Evidence map›Paper›PMID 27435080›Full record

ArticleCell stress & chaperones2016

The involvement of homocysteine in stress-induced Aβ precursor protein misprocessing and related cognitive decline in rats.

Fang Xie, Yun Zhao, Jing Ma, Jing-Bo Gong, Shi-Da Wang, Liang Zhang, Xiu-Jie Gao, Ling-Jia Qian

Open access · greenAbstract read
In one paragraph

Article in Cell stress & chaperones, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.

0numbers the graph read from it
0cells of the map it votes in
16citing papers in PubMed
1.5field-weighted citation impact, top 17% 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

16 citing papers in PubMed, 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

8 authors at 1 institution.

Fang XieDepartment of Stress Medicine, Institute of Basic Medical Sciences, #27 Taiping Road, Haidian, Beijing, 100039, People's Republic of China.
Yun ZhaoDepartment of Stress Medicine, Institute of Basic Medical Sciences, #27 Taiping Road, Haidian, Beijing, 100039, People's Republic of China.
Jing MaDepartment of Stress Medicine, Institute of Basic Medical Sciences, #27 Taiping Road, Haidian, Beijing, 100039, People's Republic of China.
Jing-Bo GongDepartment of Stress Medicine, Institute of Basic Medical Sciences, #27 Taiping Road, Haidian, Beijing, 100039, People's Republic of China.
Shi-Da WangDepartment of Stress Medicine, Institute of Basic Medical Sciences, #27 Taiping Road, Haidian, Beijing, 100039, People's Republic of China.
Liang ZhangDepartment of Stress Medicine, Institute of Basic Medical Sciences, #27 Taiping Road, Haidian, Beijing, 100039, People's Republic of China.
Xiu-Jie GaoInstitute of Health and Environmental Medicine, Tianjin, 300050, People's Republic of China.
Ling-Jia QianDepartment of Stress Medicine, Institute of Basic Medical Sciences, #27 Taiping Road, Haidian, Beijing, 100039, People's Republic of China. newjia@vip.sina.com.
Institute of Basic Medical Sciences of the Chinese Academy of Medical Sciences

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Chronic stress is a risk factor in the development of cognitive decline and even Alzheimer's disease (AD), although its underlying mechanism is not fully understood. Our previous data demonstrated that the level of homocysteine (Hcy) was significantly elevated in the plasma of stressed animals, which suggests the possibility that Hcy is a link between stress and cognitive decline. To test this hypothesis, we compared the cognitive function, plasma concentrations of Hcy, and the brain beta-amyloid (Aβ) level between rats with or without chronic unexpected mild stress (CUMS). A lower performance by rats in behavioral tests indicated that a significant cognitive decline was induced by CUMS. Stress also disturbed the normal processing of Aβ precursor protein (APP) and resulted in the accumulation of Aβ in the brains of rats, which showed a positive correlation with the hyperhomocysteinemia (HHcy) that appeared in stressed rats. Hcy-targeting intervention experiments were used to verify further the involvement of Hcy in stress-induced APP misprocessing and related cognitive decline. The results showed that diet-induced HHcy could mimic the cognitive impairment and APP misprocessing in the same manner as CUMS, while Hcy reduction by means of vitamin B complex supplements and betaine could alleviate the cognitive deficits and dysregulation of Aβ metabolism in CUMS rats. Taken together, the novel evidence from our present study suggests that Hcy is likely to be involved in chronic stress-evoked APP misprocessing and related cognitive deficits. Our results also suggested the possibility of Hcy as a target for therapy and the potential value of vitamin B and betaine intake in the prevention of stress-induced cognitive decline.

Indexed as

Alzheimer DiseaseAmyloid beta-Protein PrecursorAnimalsCognitive DysfunctionHippocampusHomocysteineMaleProtein Processing, Post-TranslationalRats, Sprague-DawleyStress, PsychologicalAmyloid beta-Protein PrecursorHomocysteineBeta-amyloidChronic unexpected mild stressCognitive declineHomocysteine

Identifiers

PMID27435080
PMCPMC5003809
OpenAlexW2496623001

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.