Evidence map›Paper›PMID 29370749›Full record

ArticleBMC neuroscience2018

Intraventricular infusion of clusterin ameliorated cognition and pathology in Tg6799 model of Alzheimer's disease.

Xue-Mei Qi, Cheng Wang, Xing-Kun Chu, Gen Li, Jian-Fang Ma

Open access · goldAbstract read
In one paragraph

Article in BMC neuroscience, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers.

0numbers the graph read from it
0cells of the map it votes in
24citing papers in PubMed
2.4field-weighted citation impact, top 9% 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

24 citing papers in PubMed, 42 citations in OpenAlex.

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  15. HDL Proteome and Alzheimer's Disease: Evidence of a Link.Antioxidants (Basel, Switzerland) · 2020
    Review
  16. Article
  17. Review
  18. Secreted Chaperones in Neurodegeneration.Frontiers in aging neuroscience · 2020
    Review
  19. Article
  20. 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

5 authors at 1 institution in 1 country.

Xue-Mei QiDepartment of Neurology and Institute of Neurology, Ruijin Hospital Affiliated to Shanghai Jiao Tong University School of Medicine, No. 197, Road Ruijin Second, Shanghai, 200025, People's Republic of China.
Cheng WangDepartment of Neurology and Institute of Neurology, Ruijin Hospital Affiliated to Shanghai Jiao Tong University School of Medicine, No. 197, Road Ruijin Second, Shanghai, 200025, People's Republic of China.
Xing-Kun ChuDepartment of Neurology and Institute of Neurology, Ruijin Hospital Affiliated to Shanghai Jiao Tong University School of Medicine, No. 197, Road Ruijin Second, Shanghai, 200025, People's Republic of China.
Gen LiDepartment of Neurology and Institute of Neurology, Ruijin Hospital Affiliated to Shanghai Jiao Tong University School of Medicine, No. 197, Road Ruijin Second, Shanghai, 200025, People's Republic of China.
Jian-Fang MaDepartment of Neurology and Institute of Neurology, Ruijin Hospital Affiliated to Shanghai Jiao Tong University School of Medicine, No. 197, Road Ruijin Second, Shanghai, 200025, People's Republic of China. majifa@hotmail.com.ORCID 0000-0002-9109-5070
Shanghai Jiao Tong University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundAlzheimer's disease (AD) is characterized by the deposition of amyloid-β (Aβ) in brain parenchyma and cerebral blood vessels as cerebral amyloid angiopathy (CAA). Clusterin, a chaperon protein associated with Aβ aggregation, toxicity and transport through blood-brain barrier, may play a key role in the development of AD. Recently, clusterin peptide D-[113-122] was shown to mimic clusterin's function and exerted therapeutic effect in atherosclerosis. In this study, we investigated whether this clusterin peptide also affected (Aβ) deposition in AD transgenic mouse.

resultsUsing a micropump, synthetic peptide 113-122 of clusterin protein (20 μg/200 μl) was infused into the lateral ventricle of 8-month 5 × FAD transgenic mouse model (Tg6799), for 2 weeks. Water-maze testing showed an improved cognitive function of the Tg6799 mice treated with clusterin. Immunocytochemistry and quantitative analysis revealed that intraventricular (icv) administration of clusterin peptide in Tg6799 mouse reduced Aβ plaques as well the severity of cerebral amyloid angiopathy. Enzyme-linked immunosorbent assay demonstrated a decreased in the soluble levels of Aβ (Aβ40 and Aβ42) in the brain. Western-blot revealed an increased level of LRP-2 after clusterin peptide treatment.

conclusionThese results suggest that icv infusion of clusterin peptide D-[113-122] offers a promising therapeutic approach to reduce Aβ deposition as well as CAA. The LRP2-mediated clearance system might be involved in the mechanism of these effects.

Indexed as

Alzheimer DiseaseAmyloid beta-PeptidesAnimalsBlood-Brain BarrierBrainCerebral Amyloid AngiopathyClusterinCognitionDisease Models, AnimalInfusions, IntraventricularMice, TransgenicAmyloid beta-PeptidesClusterinAlzheimer’s diseaseAmyloidClusterinLRP-2

Identifiers

PMID29370749
PMCPMC5785859
OpenAlexW2791391987

What OpenQuestion holds

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LicenceCC BY
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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.