Evidence map›Paper›PMID 33057949›Full record

ArticleMolecular neurobiology2021

Relationship Between Genetic Variants of ACAT1 and APOE with the Susceptibility to Dementia (SADEM Study).

Jessica Sarahi Alavez-Rubio, Nancy Martínez-Rodríguez, Jorge Escobedo-de-la-Peña, Osvaldo Garrido-Acosta, Teresa Juárez-Cedillo

Abstract read
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In one paragraph

Article in Molecular neurobiology, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
9citing papers in PubMed, 2 pooled it
0.7field-weighted citation impact, top 29% 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

9 citing papers in PubMed, 2 syntheses or guidelines pooled it, 9 citations in OpenAlex.

  1. Pooled it
  2. Pooled it
  3. Article
  4. Article
  5. Sterol O-Acyltransferase 1 (International journal of molecular sciences · 2024
    Article
  6. Article
  7. Blocking cholesterol storage to treat Alzheimer's disease.Exploration of neuroprotective therapy · 2021
    Article
  8. Article
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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 1 country.

Jessica Sarahi Alavez-RubioUniversidad Nacional Autónoma de México, Mexico City, Mexico.
Nancy Martínez-RodríguezEpidemiology, Endocrinology and Nutrition Research Unit Hospital Infantil de México Federico Gomez Mexico City Mexico Ministry of Health (SSA), Mexico City, Mexico.
Jorge Escobedo-de-la-PeñaUnidad de Investigación en Epidemiológica Clínica, Hospital General Regional Núm. 1 Dr. Carlos Mac Gregor Sánchez Navarro, Instituto Mexicano del Seguro Social, Mexico City, Mexico.
Osvaldo Garrido-AcostaFacultad de Estudios Superiores Zaragoza, Universidad Nacional Autónoma de México, Mexico City, Mexico.
Teresa Juárez-CedilloUnidad de Investigación Epidemiológica y en Servicios de Salud, Área Envejecimiento, Centro Médico Nacional Siglo XXIAQ2 Instituto Mexicano del Seguro Social, Mexico City, Mexico. terezillo@exalumno.unam.mx.ORCID http://orcid.org/0000-0002-9442-3471
Mexican Social Security Institute · MXUniversidad Nacional Autónoma de México · MXHospital Infantil de México Federico Gómez · MX

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

One of the hypotheses that have emerged to explain the origin of dementia relates the disease with altered lipid metabolism, particularly cholesterol. To maintain cholesterol homeostasis, the ACAT1 enzyme has an important function to regulate the production of Aβ. Moreover, APOE is the main cholesterol carrier in the brain, and it has been reported as a risk factor for this disease. This study evaluates the relationship between ACAT1 and APOE genetic variants with susceptibility for the development of Alzheimer's disease and other dementias. We examined four ACAT1 polymorphisms (rs2247071, rs2862616, rs3753526, rs1044925) and two in the APOE gene (rs7412, rs429358) in a group of 204 controls and 196 cases of dementia. Our results show one protective haplotype: CGCA (OR = 0.34, 95% CI = 0.23-0.46; p < 0.001) and one risk haplotype: CGGA (OR = 1.87, 95% CI = 1.34-2.60; p < 0.001) for the development of dementia. Subjects identified as APOE-ε4 allele carriers had a higher risk of developing dementia compared with non-carriers, OR = 13.33 (95% CI = 3.14-56.31). The results support the hypothesis that the ACAT1 gene, together with the APOE gene, plays an important role in susceptibility to the development of dementia and shows genetic characteristics of the Mexican population that can be used to identify the population at risk.

Indexed as

Genetic Predisposition to DiseaseGenetic VariationAgedAged, 80 and overApolipoproteins ECase-Control StudiesDementiaFemaleHaplotypesHeterozygoteHumansLinkage DisequilibriumMalePolymorphism, GeneticSterol O-AcyltransferaseApolipoproteins ESterol O-Acyltransferasesterol O-acyltransferase 1ACAT1APOECholesterolDementiaPolymorphism

Identifiers

PMID33057949
OpenAlexW3092830752

What OpenQuestion holds

Textmetadata
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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.