underlying chronic cerebral hypoperfusion (CCH). We performed middle cerebral artery occlusion (MCAO) surgery in rats to mimic acute ischemic stroke, followed by bilateral common carotid artery occlusion (BCCAo) surgery to mimic CCH. We performed behavioral tests and focused on the characterization of tauopathy through histology. Parenchymal infiltration of cerebrospinal fluid (CSF) tracers after intracisternal injection was examined to evaluate glymphatic function. In an animal model of PSD, cognitive impairment was aggravated when BCCAo was combined with MCAO. Tauopathy, manifested by tau hyperphosphorylation, was prominent in the peri-infarct area when CCH was combined. Synergistic accentuation of tauopathy was evident in the white matter. Microtubules in the neuronal axon and myelin sheath showed partial colocalization with the hyperphosphorylated tau, whereas oligodendrocytes showed near-complete colocalization. Parenchymal infiltration of CSF tracers was attenuated in the PSD model. Our experimental results suggest a hypothesis that CCH may aggravate cognitive impairment and tau hyperphosphorylation in a rat model of PSD by interfering with tau clearance through the glymphatic system. Therapeutic strategies to improve the clearance of brain metabolic wastes, including tau, may be a promising approach to prevent PSD after stroke.

Indexed as

Brain InfarctionDementiaStrokeTauopathiesAnimalsDisease Models, AnimalMaleMaze LearningRatsRats, Wistaranimal modelchronic cerebral hypoperfusionglymphatic systempost-stroke dementiatauopathy

Identifiers

PMID32967251
PMCPMC7555397
OpenAlexW3087126942

What OpenQuestion holds

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LicenceCC BY
Read underepoch 390

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.