Evidence map›Paper›PMID 39096284›Full record

ArticleACS chemical neuroscience2024

Repurposing Anidulafungin for Alzheimer's Disease via Fragment-Based Drug Discovery.

Siqi Xie, Yumei Liang, Yang Song, Tingting Li, Jianping Jia

Abstract read
In one paragraph

Article in ACS chemical neuroscience, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
3citing papers in PubMed, 1 pooled it
–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

3 citing papers in PubMed, 1 synthesis or guideline pooled it.

  1. Pooled it
  2. Article
  3. Review
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.

Siqi XieInnovation Center for Neurological Disorders and Department of Neurology, Xuanwu Hospital, Capital Medical University, National Clinical Research Center for Geriatric Diseases, Beijing 100053, P. R. China.
Yumei LiangInnovation Center for Neurological Disorders and Department of Neurology, Xuanwu Hospital, Capital Medical University, National Clinical Research Center for Geriatric Diseases, Beijing 100053, P. R. China.
Yang SongInnovation Center for Neurological Disorders and Department of Neurology, Xuanwu Hospital, Capital Medical University, National Clinical Research Center for Geriatric Diseases, Beijing 100053, P. R. China.
Tingting LiInnovation Center for Neurological Disorders and Department of Neurology, Xuanwu Hospital, Capital Medical University, National Clinical Research Center for Geriatric Diseases, Beijing 100053, P. R. China.
Jianping JiaInnovation Center for Neurological Disorders and Department of Neurology, Xuanwu Hospital, Capital Medical University, National Clinical Research Center for Geriatric Diseases, Beijing 100053, P. R. China.ORCID 0000-0003-4624-0336

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The misfolding and aggregation of beta-amyloid (Aβ) peptides have been implicated as key pathogenic events in the early stages of Alzheimer's disease (AD). Inhibiting Aβ aggregation represents a potential disease-modifying therapeutic approach to AD treatment. Previous studies have identified various molecules that inhibit Aβ aggregation, some of which share common chemical substructures (fragments) that may be key to their inhibitory activity. Employing fragment-based drug discovery (FBDD) methods may facilitate the identification of these fragments, which can subsequently be used to screen new inhibitors and provide leads for further drug development. In this study, we used an in silico FBDD approach to identify 17 fragment clusters that are significantly enriched among Aβ aggregation inhibitors. These fragments were then used to screen anti-infective agents, a promising drug class for repurposing against amyloid aggregation. This screening process identified 16 anti-infective drugs, 5 of which were chosen for further investigation. Among the 5 candidates, anidulafungin, an antifungal compound, showed high efficacy in inhibiting Aβ aggregation in vitro. Kinetic analysis revealed that anidulafungin selectively blocks the primary nucleation step of Aβ aggregation, substantially delaying Aβ fibril formation. Cell viability assays demonstrated that anidulafungin can reduce the toxicity of oligomeric Aβ on BV2 microglia cells. Molecular docking simulations predicted that anidulafungin interacted with various Aβ species, including monomers, oligomers, and fibrils, potentially explaining its activity against Aβ aggregation and toxicity. This study suggests that anidulafungin is a potential drug to be repurposed for AD, and FBDD is a promising approach for discovering drugs to combat Aβ aggregation.

Indexed as

Alzheimer DiseaseAmyloid beta-PeptidesAnidulafunginDrug DiscoveryDrug RepositioningAnimalsEchinocandinsHumansMolecular Docking SimulationPeptide FragmentsAmyloid beta-PeptidesAnidulafunginEchinocandinsPeptide Fragmentsaggregation inhibitorsAlzheimer’s diseaseanidulafunginbeta amyloiddrug repurposingfragment-based drug discovery

Identifiers

PMID39096284
PMCPMC11342299

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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.