Evidence map›Paper›PMID 28702365›Full record

ArticleBBA clinical2017

Abnormal amyloid β

G Vinothkumar, C Kedharnath, S Krishnakumar, S Sreedhar, K Preethikrishnan, S Dinesh, A Sundaram, D Balakrishnan, G Shivashekar, Sureshkumar and 1 more

Open access · hybridAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in BBA clinical, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
15citing papers in PubMed, 1 pooled it
1.2field-weighted citation impact, top 21% 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

15 citing papers in PubMed, 1 synthesis or guideline pooled it, 29 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

11 authors at 2 institutions in 1 country.

G VinothkumarDepartment of Medical Research, SRM Medical College Hospital, SRM University, Chennai, India.
C KedharnathDepartment of Nephrology, SRM Medical College Hospital, SRM University, Chennai, India.
S KrishnakumarDepartment of Nephrology, SRM Medical College Hospital, SRM University, Chennai, India.
S SreedharDepartment of Nephrology, SRM Medical College Hospital, SRM University, Chennai, India.
K PreethikrishnanDepartment of Clinical Psychology, SRM Medical College Hospital, SRM University, Chennai, India.
S DineshDepartment of Clinical Psychology, SRM Medical College Hospital, SRM University, Chennai, India.
A SundaramDepartment of Medical Research, SRM Medical College Hospital, SRM University, Chennai, India.
D BalakrishnanDepartment of Medical Research, SRM Medical College Hospital, SRM University, Chennai, India.
G ShivashekarDepartment of Pathology, SRM Medical College Hospital, SRM University, Chennai, India.
SureshkumarDepartment of Neurology, Balaji Medical College Hospital, Chrompet, Chennai, India.
P VenkataramanDepartment of Medical Research, SRM Medical College Hospital, SRM University, Chennai, India.
SRM University · INSree Balaji Dental College and Hospital · IN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundCognitive dysfunction has been increasingly recognized in chronic kidney disease (CKD) patients. Senile plaques are important pathophysiological characteristic of cognitive dysfunction. The major component of plaques is the amyloid β (Aβ) peptide released from proteolytic cleavage of amyloid precursor protein (APP). Plasma Aβ has been a focus of the growing literature on blood based biomarkers for cognitive dysfunction. Oxidative stress is prevalent in CKD and it plays an important role in cognitive dysfunction. Increased oxidative stress leads to cause cleavage of APP and Aβ production. The aim of this study is to assess the antioxidant status and Aβ

methodsA total of 60 subjects divided into 30 CKD without cognitive dysfunction and 30 CKD with cognitive dysfunction based on neuropsychological assessment tests. To compare antioxidant status and Aβ

resultsLike AD subjects, significantly increased Aβ and LPO level while decreased SOD, CAT, GPx and GSH levels were observed in plasma of CKD patients with cognitive dysfunction when compared to healthy, CKD without cognitive dysfunction and normocytic normochromic anemic subjects.

conclusionResults suggest that elevated plasma oxidative stress and Aβ were seen in CKD patients with cognitive dysfunction may be attributed to pathological changes within the brain.

Indexed as

Amyloid βAPP processingChronic kidney diseaseCognitive dysfunctionOxidative stress

Identifiers

PMID28702365
PMCPMC5491400
OpenAlexW2680611153

What Socratic holds

Textmetadata
LicenceCC BY-NC-ND
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 Socratic graph.