Evidence map›Paper›PMID 33536868›Full record

ReviewFrontiers in neuroscience2020

Animal Models of Metabolic Disorders in the Study of Neurodegenerative Diseases: An Overview.

Andreza Fabro de Bem, Rachel Krolow, Hémelin Resende Farias, Victória Linden de Rezende, Daniel Pens Gelain, José Cláudio Fonseca Moreira, João Miguel das Neves Duarte, Jade de Oliveira

Open access · goldAbstract readReview
In one paragraph

Review in Frontiers in neuroscience, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 40 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
40citing papers in PubMed, 1 pooled it
6.5field-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

40 citing papers in PubMed, 1 synthesis or guideline pooled it, 66 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

8 authors at 3 institutions in 2 countries.

Andreza Fabro de BemDepartment of Physiological Sciences, Institute of Biology, University of Brasilia, Brazilia, Brazil.
Rachel KrolowPostgraduate Program in Biological Sciences: Biochemistry, Department of Biochemistry, Institute of Basic Health Sciences, Federal University of Rio Grande do Sul, Porto Alegre, Brazil.
Hémelin Resende FariasPostgraduate Program in Biological Sciences: Biochemistry, Department of Biochemistry, Institute of Basic Health Sciences, Federal University of Rio Grande do Sul, Porto Alegre, Brazil.
Victória Linden de RezendePostgraduate Program in Biological Sciences: Biochemistry, Department of Biochemistry, Institute of Basic Health Sciences, Federal University of Rio Grande do Sul, Porto Alegre, Brazil.
Daniel Pens GelainPostgraduate Program in Biological Sciences: Biochemistry, Department of Biochemistry, Institute of Basic Health Sciences, Federal University of Rio Grande do Sul, Porto Alegre, Brazil.
José Cláudio Fonseca MoreiraPostgraduate Program in Biological Sciences: Biochemistry, Department of Biochemistry, Institute of Basic Health Sciences, Federal University of Rio Grande do Sul, Porto Alegre, Brazil.
João Miguel das Neves DuarteDepartment of Experimental Medical Science, Faculty of Medicine, Lund University, Lund, Sweden.
Jade de OliveiraPostgraduate Program in Biological Sciences: Biochemistry, Department of Biochemistry, Institute of Basic Health Sciences, Federal University of Rio Grande do Sul, Porto Alegre, Brazil.
Universidade Federal do Rio Grande do Sul · BRLund University · SEUniversidade de Brasília · BR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The incidence of metabolic disorders, as well as of neurodegenerative diseases-mainly the sporadic forms of Alzheimer's and Parkinson's disease-are increasing worldwide. Notably, obesity, diabetes, and hypercholesterolemia have been indicated as early risk factors for sporadic forms of Alzheimer's and Parkinson's disease. These conditions share a range of molecular and cellular features, including protein aggregation, oxidative stress, neuroinflammation, and blood-brain barrier dysfunction, all of which contribute to neuronal death and cognitive impairment. Rodent models of obesity, diabetes, and hypercholesterolemia exhibit all the hallmarks of these degenerative diseases, and represent an interesting approach to the study of the phenotypic features and pathogenic mechanisms of neurodegenerative disorders. We review the main pathological aspects of Alzheimer's and Parkinson's disease as summarized in rodent models of obesity, diabetes, and hypercholesterolemia.

Indexed as

Alzheimer’s diseasediabeteshypercholesterolemianeurodegenerationobesityParkinson’s diseaserodent models

Identifiers

PMID33536868
PMCPMC7848140
OpenAlexW3123815017

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.