Evidence map›Paper›PMID 30816118›Full record

ArticleScientific reports2019

Neurological sequel of chronic kidney disease: From diminished Acetylcholinesterase activity to mitochondrial dysfunctions, oxidative stress and inflammation in mice brain.

Muhammed Khairujjaman Mazumder, Rajib Paul, Pallab Bhattacharya, Anupom Borah

Open access · goldAbstract read
In one paragraph

Article in Scientific reports, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 56 papers.

0numbers the graph read from it
0cells of the map it votes in
56citing papers in PubMed
8.8field-weighted citation impact, top 2% 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

56 citing papers in PubMed, 96 citations in OpenAlex.

  1. Review
  2. Transcriptional risk score for chronic kidney disease: relation to Alzheimer's disease.Alzheimer's & dementia : the journal of the Alzheimer's Association · 2026
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  11. Cholinergic system in patients with chronic kidney disease: cognitive and renal implications.Nephrology, dialysis, transplantation : official publication of the European Dialysis and Transplant Association - European Renal Association · 2025
    Review
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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

4 authors at 2 institutions in 1 country.

Muhammed Khairujjaman MazumderCellular and Molecular Neurobiology Laboratory, Department of Life Science and Bioinformatics, Assam University, Silchar - 788011, Assam, India.
Rajib PaulCellular and Molecular Neurobiology Laboratory, Department of Life Science and Bioinformatics, Assam University, Silchar - 788011, Assam, India.
Pallab BhattacharyaDepartment of Pharmacology and Toxicology, National Institute of Pharmaceutical Education and Research (NIPER)-Ahmedabad, Gandhinagar - 382355, Gujarat, India.
Anupom BorahCellular and Molecular Neurobiology Laboratory, Department of Life Science and Bioinformatics, Assam University, Silchar - 788011, Assam, India. anupomborahh@gmail.com.
Assam University · INNational Institute of Pharmaceutical Education and Research · IN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

With increasing prevalence, chronic kidney disease (CKD) has become a global health problem. Due to the retention of uremic toxins, electrolytes and water, and the resultant metabolic disturbances, CKD affects several organs, including the nervous system. Thus, CKD patients suffer from several neurological complications, including dementia, cognitive impairment, motor abnormalities, depression, and mood and sleep disturbances. However, the mechanisms underlying the neurological complications are least elucidated. We have recently reported a highly reproducible mice model of CKD induced by high adenine diet, which exhibited psychomotor behavioral abnormalities and blood-brain barrier disruption. In the present study, using the mice model, we have investigated psycho-motor and cognitive behaviour, and the neurochemical and histopathological alterations in brain relevant to the observed behavioural abnormalities. The results demonstrate global loss of Acetylcholinesterase activity, and decrease in neuronal arborisation and dendritic spine density in discrete brain regions, of the CKD mice. Oxidative stress, inflammation, and mitochondrial dysfunctions were found in specific brain regions of the mice, which have been regarded as the underlying causes of the observed neurochemical and histopathological alterations. Thus, the present study is of immense importance, and has therapeutic implications in the management of CKD-associated neurological complications.

Indexed as

AcetylcholinesteraseAnimalsBrainDisease Models, AnimalInflammationMaleMiceMitochondriaOxidative StressRenal Insufficiency, ChronicAcetylcholinesterase

Identifiers

PMID30816118
PMCPMC6395638
OpenAlexW2918096736

What OpenQuestion holds

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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.