Evidence map›Paper›PMID 27647310›Full record

ArticleJournal of molecular neuroscience : MN2017

Upregulation of Aβ42 in the Brain and Bodily Fluids of Rhesus Monkeys with Aging.

Qiao Zhao, Jing Lu, Zitong Yao, Shubo Wang, Liming Zhu, Ju Wang, Baian Chen

Abstract read
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In one paragraph

Article in Journal of molecular neuroscience : MN, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.

0numbers the graph read from it
0cells of the map it votes in
12citing papers in PubMed
–field-weighted citation impact
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

12 citing papers in PubMed.

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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

7 authors.

Qiao ZhaoProtein Misfolding Diseases Research Laboratory, School of Basic Medical Science, Capital Medical University, No. 10, Youanmenwai, Xitoutiao, Beijing, 100069, China.
Jing LuProtein Misfolding Diseases Research Laboratory, School of Basic Medical Science, Capital Medical University, No. 10, Youanmenwai, Xitoutiao, Beijing, 100069, China.
Zitong YaoProtein Misfolding Diseases Research Laboratory, School of Basic Medical Science, Capital Medical University, No. 10, Youanmenwai, Xitoutiao, Beijing, 100069, China.
Shubo WangProtein Misfolding Diseases Research Laboratory, School of Basic Medical Science, Capital Medical University, No. 10, Youanmenwai, Xitoutiao, Beijing, 100069, China.
Liming ZhuProtein Misfolding Diseases Research Laboratory, School of Basic Medical Science, Capital Medical University, No. 10, Youanmenwai, Xitoutiao, Beijing, 100069, China.
Ju WangProtein Misfolding Diseases Research Laboratory, School of Basic Medical Science, Capital Medical University, No. 10, Youanmenwai, Xitoutiao, Beijing, 100069, China.
Baian ChenProtein Misfolding Diseases Research Laboratory, School of Basic Medical Science, Capital Medical University, No. 10, Youanmenwai, Xitoutiao, Beijing, 100069, China. baianchen@ccmu.edu.cn.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The cerebral accumulation of amyloid beta (Aβ) is one of the key pathological hallmarks of Alzheimer's disease (AD). Aβ is also found in bodily fluids such as the cerebrospinal fluid (CSF) and plasma. However, the significance of Aβ accumulation in the brain and different bodily pools, as well as its correlation with aging and cerebral amyloid pathology, is not completely understood. To better understand this question, we selected the rhesus monkey, which is phylogenetically and physiologically highly similar to the human, as a model to study. We quantified the levels of the two main Aβ isoforms (Aβ42 and Aβ40) in different sections of the brain (frontal cortex, temporal cortex, and hippocampus) and bodily fluids (CSF and plasma) of rhesus monkeys at different developmental phases (young, 5-9 years of age; mature, 10-19 years of age; and old, 21-24 years of age). We found that the levels of neuronal and insoluble Aβ42 increased significantly in the brain with aging, suggesting that this specific isoform might be directly involved in aging and AD-like pathophysiology. There was no significant change in the Aβ40 level in the brain with aging. In addition, the Aβ42 level, but not the Aβ40 level, in both the CSF and plasma increased with aging. We also identified a positive correlation between Aβ42 in the CSF and plasma and Aβ42 in the brain. Taken collectively, our results indicate that there is an association between Aβ accumulation and age. These results support the increased incidence of AD with aging.

Indexed as

Up-RegulationAgingAmyloid beta-PeptidesAnimalsBrainFemaleMacaca mulattaMalePeptide FragmentsAmyloid beta-Peptidesamyloid beta-protein (1-40)amyloid beta-protein (1-42)Peptide FragmentsAgingAlzheimer’s diseaseAmyloid beta peptideBodily fluidsRhesus monkeys

Identifiers

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Registered trials

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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.