Evidence map›Paper›PMID 33346659›Full record

ArticleJournal of medicinal chemistry2021

Glycogen Synthase Kinase 3β: A New Gold Rush in Anti-Alzheimer's Disease Multitarget Drug Discovery?

Angela De Simone, Vincenzo Tumiatti, Vincenza Andrisano, Andrea Milelli

Abstract read
In one paragraph

Article in Journal of medicinal chemistry, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 45 papers.

0numbers the graph read from it
0cells of the map it votes in
45citing 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

45 citing papers in PubMed.

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  6. Non-microglial downregulation ofbioRxiv : the preprint server for biology · 2026
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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

4 authors.

Angela De SimoneDepartment of Drug Science and Technology, University of Turin, Via Giuria 9, 10125 Torino, Italy.
Vincenzo TumiattiDepartment for Life Quality Studies, Alma Mater Studiorum-University of Bologna, Corso d' Augusto 237, 47921 Rimini, Italy.
Vincenza AndrisanoDepartment for Life Quality Studies, Alma Mater Studiorum-University of Bologna, Corso d' Augusto 237, 47921 Rimini, Italy.ORCID 0000-0003-4396-1904
Andrea MilelliDepartment for Life Quality Studies, Alma Mater Studiorum-University of Bologna, Corso d' Augusto 237, 47921 Rimini, Italy.ORCID 0000-0003-2285-7403

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Alzheimer's disease (AD), like other multifactorial diseases, is the result of a systemic breakdown of different physiological networks. As result, several lines of evidence suggest that it could be more efficiently tackled by molecules directed toward different dysregulated biochemical targets or pathways. In this context, the selection of targets to which the new molecules will be directed is crucial. For years, the design of such multitarget-directed ligands (MTDLs) has been based on the selection of main targets involved in the "cholinergic" and the "β-amyloid" hypothesis. Recently, there have been some reports on MTDLs targeting the glycogen synthase kinase 3β (GSK-3β) enzyme, due to its appealing properties. Indeed, this enzyme is involved in tau hyperphosphorylation, controls a multitude of CNS-specific signaling pathways, and establishes strict connections with several factors implicated in AD pathogenesis. In the present Miniperspective, we will discuss the reasons behind the development of GSK-3β-directed MTDLs and highlight some of the recent efforts to obtain these new classes of MTDLs as potential disease-modifying agents.

Indexed as

Drug DiscoveryAlzheimer DiseaseGlycogen Synthase Kinase 3 betaHumansPhosphorylationGlycogen Synthase Kinase 3 betaGSK3B protein, human

Identifiers

PMID33346659
PMCPMC8016207

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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.