Evidence map›Paper›PMID 30056534›Full record

ArticleNeurotoxicity research2019

Eotaxin, an Endogenous Cognitive Deteriorating Chemokine (ECDC), Is a Major Contributor to Cognitive Decline in Normal People and to Executive, Memory, and Sustained Attention Deficits, Formal Thought Disorders, and Psychopathology in Schizophrenia Patients.

Sunee Sirivichayakul, Buranee Kanchanatawan, Supaksorn Thika, André F Carvalho, Michael Maes

Abstract read
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In one paragraph

Article in Neurotoxicity research, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 36 papers.

0numbers the graph read from it
0cells of the map it votes in
36citing papers in PubMed
3.8field-weighted citation impact, top 5% 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

36 citing papers in PubMed, 82 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

5 authors at 3 institutions in 4 countries.

Sunee SirivichayakulFaculty of Medicine, Chulalongkorn University, Bangkok, Thailand.
Buranee KanchanatawanDepartment of Psychiatry, Faculty of Medicine, Chulalongkorn University, Bangkok, Thailand.
Supaksorn ThikaDepartment of Psychiatry, Faculty of Medicine, Chulalongkorn University, Bangkok, Thailand.
André F CarvalhoDepartment of Psychiatry, University of Toronto, Toronto, ON, Canada.
Michael MaesFaculty of Medicine, Chulalongkorn University, Bangkok, Thailand. dr.michaelmaes@hotmail.com.ORCID http://orcid.org/0000-0002-2012-871X
Chulalongkorn University · THBarwon Health · AUCentre for Addiction and Mental Health · CA

Funding

Asahi Glass Foundation NARatchadapiseksompotch Fund, RA60/042
6 · The paper itself

Abstract

Eotaxin is increased in neurodegenerative disorders and schizophrenia, and preclinical studies indicate that eotaxin may induce cognitive deficits. This study aims to examine whether peripheral levels of eotaxin impact cognitive functioning in healthy volunteers and formal thought disorder (FTD) and psychopathology in schizophrenia patients. Serum levels of eotaxin were assayed and cognitive tests were performed on a sample of 40 healthy participants and 80 schizophrenia patients. Among healthy participants, eotaxin levels were significantly associated with episodic/semantic memory, executive functions, Mini Mental State Examination, emotion recognition, and sustained attention. In addition, age-related effects on these cognitive measures were partly mediated by eotaxin. The super-variable "age-eotaxin" predicted a large part of the variance in cognitive functions among healthy participants, and hence, eotaxin may act as an "accelerated brain aging chemokine" (ABAC). In schizophrenia, eotaxin levels had a strong impact on formal thought disorders and psychopathology. In schizophrenia, increased eotaxin strongly impacts memory and sustained attention, which together to a large extent determine FTD. FTD together with memory deficits predicts around 92.5% of the variance in psychopathology. Moreover, the effects of eotaxin are partially mediated by executive functioning, while the effects of male sex on FTD and psychopathology are mediated by eotaxin. In healthy subjects, eotaxin strongly impacts executive functioning and multiple cognitive domains. In schizophrenia, peripheral levels of eotaxin strongly impact both negative symptoms and psychosis (hallucinations and delusions), and these eotaxin effects are mediated by impairments in frontal functioning, memory, sustained attention, and FTD. Eotaxin is an endogenous cognitive deteriorating chemokine (ECDC) and a novel therapeutic target for age-related cognitive decline and schizophrenia as well.

Indexed as

Schizophrenic PsychologyAdolescentAdultAgedAgingBiomarkersCase-Control StudiesChemokine CCL11FemaleHumansMaleMental ProcessesMiddle AgedSchizophreniaYoung AdultBiomarkersCCL11 protein, humanChemokine CCL11CytokinesImmuneInflammationInterleukinNeurocognitionSchizophrenia

Identifiers

PMID30056534
OpenAlexW2884480452

What OpenQuestion holds

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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.