Evidence map›Paper›PMID 36150560›Full record

ReviewFree radical biology & medicine2022

α-Syn overexpression, NRF2 suppression, and enhanced ferroptosis create a vicious cycle of neuronal loss in Parkinson's disease.

Anandhan A, Chen W, Nguyen N, Madhavan L, Dodson M, D D Zhang

Open access · greenAbstract readReview
In one paragraph

Review in Free radical biology & medicine, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.

0numbers the graph read from it
0cells of the map it votes in
20citing papers in PubMed
4.3field-weighted citation impact, top 4% 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

20 citing papers in PubMed, 44 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 1 institution in 1 country.

Anandhan ADepartment of Pharmacology and Toxicology, University of Arizona, Tucson, AZ, USA.
Chen WDepartment of Pharmacology and Toxicology, University of Arizona, Tucson, AZ, USA.
Nguyen NDepartment of Neurology, University of Arizona, Tucson, AZ, USA.
Madhavan LDepartment of Neurology, University of Arizona, Tucson, AZ, USA; Evelyn F McKnight Brain Institute and Bio5 Institute, University of Arizona, Tucson, AZ, USA.
Dodson MDepartment of Pharmacology and Toxicology, University of Arizona, Tucson, AZ, USA. Electronic address: dodson@pharmacy.arizona.edu.
D D ZhangDepartment of Pharmacology and Toxicology, University of Arizona, Tucson, AZ, USA; Arizona Cancer Center, University of Arizona, Tucson, AZ, 85724, USA. Electronic address: dzhang@pharmacy.arizona.edu.
University of Arizona · US

Funding

TRANSPORT OF TRACE METALS IN A POLLUTED AQUIFERP42ES004940 · NIEHS · UNIVERSITY OF ARIZONA · PI Jon D Chorover · 1990 to 2026
$68.1M
NRF Transcription Factors in Environmental Stress and Disease InterventionR35ES031575 · NIEHS · UNIVERSITY OF FLORIDA · PI Donna D Zhang · 2020 to 2026
$7.1M
NIEHS NIH HHS P42 ES004940NIEHS NIH HHS R35 ES031575
6 · The paper itself

Abstract

Parkinson's disease (PD) is the second most common neurodegenerative disorder, affecting millions each year. Most PD cases (∼90%) are sporadic, resulting from the age-dependent accumulation of pathogenic effects. One key pathological hallmark of PD progression is the accumulation of alpha-synuclein (α-syn), which has been shown to negatively affect neuronal function and viability. Here, using 3- and 6-month-old Nrf2

Indexed as

FerroptosisNeurodegenerative DiseasesParkinson Diseasealpha-SynucleinAnimalsHumansInfantMiceNF-E2-Related Factor 2alpha-SynucleinNFE2L2 protein, humanNfe2l2 protein, mouseNF-E2-Related Factor 2agingalpha-synucleinferroptosisNrf2Parkinson's disease

Identifiers

PMID36150560
PMCPMC9841923
OpenAlexW4297877955

What OpenQuestion holds

Textmetadata
LicenceTDM
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.