ArticleBiochemistry2010
Hydralazine modifies Aβ fibril formation and prevents modification by lipids in vitro.
Article in Biochemistry, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.
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Who cites it
13 citing papers in PubMed, 31 citations in OpenAlex.
- Hydralazine inhibits cysteamine dioxygenase to treat preeclampsia and senesce glioblastoma.Science advances · 2025Article
- Scars of oxidative stress: protein carbonylation and beta cell dysfunction in diabetes.Frontiers in endocrinology · 2025Review
- Review
- Beyond lecanemab: Examining Phase III potential in Alzheimer's therapeutics.PCN reports : psychiatry and clinical neurosciences · 2024Article
- Mitochondrial dysfunction in neurodegenerative disorders.Neurotherapeutics : the journal of the American Society for Experimental NeuroTherapeutics · 2024Review
- sc2MeNetDrug: A computational tool to uncover inter-cell signaling targets and identify relevant drugs based on single cell RNA-seq data.PLoS computational biology · 2024Article
- Roles of Oxidative Stress in Synaptic Dysfunction and Neuronal Cell Death in Alzheimer's Disease.Antioxidants (Basel, Switzerland) · 2023Review
- Exploring Molecular Targets for Mitochondrial Therapies in Neurodegenerative Diseases.International journal of molecular sciences · 2023Review
- Hydralazine Revives Cellular and Ocular Lens Health-Span by Ameliorating the Aging and Oxidative-Dependent Loss of the Nrf2-Activated Cellular Stress Response.Antioxidants (Basel, Switzerland) · 2023Article
- Molecular Mechanisms and Genetics of Oxidative Stress in Alzheimer's Disease.Journal of Alzheimer's disease : JAD · 2019Review
- Hydralazine Protects Nigrostriatal Dopaminergic Neurons From MPPFrontiers in neurology · 2019Article
- Hydralazine induces stress resistance and extends C. elegans lifespan by activating the NRF2/SKN-1 signalling pathway.Nature communications · 2017Article
- Small molecule screening in context: lipid-catalyzed amyloid formation.Protein science : a publication of the Protein Society · 2014Article
Corrections and comments
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Authors and funding
9 authors at 1 institution in 1 country.
Funding
Abstract
Lipid oxidative damage and amyloid β (Aβ) misfolding contribute to Alzheimer's disease (AD) pathology. Thus, the prevention of oxidative damage and Aβ misfolding are attractive targets for drug discovery. At present, no AD drugs approved by the Food and Drug Administration (FDA) prevent or halt disease progression. Hydralazine, a smooth muscle relaxant, is a potential drug candidate for AD drug therapy as it reduces Aβ production and prevents oxidative damage via its antioxidant hydrazide group. We evaluated the efficacy of hydralazine, and related hydrazides, in reducing (1) Aβ misfolding and (2) Aβ protein modification by the reactive lipid 4-hydroxy-2-nonenal (HNE) using transmission electron microscopy and Western blotting. While hydralazine did not prevent Aβ aggregation as measured using the protease protection assay, there were more oligomeric species observed by electron microscopy. Hydralazine prevented lipid modification of Aβ, and Aβ was used as a proxy for classes of proteins which either misfold or are modified by HNE. All of the other hydrazides prevented lipid modification of Aβ and also did not prevent Aβ aggregation. Surprisingly, a few of the compounds, carbazochrome and niclosamide, appeared to augment Aβ formation. Thus, hydrazides reduced lipid oxidative damage, and hydralazine additionally reduced Aβ misfolding. While hydralazine would require specific chemical modifications for use as an AD therapeutic itself (to improve blood brain barrier permeability, reduce vasoactive side effects, and optimization for amyloid inhibition), this study suggests its potential merit for further AD drug development.
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