Evidence map›Paper›PMID 35204286›Full record

ReviewAntioxidants (Basel, Switzerland)2022

CNS Redox Homeostasis and Dysfunction in Neurodegenerative Diseases.

Gundars Goldsteins, Vili Hakosalo, Merja Jaronen, Meike Hedwig Keuters, Šárka Lehtonen, Jari Koistinaho

Open access · goldAbstract readReview
In one paragraph

Review in Antioxidants (Basel, Switzerland), 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 26 papers.

0numbers the graph read from it
0cells of the map it votes in
26citing papers in PubMed
2.8field-weighted citation impact, top 8% 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

26 citing papers in PubMed, 26 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

6 authors at 2 institutions in 1 country.

Gundars GoldsteinsA.I.Virtanen Institute for Molecular Sciences, University of Eastern Finland, 70211 Kuopio, Finland.
Vili HakosaloA.I.Virtanen Institute for Molecular Sciences, University of Eastern Finland, 70211 Kuopio, Finland.
Merja JaronenA.I.Virtanen Institute for Molecular Sciences, University of Eastern Finland, 70211 Kuopio, Finland.
Meike Hedwig KeutersNeuroscience Center, University of Helsinki, 00014 Helsinki, Finland.
Šárka LehtonenA.I.Virtanen Institute for Molecular Sciences, University of Eastern Finland, 70211 Kuopio, Finland.ORCID 0000-0002-5055-9414
Jari KoistinahoA.I.Virtanen Institute for Molecular Sciences, University of Eastern Finland, 70211 Kuopio, Finland.
University of Eastern Finland · FIUniversity of Helsinki · FI

Funding

Academy of Finland 334525
6 · The paper itself

Abstract

A single paragraph of about 200 words maximum. Neurodegenerative diseases (ND), such as Alzheimer's disease, Parkinson's disease, and amyotrophic lateral sclerosis, pose a global challenge in the aging population due to the lack of treatments for their cure. Despite various disease-specific clinical symptoms, ND have some fundamental common pathological mechanisms involving oxidative stress and neuroinflammation. The present review focuses on the major causes of central nervous system (CNS) redox homeostasis imbalance comprising mitochondrial dysfunction and endoplasmic reticulum (ER) stress. Mitochondrial disturbances, leading to reduced mitochondrial function and elevated reactive oxygen species (ROS) production, are thought to be a major contributor to the pathogenesis of ND. ER dysfunction has been implicated in ND in which protein misfolding evidently causes ER stress. The consequences of ER stress ranges from an increase in ROS production to altered calcium efflux and proinflammatory signaling in glial cells. Both pathological pathways have links to ferroptotic cell death, which has been implicated to play an important role in ND. Pharmacological targeting of these pathological pathways may help alleviate or slow down neurodegeneration.

Indexed as

Alzheimer’s diseaseamyotrophic lateral sclerosisendoplasmic reticulum (ER) stressferroptosismitochondrianeuroinflammationParkinson’s diseasereactive oxygen species (ROS)unfolded protein response (UPR)

Identifiers

PMID35204286
PMCPMC8869494
OpenAlexW4213028663

What OpenQuestion holds

Textmetadata
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.