Evidence map›Paper›PMID 37315033›Full record

ArticlePloS one2023

Evaluation of 18F labeled glial fibrillary acidic protein binding nanobody and its brain shuttle peptide fusion proteins using a neuroinflammation rat model.

Takahiro Morito, Ryuichi Harada, Ren Iwata, Yoichi Ishikawa, Nobuyuki Okamura, Yukitsuka Kudo, Shozo Furumoto, Kazuhiko Yanai, Manabu Tashiro

Open access · goldAbstract read
In one paragraph

Article in PloS one, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.

0numbers the graph read from it
0cells of the map it votes in
1citing papers in PubMed
0.5field-weighted citation impact, top 34% 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

1 citing paper in PubMed, 2 citations in OpenAlex.

  1. 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

9 authors at 2 institutions in 1 country.

Takahiro MoritoDivision of Cyclotron Nuclear Medicine, Tohoku University Graduate School of Medicine, Sendai, Miyagi, Japan.
Ryuichi HaradaDepartment of Pharmacology, Tohoku University Graduate School of Medicine, Sendai, Miyagi, Japan.ORCID 0000-0001-8538-8814
Ren IwataDivision of Radiopharmaceutical Chemistry, Cyclotron and Radioisotope Center, Tohoku University, Sendai, Miyagi, Japan.
Yoichi IshikawaDivision of Radiopharmaceutical Chemistry, Cyclotron and Radioisotope Center, Tohoku University, Sendai, Miyagi, Japan.
Nobuyuki OkamuraDivision of Pharmacology, Faculty of Medicine, Tohoku Medical and Pharmaceutical University, Sendai, Miyagi, Japan.
Yukitsuka KudoInstitute of Development, Aging and Cancer, Tohoku University, Sendai, Miyagi, Japan.
Shozo FurumotoDivision of Radiopharmaceutical Chemistry, Cyclotron and Radioisotope Center, Tohoku University, Sendai, Miyagi, Japan.
Kazuhiko YanaiDivision of Cyclotron Nuclear Medicine, Tohoku University Graduate School of Medicine, Sendai, Miyagi, Japan.
Manabu TashiroDivision of Cyclotron Nuclear Medicine, Tohoku University Graduate School of Medicine, Sendai, Miyagi, Japan.
Tohoku University · JPTohoku Medical and Pharmaceutical University · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Astrogliosis is a crucial feature of neuroinflammation and is characterized by the significant upregulation of glial fibrillary acidic protein (GFAP) expression. Hence, visualizing GFAP in the living brain of patients with damaged central nervous system using positron emission tomography (PET) is of great importance, and it is expected to depict neuroinflammation more directly than existing neuroinflammation imaging markers. However, no PET radiotracers for GFAP are currently available. Therefore, neuroimaging with antibody-like affinity proteins could be a viable strategy for visualizing imaging targets that small molecules rarely recognize, such as GFAP, while we need to overcome the challenges of slow clearance and low brain permeability. The E9 nanobody, a small-affinity protein with high affinity and selectivity for GFAP, was utilized in this study. E9 was engineered by fusing a brain shuttle peptide that facilitates blood-brain barrier permeation via two different types of linker domains: E9-GS-ApoE (EGA) and E9-EAK-ApoE (EEA). E9, EGA and EEA were radiolabeled with fluorine-18 using cell-free protein radiosynthesis. In vitro autoradiography showed that all radiolabeled proteins exhibited a significant difference in neuroinflammation in the brain sections created from a rat model constructed by injecting lipopolysaccharide (LPS) into the unilateral striatum of wildtype rats, and an excess competitor displaced their binding. However, exploratory in vivo PET imaging and ex vivo biodistribution studies in the rat model failed to distinguish neuroinflammatory lesions within 3 h of 18F-EEA intravenous injection. This study contributes to a better understanding of the characteristics of small-affinity proteins fused with a brain shuttle peptide for further research into the use of protein molecules as PET tracers for imaging neuropathology.

Indexed as

Neuroinflammatory DiseasesTomography, X-Ray ComputedAnimalsApolipoproteins EBrainFluorine RadioisotopesGlial Fibrillary Acidic ProteinPeptidesRatsSingle-Domain AntibodiesTissue DistributionApolipoproteins EFluorine-18Fluorine RadioisotopesGlial Fibrillary Acidic ProteinPeptidesSingle-Domain Antibodies

Identifiers

PMID37315033
PMCPMC10266665
OpenAlexW4380627733

What OpenQuestion holds

Textmetadata
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.