Evidence map›Paper›PMID 37069416›Full record

ArticleNeurochemical research2023

APP96-110 Elicits Neuroprotective Effects Following Ischemic Insult in Animal Models.

Renée Kosonen, Ji Young Chang, Seowoo Lee, Jiwon Kim, Jong Youl Kim, Jong Eun Lee

Open access · greenAbstract read
PubMed Publisher
In one paragraph

Article in Neurochemical research, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

0numbers the graph read from it
0cells of the map it votes in
0citing papers in PubMed
0.4field-weighted citation impact, top 41% 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

0 citing papers in PubMed, 2 citations in OpenAlex.

No citing paper in PubMed yet.

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

6 authors at 1 institution in 1 country.

Renée KosonenDepartment of Anatomy, Yonsei University College of Medicine, Seoul, 03722, South Korea.ORCID http://orcid.org/0000-0003-1039-0682
Ji Young ChangDepartment of Anatomy, Yonsei University College of Medicine, Seoul, 03722, South Korea.ORCID http://orcid.org/0000-0001-9292-9551
Seowoo LeeDepartment of Anatomy, Yonsei University College of Medicine, Seoul, 03722, South Korea.
Jiwon KimDepartment of Anatomy, Yonsei University College of Medicine, Seoul, 03722, South Korea.ORCID http://orcid.org/0000-0001-6493-4484
Jong Youl KimDepartment of Anatomy, Yonsei University College of Medicine, Seoul, 03722, South Korea.ORCID http://orcid.org/0000-0002-8340-2894
Jong Eun LeeDepartment of Anatomy, Yonsei University College of Medicine, Seoul, 03722, South Korea. jelee@yuhs.ac.ORCID http://orcid.org/0000-0001-6203-7413
Yonsei University · KR

Funding

National Research Foundation of Korea NRF-2021R1A2C2008034
6 · The paper itself

Abstract

Competitive amyloidogenic pathways play an important role in many neurological diseases such as the onset of various degenerative diseases and ischemic stroke. Overexpression of amyloid precursor protein (APP) and amyloid-beta is modulated via the amyloidogenic pathway, which plays a crucial role in neuroinflammation. During ischemic conditions, the activity of the anti-inflammatory non-amyloidogenic pathway decreases, thus increasing the activity of amyloidogenic pathway. The soluble alpha form of APP (sAPPα), formed via the non-amyloidogenic pathway, exhibits neuroprotective effects against neurological diseases. sAPPα is thought to have a modulatory effect on several cell survival pathways, including its ability to inhibit the phosphoinositide 3-kinases (PI3K) pathway, thereby inhibiting the inflammatory response. The APP derivative, APP96-110, could act as a functional substitute for native sAPPα. Herein, we investigated whether APP96-110 has neuroprotective effects against neuroinflammation and damage following cerebral ischemic stroke. Treatment with diluted APP96-110 (0.005 mg/kg) in mice after 30 min of transient middle cerebral artery occlusion (tMCAO) showed improved motor function and reduced expression of the inflammatory marker CD86. APP96-110 decreased the infarct size and induced an anti-inflammatory response by inhibiting the PI3K pathway. These results suggest that the treatment of APP96-110 is efficacious in reducing neuroinflammation and infarct size in ischemic stroke.

Indexed as

Ischemic StrokeNeuroprotective AgentsStrokeAmyloid beta-Protein PrecursorAnimalsAnti-Inflammatory AgentsInfarction, Middle Cerebral ArteryMiceModels, AnimalNeuroinflammatory DiseasesPhosphatidylinositol 3-KinasesRatsRats, Sprague-DawleyAmyloid beta-Protein PrecursorAnti-Inflammatory AgentsNeuroprotective AgentsPhosphatidylinositol 3-KinasesAmyloid precursor proteinAPP96-110Ischemic strokeMicrogliaNeuroinflammation

Identifiers

PMID37069416
OpenAlexW4366140917

What OpenQuestion holds

Textmetadata
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.