Evidence map›Paper›PMID 32209731›Full record

ArticleAging2020

Intranasal delivery of 9-cis retinoic acid reduces beta-amyloid deposition via inhibiting astrocyte-mediated inflammation.

Hong Zhao, Shuo Li, Zhuo Li, Shuo Yang, Dandan Li, Jiaolin Zheng, Hongmei Gao, Ling Yun, YingLi Gu, Longxuan Li and 2 more

Open access · greenAbstract read
In one paragraph

Article in Aging, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.

0numbers the graph read from it
0cells of the map it votes in
8citing papers in PubMed
1.1field-weighted citation impact, top 24% 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

8 citing papers in PubMed, 12 citations in OpenAlex.

  1. Article
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  7. Review
  8. Sodium Butyrate Protects N2a Cells against AMediators of inflammation · 2020
    Article
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 at 6 institutions in 2 countries.

Hong ZhaoDepartment of Neurology, The Fourth Hospital of Harbin Medical University, Harbin, China.
Shuo LiDepartment of Ultrasonography, The Fourth Hospital of Harbin Medical University, Harbin, China.
Zhuo LiDepartment of Endocrinology, The First Hospital of Jilin University, Changchun, China.
Shuo YangDepartment of Neurology, The Fourth Hospital of Harbin Medical University, Harbin, China.
Dandan LiDepartment of Neurology, The Second Hospital of Heilongjiang Province, Harbin, China.
Jiaolin ZhengDepartment of Neurology, The Second Hospital of Harbin Medical University, Harbin, China.
Hongmei GaoDepartment of Neurology, The Fourth Hospital of Harbin Medical University, Harbin, China.
Ling YunDepartment of Neurology, The Fourth Hospital of Harbin Medical University, Harbin, China.
YingLi GuDepartment of Neurology, The Fourth Hospital of Harbin Medical University, Harbin, China.
Longxuan LiDepartment of Neurology, Gongli Hospital of The Second Military Medical University, Shanghai, China.
Jing ZhaoDepartment of Neuroscience, Mayo Clinic, Jacksonville, FL 32224, USA.
Yuan FuDepartment of Neurology, The Fourth Hospital of Harbin Medical University, Harbin, China.
Harbin Medical University · CNFourth Affiliated Hospital of Harbin Medical University · CNFirst Hospital of Jilin University · CNMayo Clinic in Florida · USSecond Affiliated Hospital of Harbin Medical University · CNSecond Military Medical University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Alzheimer's disease (AD) is associated with the accumulation and deposition of a beta-amyloid (Αβ) peptide in the brain, resulting in increased neuroinflammation and synaptic dysfunction. Intranasal delivery of targeted drugs to the brain represents a noninvasive pathway that bypasses the blood-brain barrier and minimizes systemic exposure. The aim of this study was to evaluate the therapeutic effect of intranasally delivered 9-cis retinoic acid (RA) on the neuropathology of an AD mouse model. Herein, we observed dramatically decreased Αβ deposition in the brains of amyloid precursor protein (APP) and presenilin 1 (PS1) double-transgenic mice (APP/PS1) treated intranasally with 9-cis RA for 4 weeks compared to that in the brains of vehicle-treated mice. Importantly, intranasal delivery of 9-cis RA suppressed Αβ-associated astrocyte activation and neuroinflammation and ultimately restored synaptic deficits in APP/PS1 transgenic mice. These results support the critical roles of Αβ-associated neuroinflammation responses to synaptic deficits, particularly during the deposition of Αβ. Our findings provide strong evidence that intranasally delivered 9-cis RA attenuates neuronal dysfunction in an AD mouse model and is a promising therapeutic strategy for the prevention and treatment of AD.

Indexed as

Administration, IntranasalAlitretinoinAlzheimer DiseaseAmyloid beta-PeptidesAmyloid beta-Protein PrecursorAnimalsAstrocytesBrainDisease Models, AnimalInflammationInflammation MediatorsMiceMice, TransgenicMicrogliaPresenilin-1AlitretinoinAmyloid beta-PeptidesAmyloid beta-Protein PrecursorInflammation MediatorsPresenilin-1presenilin 1, mouse9-cis retinoic acidAlzheimer's diseaseastrocyte activationbeta-amyloidintranasal delivery

Identifiers

PMID32209731
PMCPMC7138573
OpenAlexW3013937331

What OpenQuestion holds

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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 OpenQuestion graph.