Evidence map›Paper›PMID 35745036›Full record

ArticleMolecules (Basel, Switzerland)2022

1,8-Cineole Ameliorates Advanced Glycation End Products-Induced Alzheimer's Disease-like Pathology In Vitro and In Vivo.

Fengmao An, Yuhan Bai, Xinran Xuan, Ming Bian, Guowei Zhang, Chengxi Wei

Open access · goldAbstract read
In one paragraph

Article in Molecules (Basel, Switzerland), 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
14citing papers in PubMed, 1 pooled it
3.5field-weighted citation impact, top 6% 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

14 citing papers in PubMed, 1 synthesis or guideline pooled it, 30 citations in OpenAlex.

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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

6 authors at 1 institution in 1 country.

Fengmao AnInstitute of Pharmaceutical Chemistry and Pharmacology, Inner Mongolia Minzu University, Tongliao 028000, China.
Yuhan BaiFirst Clinical Medical College, Inner Mongolia Minzu University, Tongliao 028000, China.
Xinran XuanFirst Clinical Medical College, Inner Mongolia Minzu University, Tongliao 028000, China.
Ming BianInstitute of Pharmaceutical Chemistry and Pharmacology, Inner Mongolia Minzu University, Tongliao 028000, China.
Guowei ZhangCollege of Nursing, Inner Mongolia Minzu University, Tongliao 028000, China.
Chengxi WeiInstitute of Pharmaceutical Chemistry and Pharmacology, Inner Mongolia Minzu University, Tongliao 028000, China.
Minzu University of China · CN

Funding

Central Government Funds for Guiding Local Scientific and Technological Development of Inner Mongolia Autonomous Region 2021ZY0014Inner Mongolia Key Laboratory of Mongolian Medicine Pharmacology for Cardio-Cerebral Vascular System MDK2017039National Natural Science Foundation of China 82160823, 82160958, 81660720, 81660675PhD Science Research Initiation Foundation of Inner Mongolia Minzu University BS406Program for Young Talents of Science and Technology in Universities of Inner Mongolia Autonomous Region NJYT-20-B24The Natural Science Foundation of Inner Mongolia 2018JQ01
6 · The paper itself

Abstract

Advanced glycation end products (AGEs) are stable products produced by the reaction of macromolecules such as proteins, lipids or nucleic acids with glucose or other reducing monosaccharides, which can be identified by immunohistochemistry in the senile plaques and neurofibrillary tangles of Alzheimer's disease (AD) patients. Growing evidence suggests that AGEs are important risk factors for the development and progression of AD. 1,8-cineole (CIN) is a monoterpenoid compound which exists in many plant essential oils and has been proven to have neuroprotective activity, but its specific effect and molecular mechanisms are not clear. In this study, AGEs-induced neuronal injury and intracerebroventricular-AGE animals as the possible models for AD were employed to investigate the effects of CIN on AD pathology as well as the molecular mechanisms involved both in vivo and in vitro. Our study demonstrated that CIN could ameliorate tau phosphorylation by down-regulating the activity of GSK-3β and reducing Aβ production by inhibiting the activity of BACE-1 both in vivo and in vitro. It is suggested that CIN has certain therapeutic value in the treatment of AD.

Indexed as

Alzheimer DiseaseAmyloid beta-PeptidesAnimalsEucalyptolGlycation End Products, AdvancedGlycogen Synthase Kinase 3 betaHumansPhosphorylationtau ProteinsAmyloid beta-PeptidesEucalyptolGlycation End Products, AdvancedGlycogen Synthase Kinase 3 betatau Proteins1,8-cineoleadvanced glycation end productsAlzheimer’s diseasetau hyperphosphorylationβ-amyloid

Identifiers

PMID35745036
PMCPMC9229467
OpenAlexW4283119791

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.