Evidence map›Paper›PMID 39483494›Full record

ArticleNeuroSci2024

RETRACTED: Cytotoxic Effect of Amyloid-β1-42 Oligomers on Endoplasmic Reticulum and Golgi Apparatus Arrangement in SH-SY5Y Neuroblastoma Cells.

José J Jarero-Basulto, Yadira Gasca-Martínez, Martha C Rivera-Cervantes, Deisy Gasca-Martínez, Nidia Jannette Carrillo-González, Carlos Beas-Zárate, Graciela Gudiño-Cabrera

RetractedAbstract readRetracted Publication
In one paragraph

Article in NeuroSci, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It has been retracted, and should not be counted. Cited by 7 papers.

0numbers the graph read from it
0cells of the map it votes in
7citing papers in PubMed
–field-weighted citation impact
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

7 citing papers in PubMed.

  1. Amyloid-β "Co-assembles" with Coatomer Subunit Delta (δ-COP).The journal of physical chemistry letters · 2026
    Article
  2. Article
  3. Article
  4. Anti-Amyloid Aggregation Effects of Gobaishi (Molecules (Basel, Switzerland) · 2025
    Article
  5. Article
  6. Article
  7. Review
4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

7 authors.

José J Jarero-BasultoCellular Neurobiology Laboratory, Cell and Molecular Biology Department, University Center of Biological and Agricultural Sciences (CUCBA), University of Guadalajara, Zapopan 45220, Mexico; jose.jarero@academicos.udg.mx (J.J.J.-B.); mrivera@academicos.udg.mx (M.C.R.-C.).
Yadira Gasca-MartínezDevelopment and Neural Regeneration Laboratory, Cell and Molecular Biology Department, University Center of Biological and Agricultural Sciences (CUCBA), University of Guadalajara, Zapopan 45220, Mexico; yadira.gasca3953@alumnos.udg.mx (Y.G.-M.); nidia.carrillo@academicos.udg.mx (N.J.C.-G.).
Martha C Rivera-CervantesCellular Neurobiology Laboratory, Cell and Molecular Biology Department, University Center of Biological and Agricultural Sciences (CUCBA), University of Guadalajara, Zapopan 45220, Mexico; jose.jarero@academicos.udg.mx (J.J.J.-B.); mrivera@academicos.udg.mx (M.C.R.-C.).ORCID 0000-0002-7601-6944
Deisy Gasca-MartínezBehavioral Analysis Unit, Neurobiology Institute, Campus UNAM, Juriquilla 76230, Mexico; gasca@inb.unam.mx.ORCID 0000-0001-5794-7383
Nidia Jannette Carrillo-GonzálezDevelopment and Neural Regeneration Laboratory, Cell and Molecular Biology Department, University Center of Biological and Agricultural Sciences (CUCBA), University of Guadalajara, Zapopan 45220, Mexico; yadira.gasca3953@alumnos.udg.mx (Y.G.-M.); nidia.carrillo@academicos.udg.mx (N.J.C.-G.).ORCID 0000-0002-3116-6930
Carlos Beas-ZárateNeurobiotechnology Laboratory, Cell and Molecular Biology Department, University Center of Biological and Agricultural Sciences (CUCBA), University of Guadalajara, Zapopan 45220, Mexico; carlosbeas55@gmail.com.ORCID 0000-0002-2922-2868
Graciela Gudiño-CabreraDevelopment and Neural Regeneration Laboratory, Cell and Molecular Biology Department, University Center of Biological and Agricultural Sciences (CUCBA), University of Guadalajara, Zapopan 45220, Mexico; yadira.gasca3953@alumnos.udg.mx (Y.G.-M.); nidia.carrillo@academicos.udg.mx (N.J.C.-G.).ORCID 0000-0003-3170-6535

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Amyloid-β oligomers are a cytotoxic structure that is key for the establishment of the beginning stages of Alzheimer's disease (AD). These structures promote subcellular alterations that cause synaptic dysfunction, loss of cell communication, and even cell death, generating cognitive deficits. The aim of this study was to investigate the cytotoxic effects of amyloid-β1-42 oligomers (AβOs) on the membranous organelles involved in protein processing: the endoplasmic reticulum (ER) and Golgi apparatus (GA). The results obtained with 10 μM AβOs in SH-SY5Y neuroblastoma cells showed that oligomeric structures are more toxic than monomers because they cause cell viability to decrease as exposure time increases. Survivor cells were analyzed to further understand the toxic effects of AβOs on intracellular organelles. Survivor cells showed morphological alterations associated with abnormal cytoskeleton modification 72-96 h after exposure to AβOs. Moreover, the ER and GA presented rearrangement throughout the cytoplasmic space, which could be attributed to a lack of constitutive protein processing or to previous abnormal cytoskeleton modification. Interestingly, the disorganization of both ER and GA organelles exposed to AβOs is likely an early pathological alteration that could be related to aberrant protein processing and accumulation in AD.

Indexed as

amyloid-βamyloid-β1-42 oligomerscytoskeleton modificationendoplasmic reticulum rearrangementGolgi apparatus rearrangement

Identifiers

PMID39483494
PMCPMC11469764

What Socratic 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 Socratic graph.