Evidence map›Paper›PMID 31658360›Full record

ArticleBritish journal of pharmacology2020

Neurotrophic interactions between neurons and astrocytes following AAV1-Rheb(S16H) transduction in the hippocampus in vivo.

Min-Tae Jeon, Gyeong Joon Moon, Sehwan Kim, Minji Choi, Yong-Seok Oh, Dong Woon Kim, Hyung-Jun Kim, Kea Joo Lee, Youngshik Choe, Chang Man Ha and 7 more

Open access · hybridAbstract read
In one paragraph

Article in British journal of pharmacology, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
17citing papers in PubMed, 1 pooled it
1.2field-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

17 citing papers in PubMed, 1 synthesis or guideline pooled it, 20 citations in OpenAlex.

  1. Pooled it
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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

17 authors at 8 institutions in 2 countries.

Min-Tae JeonSchool of Life Sciences, Kyungpook National University, Daegu, Korea.
Gyeong Joon MoonSchool of Life Sciences, Kyungpook National University, Daegu, Korea.ORCID 0000-0002-2851-9563
Sehwan KimSchool of Life Sciences, Kyungpook National University, Daegu, Korea.
Minji ChoiDepartment of Science in Korean Medicine, Graduate School, Kyung Hee University, Seoul, Korea.
Yong-Seok OhDepartment of Brain-Cognitive Science, Daegu-Gyeongbuk Institute of Science and Technology, Daegu, Korea.ORCID 0000-0002-9039-2014
Dong Woon KimDepartment of Anatomy, Brain Research Institute, Chungnam National University School of Medicine, Daejeon, Korea.ORCID 0000-0001-7691-1394
Hyung-Jun KimDepartment of Neural Development and Disease, Department of Structure and Function of Neural Network, Korea Brain Research Institute, Daegu, Korea.
Kea Joo LeeDepartment of Neural Development and Disease, Department of Structure and Function of Neural Network, Korea Brain Research Institute, Daegu, Korea.ORCID 0000-0002-1366-4709
Youngshik ChoeDepartment of Neural Development and Disease, Department of Structure and Function of Neural Network, Korea Brain Research Institute, Daegu, Korea.
Chang Man HaDepartment of Neural Development and Disease, Department of Structure and Function of Neural Network, Korea Brain Research Institute, Daegu, Korea.
Il-Sung JangDepartment of Pharmacology, School of Dentistry, Kyungpook National University, Daegu, Korea.
Michiko NakamuraBrain Science and Engineering Institute, Kyungpook National University, Daegu, Korea.
Catriona McLeanVictorian Brain Bank Network, Florey Institute of Neuroscience and Mental Health, Parkville, Victoria, Australia.
Won-Suk ChungDepartment of Biological Sciences, Korea Advanced Institute of Science and Technology (KAIST), Daejeon, Korea.
Won-Ho ShinPredictive Model Research Center, Korea Institute of Toxicology, Daejeon, Korea.
Seok-Geun LeeDepartment of Science in Korean Medicine, Graduate School, Kyung Hee University, Seoul, Korea.ORCID 0000-0002-0060-5777
Sang Ryong KimSchool of Life Sciences, Kyungpook National University, Daegu, Korea.ORCID 0000-0003-0299-1613
Kyungpook National University · KRKorea Brain Research Institute · KRDaegu Gyeongbuk Institute of Science and Technology · KRKorea Advanced Institute of Science and Technology · KRChungnam National University · KRFlorey Institute of Neuroscience and Mental Health · AUKyung Hee Cyber University · KRKyung Hee University · KR

Funding

KBRI Research Program of the Ministry of Science, ICT & Future Planning 18-BR-02-06KBRI Research Program of the Ministry of Science, ICT & Future Planning 18-BR-03-01KBRI Research Program of the Ministry of Science, ICT & Future Planning 18-RB-03-03Ministry of Health & Welfare HI14C1135Ministry of Health & Welfare HI15C1928National Research Foundation of Korea NRF-2017R1A2B4002675National Research Foundation of Korea NRF-2017R1D1A1B03032218
6 · The paper itself

Abstract

background and purposeWe recently reported that AAV1-Rheb(S16H) transduction could protect hippocampal neurons through the induction of brain-derived neurotrophic factor (BDNF) in the rat hippocampus in vivo. It is still unclear how neuronal BDNF produced by AAV1-Rheb(S16H) transduction induces neuroprotective effects in the hippocampus and whether its up-regulation contributes to the enhance of a neuroprotective system in the adult brain. EXPERIMENTAL APPROACH: To determine the presence of a neuroprotective system in the hippocampus of patients with Alzheimer's disease (AD), we examined the levels of glial fibrillary acidic protein, BDNF and ciliary neurotrophic factor (CNTF) and their receptors, tropomyocin receptor kinase B (TrkB) and CNTF receptor α(CNTFRα), in the hippocampus of AD patients. We also determined whether AAV1-Rheb(S16H) transduction stimulates astroglial activation and whether reactive astrocytes contribute to neuroprotection in models of hippocampal neurotoxicity in vivo and in vitro. KEY

resultsAD patients may have a potential neuroprotective system, demonstrated by increased levels of full-length TrkB and CNTFRα in the hippocampus. Further AAV1-Rheb(S16H) transduction induced sustained increases in the levels of full-length TrkB and CNTFRα in reactive astrocytes and hippocampal neurons. Moreover, neuronal BDNF produced by Rheb(S16H) transduction of hippocampal neurons induced reactive astrocytes, resulting in CNTF production through the activation of astrocytic TrkB and the up-regulation of neuronal BDNF and astrocytic CNTF which had synergistic effects on the survival of hippocampal neurons in vivo. CONCLUSIONS AND IMPLICATIONS: The results demonstrated that Rheb(S16H) transduction of hippocampal neurons could strengthen the neuroprotective system and this intensified system may have a therapeutic value against neurodegeneration in the adult brain.

Indexed as

AstrocytesNeuroprotective AgentsBrain-Derived Neurotrophic FactorGlial Fibrillary Acidic ProteinHippocampusHumansNeuronsRas Homolog Enriched in Brain ProteinBrain-Derived Neurotrophic FactorGlial Fibrillary Acidic ProteinNeuroprotective AgentsRas Homolog Enriched in Brain ProteinRHEB protein, human

Identifiers

PMID31658360
PMCPMC7012949
OpenAlexW2982511428

What Socratic holds

Textmetadata
LicenceCC BY-NC
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.