Evidence map›Paper›PMID 37995080›Full record

ReviewMolecular neurobiology2024

Potential Use of the Cholesterol Transfer Inhibitor U18666A as a Potent Research Tool for the Study of Cholesterol Mechanisms in Neurodegenerative Disorders.

Saman Yasamineh, Fatemeh Jabbari Mehrabani, Ehsan Derafsh, Renizo Danihiel Cosimi, Amir Mohammad Karimi Forood, Siamak Soltani, Meead Hadi, Omid Gholizadeh

Abstract readReview
PubMed Publisher
In one paragraph

Review in Molecular neurobiology, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.

0numbers the graph read from it
0cells of the map it votes in
10citing 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

10 citing papers in PubMed.

  1. Article
  2. Review
  3. Review
  4. 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

8 authors.

Saman YasaminehViro & Biotech, Tehran, Iran.
Fatemeh Jabbari MehrabaniDepartment of Nanobiotechnology, Tehran, Iran.
Ehsan DerafshWindsor University School of Medicine, Cayon, Saint Kitts and Nevis.
Renizo Danihiel CosimiBiology, Molecular Research Center, Biology, Santiago, Chile.
Amir Mohammad Karimi ForoodBiomedical Engineering Department, Shahed University, Tehran, Iran.
Siamak SoltaniDepartment of Forensic Medicine, School of Medicine, Iran University of Medical Sciences, Tehran, Iran.
Meead HadiDepartment Of Microbiology, Faculty of Basic Sciences, Tehran Central Branch, Islamic Azad University, Tehran, Iran.
Omid GholizadehViro & Biotech, Tehran, Iran. ogholizade1374@gmail.com.ORCID http://orcid.org/0000-0002-2208-6437

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Cholesterol is an essential component of mammalian cell membranes and a precursor for crucial signaling molecules. The brain contains the highest level of cholesterol in the body, and abnormal cholesterol metabolism links to many neurodegenerative disorders. The results indicate that faulty cholesterol metabolism is a common feature among people living with neurodegenerative conditions. The researchers suggest that restoring cholesterol levels may become a beneficial new strategy in treating certain neurodegenerative conditions. Several neurodegenerative disorders, such as Alzheimer's disease (AD), Niemann-Pick type C (NPC) disease, and Parkinson's disease (PD), have been connected to abnormalities in brain cholesterol metabolism. Consequently, using a lipid research tool is vital to study further and understand the effect of lipids in neurodegenerative disorders such as NPC, AD, PD, and Huntington's disease (HD). U18666A, also known as 3-(2-(diethylamino) ethoxy) androst-5-en-17-one, is a pharmaceutical drug that suppresses cholesterol trafficking and is a well-known class-2 amphiphile. U18666A has performed many functions, allowing for essential discoveries in lipid studies and shedding light on the pathophysiology of neurodegenerative disorders. Additionally, U18666A prevented the downregulation of low-density lipoprotein (LDL) receptors that are induced by LDL and led to the buildup of cholesterol in lysosomes. Numerous studies show that U18666A impacts the function of cholesterol trafficking to control the metabolism and transport of amyloid precursor proteins (APPs). Treating cortical neurons with U18666A may provide a new in vitro model system for studying the underlying molecular process of NPC, AD, HD, and PD. In this article, we review the mechanism and function of U18666A as a vital tool for studying cholesterol mechanisms in neurological diseases related to abnormal cholesterol metabolism, such as AD, NPC, HD, and PD.

Indexed as

AndrostenesCholesterolNeurodegenerative DiseasesAnimalsHumans3-beta-(2-(diethylamino)ethoxy)androst-5-en-17-oneAndrostenesCholesterolAlzheimer’s disease (AD)CholesterolNeurodegenerative diseasesNiemann-Pick type C (NPC) diseaseU18666A

Identifiers

PMID37995080

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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.